About   Help   FAQ
Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Krastm4Tyj
targeted mutation 4, Tyler Jacks
MGI:2429948
Summary 253 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
ht1
Krastm4Tyj/Kras+ involves: 129S4/SvJae MGI:3716404
cn2
Krastm4Tyj/Krastm4Tyj B6.129S4-Krastm4Tyj MGI:5440073
cn3
Krastm4Tyj/Kras+ B6.129S4-Krastm4Tyj MGI:5304807
cn4
Krastm4Tyj/Kras+ either: (involves: 129S4/SvJae) or (involves: 129S4/SvJae * C3H/HeJ) MGI:4836591
cn5
Krastm4Tyj/Kras+ involves: 129S4/SvJae MGI:3842379
cn6
Krastm4Tyj/Kras+ involves: 129S4/SvJae * C57BL/6 MGI:5528689
cn7
Krastm4Tyj/Kras+ involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5659878
cn8
Krastm4Tyj/Kras+
Tg(TPO-cre)1Shk/0
129.Cg-Krastm4Tyj Tg(Tpo-cre)1Shk MGI:5897670
cn9
Krastm4Tyj/Kras+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
129.Cg-Krastm4Tyj Tg(Tpo-cre)1Shk Ptentm2.1Ppp MGI:5897668
cn10
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
B6.129(Cg)-Krastm4Tyj Ptf1atm1.1(cre)Cvw MGI:3836557
cn11
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
B6.129-Krastm4Tyj Tgfbr2tm1.2Hlm MGI:5304695
cn12
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
B6.Cg-Krastm4Tyj Map2k7tm1.1Twad/Map2k7tm1.2Twad MGI:4948962
cn13
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(MUC1)79.24Gend/0
B6.Cg-Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend MGI:3836556
cn14
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
B6J.Cg-Tg(Tyr-cre/ERT2)13Bos Cdkn2atm2.1Nesh Krastm4Tyj MGI:5752237
cn15
Apctm2Rak/Apctm2Rak
Krastm4Tyj/Kras+
involves: 129 * 129S4/SvJae * C57BL/6J * SJL MGI:5432240
cn16
Krastm4Tyj/Kras+
Tg(Gfap-cre)77.6Mvs/0
involves: 129 * BALB/c * C57BL/6NHsd MGI:4849444
cn17
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trp53tm1Brn/Trp53+
involves: 129 * C57BL/6 * CBA MGI:7736740
cn18
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Trp53tm1Brn/Trp53+
involves: 129 * C57BL/6 * CBA MGI:7736726
cn19
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
involves: 129 * C57BL/6 * CBA MGI:7736747
cn20
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA MGI:7736746
cn21
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308954
cn22
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308963
cn23
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308962
cn24
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308961
cn25
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308959
cn26
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308946
cn27
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
involves: 129 * C57BL/6 * CBA * FVB/N MGI:5308951
cn28
Krastm4Tyj/Kras+
Tg(Scgb1a1-cre)1Kkw/?
involves: 129 * C57BL/6 * FVB/N MGI:3624415
cn29
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Prdm1tm1Clme/Prdm1tm1Clme
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
involves: 129 * C57BL/6NCrl * FVB/N MGI:6296000
cn30
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
involves: 129 * C57BL/6NCrl * FVB/N MGI:6296002
cn31
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129 * FVB/N MGI:3695424
cn32
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129 * FVB/N MGI:3695421
cn33
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129 * FVB/N MGI:3695428
cn34
Albtm1(cre/ERT2)Mtz/Alb+
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae MGI:6256733
cn35
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Trp53tm1Tyj/Trp53tm1Tyj
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6 MGI:4948964
cn36
Krastm4Tyj/Kras+
Raf1tm2Bacc/Raf1tm2Bacc
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5510702
cn37
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716963
cn38
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716966
cn39
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5562914
cn40
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae MGI:3716968
cn41
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7tm1.1Ysun
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5562910
cn42
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:5510703
cn43
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae MGI:4441491
cn44
Krastm4Tyj/Kras+
Krt19tm1(cre/ERT)Ggu/Krt19+
Ptentm2Mak/Ptentm2Mak
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac MGI:6256734
cn45
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Shhtm2(cre/ERT2)Cjt/Shh+
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac MGI:5298088
cn46
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Krt19tm1(cre/ERT)Ggu/Krt19+
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac MGI:5298083
cn47
Hprt1tm1(CAG-BRF1)Gu/Hprt1+
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * 129S7/SvEvBrd * FVB/N MGI:6403693
cn48
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N MGI:6377665
cn49
Cd9tm1c(EUCOMM)Hmgu/Cd9tm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N MGI:6377669
cn50
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N MGI:6377664
cn51
Cd9tm1c(EUCOMM)Hmgu/Cd9tm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N MGI:6377668
cn52
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N MGI:6377671
cn53
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N MGI:6377672
cn54
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441490
cn55
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441492
cn56
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441486
cn57
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N MGI:4441488
cn58
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5528686
cn59
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5559052
cn60
Krastm4Tyj/Kras+
Myod1tm1.1(cre/ERT,TVA)Gcg/Myod1+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5547939
cn61
Krastm4Tyj/Kras+
Lrrc17tm1Nik/Lrrc17+
Srpk2tm1Nik/Srpk2+
Tg(Mx1-cre)1Cgn/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA MGI:4460775
cn62
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Tg(Trp53)bSrn/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA MGI:4948965
cn63
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428898
cn64
Krastm4Tyj/Krastm4Tyj
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:4819844
cn65
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:5428907
cn66
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:6256730
cn67
Krastm4Tyj/Kras+
Ptentm2Mak/Pten+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA MGI:6256732
cn68
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:5486065
cn69
Cdkn2atm2.1Nesh/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835045
cn70
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB MGI:4835041
cn71
Krastm4Tyj/Kras+
Tg(CAG-Bgeo,-tsA58T)T26Ichi/0
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5604750
cn72
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:3776026
cn73
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Gev/Trp53tm1Gev
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5635880
cn74
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N MGI:5659893
cn75
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6N * FVB/N MGI:6377667
cn76
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre/ERT)20Efu/0
involves: 129P2/OlaHsd * 129S4/SvJae * CD-1 MGI:5298084
cn77
Apctm2.1Cip/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:3776028
cn78
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB MGI:4835046
cn79
Cdkn2atm2Brn/Cdkn2atm2Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S4/SvJae * FVB/N MGI:5484548
cn80
Krastm4Tyj/Kras+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Meox2tm1(cre)Sor/Meox2+
involves: 129P2/OlaHsd * 129S4/SvJaeSor * FVB/N MGI:3716399
cn81
Brca2tm1Brn/Brca2tm1Cam
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940096
cn82
Brca2tm1Cam/Brca2tm1Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940102
cn83
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
involves: 129P2/OlaHsd * C57BL/6 * FVB MGI:5486056
cn84
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3695431
cn85
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3695432
cn86
Krastm4Tyj/Krastm4Tyj
Bhlha15tm3(cre/ERT2)Skz/Bhlha15+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3821739
cn87
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4839216
cn88
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:3032576
cn89
Krastm4Tyj/Kras+
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ MGI:4839215
cn90
Bak1tm1Thsn/Bak1tm1Thsn
Baxtm1Sjk/Baxtm2Sjk
Krastm4Tyj/Kras+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5559061
cn91
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/Gt(ROSA)26Sor+
Tg(Flt3-cre)#Ccb/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:6273518
cn92
Gfi1tm5.1(GFI1*)Tmo/Gfi1tm5.1(GFI1*)Tmo
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA MGI:5468269
cn93
Gfi1tm5.1(GFI1*)Tmo/Gfi1+
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA MGI:5468270
cn94
Gfi1tm6.1(GFI1)Tmo/Gfi1tm6.1(GFI1)Tmo
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA MGI:5468271
cn95
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3695569
cn96
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3695567
cn97
Krastm4Tyj/Kras+
Tg(Erbb2*)#Maed/0
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6J MGI:6192639
cn98
Krastm4Tyj/Krastm4Tyj
Ptpn11tm1Gsf/Ptpn11tm1Gsf
Tg(Six3-cre)69Frty/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:6384017
cn99
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3695568
cn100
Krastm4Tyj/Krastm4Tyj
Trim33tm1Los/Trim33tm1Los
Tg(Pdx1-cre)89.1Dam/0
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 * DBA/2 MGI:4355873
cn101
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scribtm1.1Phum
involves: 129S4/SvJae MGI:5638045
cn102
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scrib+
involves: 129S4/SvJae MGI:5638047
cn103
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
involves: 129S4/SvJae MGI:3716965
cn104
Krastm4Tyj/Kras+
Rbl2tm2Tyj/Rbl2tm2Tyj
involves: 129S4/SvJae MGI:3842378
cn105
Krastm4Tyj/Kras+
Ube2sem1Ysun/Ube2sem1Ysun
involves: 129S4/SvJae MGI:7710917
cn106
Dhx33em1Yazh/Dhx33+
Krastm4Tyj/Kras+
involves: 129S4/SvJae MGI:6502114
cn107
Dhx33em1Yazh/Dhx33em1Yazh
Krastm4Tyj/Kras+
involves: 129S4/SvJae MGI:6502111
cn108
Krastm4Tyj/Kras+
Rb1tm3Tyj/Rb1tm3Tyj
involves: 129S4/SvJae MGI:3842377
cn109
Fastm1Ach/Fastm1Ach
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae MGI:5014515
cn110
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae MGI:5014516
cn111
Krastm4Tyj/Kras+
Trp53tm4Att/Trp53tm4Att
involves: 129S4/SvJae MGI:5140101
cn112
Krastm4Tyj/Krastm4Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae MGI:4818400
cn113
Krastm4Tyj/Krastm4Tyj
Tg(Cela1-cre/ERT)1Dam/0
involves: 129S4/SvJae MGI:3821750
cn114
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm3(CAG-luc)Tyj/Gt(ROSA)26Sor+
involves: 129S4/SvJae MGI:3818747
cn115
Krastm4Tyj/Kras+
Tg(Prm-cre)58Og/0
involves: 129S4/SvJae MGI:3716392
cn116
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Scgb1a1-rtTA)1Jaw/0
involves: 129S4/SvJae MGI:4368025
cn117
Gt(ROSA)26Sortm1(RAC1*)Jkis/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
involves: 129S4/SvJae MGI:5437472
cn118
Krastm4Tyj/Kras+
Trp53tm1Lejo/Trp53tm1Lejo
involves: 129S4/SvJae MGI:5441555
cn119
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
involves: 129S4/SvJae MGI:5491219
cn120
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Tg(Cela1-cre/ERT)1Dam/0
involves: 129S4/SvJae MGI:5510699
cn121
Krastm4Tyj/Kras+
Tg(Cela1-cre/ERT)1Dam/0
involves: 129S4/SvJae MGI:5510700
cn122
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae MGI:5510701
cn123
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
involves: 129S4/SvJae MGI:3776023
cn124
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
involves: 129S4/SvJae MGI:3716967
cn125
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Pms2tm2(cre)Lisk/Pms2tm2(cre)Lisk
involves: 129S4/SvJae * 129S4/SvJaeSor MGI:5543250
cn126
Krastm4Tyj/Kras+
Meox2tm1(cre)Sor/Meox2+
involves: 129S4/SvJae * 129S4/SvJaeSor MGI:3716398
cn127
Gt(ROSA)26Sortm1(Notch1)Dam/Gt(ROSA)26Sor+
Krastm4Tyj/Krastm4Tyj
Tg(Cela1-cre/ERT)1Dam/0
involves: 129S4/SvJae * 129S4/SvJaeSor MGI:3821751
cn128
Gt(ROSA)26Sortm1(Notch1)Dam/Gt(ROSA)26Sor+
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6 * CBA MGI:3821752
cn129
Cdkn2atm1.1Gsu/Cdkn2atm1.1Gsu
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6J * FVB/N MGI:5502380
cn130
Krastm4Tyj/Kras+
Krt19tm1(cre/ERT)Ggu/Krt19+
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5298082
cn131
Krastm4Tyj/Kras+
Shhtm2(cre/ERT2)Cjt/Shh+
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5298087
cn132
Krastm4Tyj/Kras+
Stk11tm1.2Rdp/Stk11tm1.2Rdp
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5515885
cn133
Gt(ROSA)26Sortm2(Pik3ca*)Dsa/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae * 129S6/SvEvTac MGI:5510696
cn134
Krastm4Tyj/Kras+
Pik3r2tm1Lca/Pik3r2tm1Lca
involves: 129S4/SvJae * 129S6/SvEvTac MGI:3834444
cn135
Krastm4Tyj/Kras+
Pik3r1tm1Lca/Pik3r1+
Pik3r2tm1Lca/Pik3r2tm1Lca
involves: 129S4/SvJae * 129S6/SvEvTac MGI:3834445
cn136
Krastm4Tyj/Kras+
Pik3r1tm1Lca/Pik3r1tm1Lca
Pik3r2tm1Lca/Pik3r2tm1Lca
involves: 129S4/SvJae * 129S6/SvEvTac MGI:3834443
cn137
Col1a1tm5(tetO-GFP/RNAi:Cdkn2a)Slowe/Col1a1+
Gt(ROSA)26Sortm1(Luc)Kael/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Krastm4Tyj/Kras+
Tg(Scgb1a1-rtTA)1Jaw/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 MGI:4999988
cn138
Krastm4Tyj/Kras+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Tg(Krt1-15-cre/PGR*)22Cot/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL/J MGI:5556259
cn139
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Hmga2tm1.1Mmw/Hmga2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * FVB/N MGI:6295996
cn140
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Vil1-cre)20Syr/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5013409
cn141
Krastm4Tyj/Kras+
Stk11tm1.1Rdp/Stk11tm1.2Rdp
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659881
cn142
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659896
cn143
Krastm4Tyj/Kras+
Stk11tm1.1Rdp/Stk11tm1.1Rdp
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N MGI:5659880
cn144
Gt(ROSA)26Sortm1(Tva)Dsa/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6J MGI:3814193
cn145
Krastm4Tyj/Kras+
Tg(Cdh5-cre/ERT2)1Rha/0
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6NCrl * FVB MGI:7435431
cn146
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N MGI:5502381
cn147
Fgfr3tm4Cxd/Fgfr3+
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N MGI:5141739
cn148
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm1(sb13)Tuv/Gt(ROSA)26Sor+
Tg(Pdx1-cre)6Tuv/0
TgTn(sb-T2/Onc)#Dla/0
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N MGI:5438089
cn149
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Amhr2tm3(cre)Bhr/Amhr2+
involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6 MGI:5432231
cn150
Brf1tm1Arte/Brf1tm1Arte
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * 129S7/SvEvBrd * FVB/N MGI:6403690
cn151
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Tg(CYP19A1-cre)1Jri/0
involves: 129S4/SvJae * 129X1/SvJ * C57BL/6 MGI:5432224
cn152
Ctnnb1tm1Mmt/Ctnnb1tm1Mmt
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * 129X1/SvJ * FVB/N MGI:5790500
cn153
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * 129X1/SvJ * FVB/N MGI:5141743
cn154
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * BALB/c * C57BL/6 MGI:5013916
cn155
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA MGI:3035835
cn156
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA MGI:5013917
cn157
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Gfap-cre)77.6Mvs/0
involves: 129S4/SvJae * BALB/c * C57BL/6NHsd MGI:4849441
cn158
Krastm4Tyj/Kras+
Tg(Tek-cre)12Flv/0
involves: 129S4/SvJae * C3H * C57BL/6 MGI:3716393
cn159
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Scgb1a1-cre)1Tauc/0
involves: 129S4/SvJae * C57BL/6 MGI:4943568
cn160
Krastm4Tyj/Kras+
Siva1tm1.1Att/Siva1tm1.2Att
involves: 129S4/SvJae * C57BL/6 MGI:5659853
cn161
Krastm4Tyj/Kras+
Tg(MUC1)79.24Gend/0
involves: 129S4/SvJae * C57BL/6 MGI:4411919
cn162
Krastm4Tyj/Kras+
Siva1tm1.2Att/Siva1+
involves: 129S4/SvJae * C57BL/6 MGI:5659856
cn163
Krastm4Tyj/Kras+
Plcl1tm1.1Matk/Plcl1tm1.1Matk
involves: 129S4/SvJae * C57BL/6 MGI:5607955
cn164
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
involves: 129S4/SvJae * C57BL/6 MGI:5559056
cn165
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
involves: 129S4/SvJae * C57BL/6 MGI:5528687
cn166
Krastm4Tyj/Kras+
Tg(IVL-cre/ERT2)1Blpn/0
involves: 129S4/SvJae * C57BL/6 MGI:5298090
cn167
Braftm2Cpri/Braf+
Krastm4Tyj/Kras+
involves: 129S4/SvJae * C57BL/6 MGI:5440071
cn168
Diras2em1Gpt/Diras2em1Gpt
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
Ube2ftm1c(EUCOMM)Hmgu/Ube2ftm1c(EUCOMM)Hmgu
involves: 129S4/SvJae * C57BL/6 MGI:7738284
cn169
Krastm4Tyj/Kras+
Ralatm1.2Cjm/Ralatm1.2Cjm
Ralbtm1.1Cjm/Ralbtm1.2Cjm
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5505293
cn170
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * CBA/J MGI:6505552
cn171
Krastm4Tyj/Kras+
Tg(Krt1-15-cre/PGR*)22Cot/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL/J MGI:5556244
cn172
Fbxw7tm1Iken/Fbxw7tm1Iken
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA MGI:6157296
cn173
Fbxw7tm1Iken/Fbxw7+
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA MGI:6157295
cn174
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:5441554
cn175
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3821753
cn176
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:2687206
cn177
Krastm4Tyj/Kras+
Tg(Fabp7-cre,-lacZ)3Gtm/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3810650
cn178
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:5582314
cn179
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA MGI:3695430
cn180
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:2687217
cn181
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:5308806
cn182
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:5308964
cn183
Krastm4Tyj/Kras+
Tg(KRT14-cre/ERT)20Efu/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N MGI:5659911
cn184
Krastm4Tyj/Kras+
Tg(CAG-HPV16E6E7,-luc)#Mspi/0
Tg(KRT14-cre/ERT)20Efu/0
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N * FVB/NJ MGI:5659910
cn185
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
involves: 129S4/SvJae * C57BL/6 * DBA MGI:5428897
cn186
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4355874
cn187
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre)89.1Dam/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4355875
cn188
Braftm1Rima/Braf+
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)1Lru/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4458349
cn189
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5705321
cn190
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5705328
cn191
Krastm4Tyj/Kras+
Tg(Slco1c1-icre/ERT2)1Mash/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB MGI:7435433
cn192
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * C57BL/6 * FVB MGI:4835044
cn193
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm3.1Tyj/Trp53+
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:6505560
cn194
Brca1tm1Thl/Brca1tm2Rjbr
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494465
cn195
Brca1tm1Thl/Brca1tm1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494464
cn196
Brca1tm1Thl/Brca1tm3.1Rjbr
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:5494462
cn197
Gt(ROSA)26Sortm1(MYC/ERT2)Gev/Gt(ROSA)26Sortm1(MYC/ERT2)Gev
Krastm4Tyj/Krastm4Tyj
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:3821936
cn198
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4941337
cn199
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4941336
cn200
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:6505545
cn201
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm3Tyj/Trp53+
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:4940098
cn202
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Zdhhc20em1Jdo/Zdhhc20em1Jdo
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * C57BL/6 * FVB/N MGI:7711290
cn203
Apctm2Rak/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * C57BL/6 * FVB/N * SJL MGI:6505558
cn204
Krastm4Tyj/Kras+
Ube2cem1Gpt/Ube2cem1Gpt
involves: 129S4/SvJae * C57BL/6J MGI:7710915
cn205
Ggctem1.2Smoc/Ggctem1.2Smoc
Krastm4Tyj/Kras+
involves: 129S4/SvJae * C57BL/6J MGI:7261333
cn206
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
involves: 129S4/SvJae * C57BL/6J MGI:4836596
cn207
Deptortm1.2Ysun/Deptortm1.2Ysun
Krastm4Tyj/Kras+
Ube2cem1Gpt/Ube2cem1Gpt
involves: 129S4/SvJae * C57BL/6J MGI:7710919
cn208
Diras2em1Gpt/Diras2em1Gpt
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
involves: 129S4/SvJae * C57BL/6J * C57BL/6JGpt MGI:7738283
cn209
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
Ube2ftm1c(EUCOMM)Hmgu/Ube2ftm1c(EUCOMM)Hmgu
involves: 129S4/SvJae * C57BL/6J * C57BL/6N MGI:7738261
cn210
Chaf1btm2c(EUCOMM)Hmgu/Chaf1b+
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
involves: 129S4/SvJae * C57BL/6J * C57BL/6N * CBA/J MGI:6267351
cn211
Krastm4Tyj/Kras+
Tg(Krt1-15-cre/PGR*)22Cot/0
involves: 129S4/SvJae * C57BL/6J * SJL/J MGI:5298086
cn212
Krastm4Tyj/Kras+
Stk11tm1.1Gne/Stk11tm1.1Gne
involves: 129S4/SvJae * C57BL/6N MGI:5484547
cn213
Krastm4Tyj/Krastm4Tyj
Tg(Cela1-cre/ERT2)1Stof/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3821737
cn214
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
involves: 129S4/SvJae * C57BL/6 * SJL MGI:3821738
cn215
Krastm4Tyj/Kras+
Tg(MMTV-cre)4Mam/0
involves: 129S4/SvJae * FVB MGI:3044680
cn216
Krastm4Tyj/Kras+
Tg(Cdh5-cre/ERT2)1Rha/0
involves: 129S4/SvJae * FVB MGI:7435429
cn217
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
involves: 129S4/SvJae * FVB MGI:4835047
cn218
Krastm4Tyj/Kras+
Rab11fip1tm1.1Jicn/Rab11fip1tm1.1Jicn
Tg(Pdx1-cre)6Tuv/0
Trp53tm2.1Tyj/Trp53+
involves: 129S4/SvJae * FVB/N MGI:6113915
cn219
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Usp9x+
involves: 129S4/SvJae * FVB/N MGI:5438091
cn220
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Y
involves: 129S4/SvJae * FVB/N MGI:5438090
cn221
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
involves: 129S4/SvJae * FVB/N MGI:5494463
cn222
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/?
involves: 129S4/SvJae * FVB/N MGI:3032575
cn223
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * FVB/N MGI:5141742
cn224
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
involves: 129S4/SvJae * FVB/N MGI:3044567
cn225
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
involves: 129S4/SvJae * FVB/N MGI:5141740
cn226
Krastm4Tyj/Kras+
Tg(Tg-cre/ERT2)#Mmcm/0
involves: 129S4/SvJae * FVB/NCr MGI:5780080
cn227
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scribtm1.1Phum
Tg(Pbsn-cre)20Fwan/0
involves: 129S4/SvJae * FVB/NCrl MGI:5300204
cn228
Krastm4Tyj/Kras+
Tg(Pbsn-cre)20Fwan/0
involves: 129S4/SvJae * FVB/NCrl MGI:5300203
cn229
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scrib+
Tg(Pbsn-cre)20Fwan/0
involves: 129S4/SvJae * FVB/NCrl MGI:5300205
cn230
Krastm4Tyj/Kras+
Sftpctm1(cre/ERT2)Blh/Sftpc+
Trp53tm5Tyj/Trp53+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 MGI:5317171
cn231
Krastm4Tyj/Kras+
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
Trp53tm5Tyj/Trp53+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 MGI:5317170
cn232
Krastm4Tyj/Krastm4Tyj
Ugdhtm1.1Xzh/Ugdhtm1.1Xzh
H2az2Tg(Wnt1-cre)11Rth/H2az2+
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * CBA/J MGI:5430385
cn233
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:3695426
cn234
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:3695422
cn235
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N MGI:3695429
cn236
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940100
cn237
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N MGI:4940099
cn238
Epha2tm1Jrui/Epha2tm1Jrui
Krastm4Tyj/Kras+
Trp53tm2.1Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
involves: 129S/SvEv * 129S4/SvJae * FVB/N MGI:6113916
cn239
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182tm1.1Dgk
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704424
cn240
Krastm4Tyj/Kras+
Mapk8tm1Wag/Mapk8+
Mapk9tm1Mka/Mapk9tm1Mka
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:4948963
cn241
Gt(ROSA)26Sortm1(CAG-Mir182)Dgk/Gt(ROSA)26Sortm1(CAG-Mir182)Dgk
Krastm4Tyj/Krastm4Tyj
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704425
cn242
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182+
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:5704427
cn243
Krastm4Tyj/Kras+
Pax7tm2.1(cre/ERT2)Fan/Pax7+
Trp53tm1Brn/Trp53tm1Brn
involves: 129/Sv * 129P2/OlaHsd * 129X1/SvJ * C57BL/6 MGI:5547938
cn244
Pggt1btm1Mbrg/Pggt1btm1Mbrg
Krastm4Tyj/Kras+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714152
cn245
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1b+
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714154
cn246
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:3714153
cn247
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722605
cn248
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722603
cn249
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm3Glo
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR MGI:3722604
cn250
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Krastm4Tyj/Kras+
involves: 129/Sv * 129S4/SvJae * C57BL/6 * FVB/N * SJL MGI:5659895
cn251
Krastm4Tyj/Kras+
Tg(SFTPC-rtTA)5Jaw/0
Tg(tetO-cre)1Jaw/0
involves: 129/Sv * C57BL/6 MGI:3716394
cn252
Krastm4Tyj/Kras+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * C57BL/6 * FVB * ICR MGI:3722600
cn253
Krastm4Tyj/Kras+
Trp53tm3Glo/Trp53+
Tg(KRT5-cre/PGR)1Der/?
involves: 129/Sv * C57BL/6 * FVB * ICR MGI:3722602


Genotype
MGI:3716404
ht1
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• treatment with adenoviral Cre to induce oncogenic Kras expression results in lung tumor development, but causes a lower tumor burden and decreased overall tumor area compared to induced mutants on a Spry2-null background (J:119477)
• 20% and 100% of mice develop lung lesions at 6 weeks and 20 weeks, respectively, post intranasal adenoviral cre administration (J:216266)
• all mice delivered with an adenovirus expressing cre recombinase through nasal inhalation at 8 weeks of age develop lung tumors (J:299900)
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) (J:207982)
• treatment with MLN4924, a small molecular inhibitor of NAE, beginning at 13 weeks after Ad-Cre administration reduces tumor burden, with a reduction in both number of hyperplastic areas and adenomas and size of the tumors (J:207982)
• mice intratracheally administered an adenovirus expressing cre recombinase (Ad-cre) develop multiple lung adenomas (J:333347)
• a few adenocarcinomas develop in mice following Ad-Cre administration (J:207982)
• mice intratracheally administered Ad-cre develop a few adenocarcinomas (J:333347)

respiratory system
• treatment with adenoviral Cre to induce oncogenic Kras expression results in lung tumor development, but causes a lower tumor burden and decreased overall tumor area compared to induced mutants on a Spry2-null background (J:119477)
• 20% and 100% of mice develop lung lesions at 6 weeks and 20 weeks, respectively, post intranasal adenoviral cre administration (J:216266)
• all mice delivered with an adenovirus expressing cre recombinase through nasal inhalation at 8 weeks of age develop lung tumors (J:299900)
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) (J:207982)
• treatment with MLN4924, a small molecular inhibitor of NAE, beginning at 13 weeks after Ad-Cre administration reduces tumor burden, with a reduction in both number of hyperplastic areas and adenomas and size of the tumors (J:207982)
• mice intratracheally administered an adenovirus expressing cre recombinase (Ad-cre) develop multiple lung adenomas (J:333347)
• a few adenocarcinomas develop in mice following Ad-Cre administration (J:207982)
• mice intratracheally administered Ad-cre develop a few adenocarcinomas (J:333347)

mortality/aging
• mice intratracheally administered Ad-cre have a median survival time of approximately 130 days with 100% death by 175 days

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:207982




Genotype
MGI:5440073
cn2
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Genetic
Background
B6.129S4-Krastm4Tyj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• primary mouse embryonic fibroblast treated with adenoviral-cre exhibit enhanced growth rate compared with wild-type cells




Genotype
MGI:5304807
cn3
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
B6.129S4-Krastm4Tyj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 79 days

neoplasm
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction

respiratory system
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop noninvasive adenoma and adenocarcinoma over a 6-10 week period, characterized by epithelial cell proliferation without destruction of alveolar walls or stromal reaction




Genotype
MGI:4836591
cn4
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
either: (involves: 129S4/SvJae) or (involves: 129S4/SvJae * C3H/HeJ)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• after ovarian intrabursal injection of an adenovirus expressing Cre, mutants develop benign ovarian endometriosis-like lesions, however no invasive ovarian tumors are seen up to 10 months following adenoviral injection

growth/size/body
• 47% of mutants develop peritoneal endometriosis following ovarian intrabursal injection of an adenovirus expressing Cre
• however, mice injected with adenovirus expressing Cre directly into the peritoneum do not develop peritoneal endometriosis

reproductive system
• after ovarian intrabursal injection of an adenovirus expressing Cre, mutants develop benign ovarian endometriosis-like lesions, however no invasive ovarian tumors are seen up to 10 months following adenoviral injection

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
endometriosis DOID:289 J:96296




Genotype
MGI:3842379
cn5
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median life span of cre adenovirus-treated mice is 32 weeks

neoplasm
• tumors from cre adenovirus-treated mice exhibit increased cell proliferation compared to in tumors from Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice
• cre adenovirus-treated mice develop smaller tumors than in cre adenovirus-treated Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice
• mice treated with adenovirus cre develop lung lesions in 4 to 6 months (J:147590)
• cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia (J:147590)
• cre adenovirus-treated mice develop fewer tumors than in Krastm4Tyj/Kras+ Rb1tm3Tyj/Rb1tm3Tyj mice (J:147590)
• large tumors easily visible on the surface of the lungs at eight weeks after Cre-adenovirus treatment (J:158937)
• presence of atypical adenomatous hyperplasia after Cre-adenovirus treatment
• the most common lesion is adenocarcinoma after Cre-adenovirus treatment
• in cre adenovirus-treated mice

respiratory system
• mice treated with adenovirus cre develop lung lesions in 4 to 6 months (J:147590)
• cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia (J:147590)
• cre adenovirus-treated mice develop fewer tumors than in Krastm4Tyj/Kras+ Rb1tm3Tyj/Rb1tm3Tyj mice (J:147590)
• large tumors easily visible on the surface of the lungs at eight weeks after Cre-adenovirus treatment (J:158937)
• presence of atypical adenomatous hyperplasia after Cre-adenovirus treatment
• the most common lesion is adenocarcinoma after Cre-adenovirus treatment
• in cre adenovirus-treated mice
• in cre adenovirus-treated mice
• cre adenovirus-treated mice develop bronchiolar hyperplasia and dysplasia unlike wild-type mice
• in cre adenovirus-treated mice
• presence of epithelial hyperplasia after Cre-adenovirus treatment

immune system
• following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice

hematopoietic system
• following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice

reproductive system
• following injection of a cre adenovirus in the ovarian bursa, mice develop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Krastm4Tyj micefollowing injection of a cre adenovirus in the ovarian bursa, mice develop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Krastm4Tyj mice




Genotype
MGI:5528689
cn6
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus

respiratory system
• lung adenocarcinomas cover 11% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:203686




Genotype
MGI:5659878
cn7
Allelic
Composition
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a median survival of 24 weeks after ad-cre inoculation

neoplasm
• mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness
• all tumors of ad-cre inoculated mice are adenocarincomas
• metastasis or local invasion is not seen in ad-cre inoculated mice

respiratory system
• mice inoculated with ad-cre by inhalation develop lung tumors with high multiplicity, long latency, and low aggressiveness
• all tumors of ad-cre inoculated mice are adenocarincomas
• metastasis or local invasion is not seen in ad-cre inoculated mice




Genotype
MGI:5897670
cn8
Allelic
Composition
Krastm4Tyj/Kras+
Tg(TPO-cre)1Shk/0
Genetic
Background
129.Cg-Krastm4Tyj Tg(Tpo-cre)1Shk
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(TPO-cre)1Shk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• mice are indistinguishable from wild-type mice and show no alterations of the thyroid gland




Genotype
MGI:5897668
cn9
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(TPO-cre)1Shk/0
Genetic
Background
129.Cg-Krastm4Tyj Tg(Tpo-cre)1Shk Ptentm2.1Ppp
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Tg(TPO-cre)1Shk mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% of mice die within 7 weeks from birth and none survive over 4 months of age
• treatment with LY294002, an inhibitor of PI3K, twice a week starting at 3 weeks of age prolongs survival of mice

endocrine/exocrine glands
• mice develop thyroids 200- to 500-fold larger than controls
• mice rapidly develop thyroid follicular carcinomas
• 30-90% of the thyroid glands are replaced by microfollicular to solid areas, indicating thyroid follicular cancer, including capsular, muscle, and vascular invasion

homeostasis/metabolism

neoplasm
• mice rapidly develop thyroid follicular carcinomas
• 30-90% of the thyroid glands are replaced by microfollicular to solid areas, indicating thyroid follicular cancer, including capsular, muscle, and vascular invasion
• all mice surviving at least 12 weeks develop thyroglobulin-positive lung metastases




Genotype
MGI:3836557
cn10
Allelic
Composition
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
B6.129(Cg)-Krastm4Tyj Ptf1atm1.1(cre)Cvw
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• pancreatic tumors exhibit higher proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes
• at 34 weeks of age, 4 of 10 mice develop metastasis to the lung and liver compared to 6 of 10 metastasis at 48 weeks in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes

endocrine/exocrine glands
• pancreatic weight is greater than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes
• pancreatic tumors exhibit higher proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes

growth/size/body
• pancreatic weight is greater than in Krastm4Tyj Ptf1atm1.1(cre)Cvw heterozygotes




Genotype
MGI:5304695
cn11
Allelic
Composition
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
Genetic
Background
B6.129-Krastm4Tyj Tgfbr2tm1.2Hlm
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tgfbr2tm1.2Hlm mutation (0 available); any Tgfbr2 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase have a median survival of 43 days

neoplasm
• tumors of Cre adenoviral treated mutants show transmural invasion of vessels and pleural invasion, and regional metastases to mediastinal lymph nodes
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop tumors similar to human mixed subtype adenocarcinomas; they show progression of a pure noninvasive lung adenocarcinoma to an adenocarcinoma with mixed invasive morphology and metastatic potential
• tumors of mutants treated with Cre adenovirus show evidence of inflammatory cell recruitment and tumor microenvironment remodeling with neoangiogenesis not seen in homozygous cre adenovirus treated Krastm4Tyj mice

hematopoietic system
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit and increase in B cells in the lungs compared to homozygous cre adenovirus treated Krastm4Tyj mice
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit and increase in T cells in the lungs compared to homozygous cre adenovirus treated Krastm4Tyj mice
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit a lower myeloid cell population in the lungs than controls

immune system
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit and increase in B cells in the lungs compared to homozygous cre adenovirus treated Krastm4Tyj mice
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit and increase in T cells in the lungs compared to homozygous cre adenovirus treated Krastm4Tyj mice
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase exhibit a lower myeloid cell population in the lungs than controls

respiratory system
• mutants with an intranasal instillation of an adenovirus expressing Cre recombinase develop tumors similar to human mixed subtype adenocarcinomas; they show progression of a pure noninvasive lung adenocarcinoma to an adenocarcinoma with mixed invasive morphology and metastatic potential
• tumors of mutants treated with Cre adenovirus show evidence of inflammatory cell recruitment and tumor microenvironment remodeling with neoangiogenesis not seen in homozygous cre adenovirus treated Krastm4Tyj mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:177379




Genotype
MGI:4948962
cn12
Allelic
Composition
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Genetic
Background
B6.Cg-Krastm4Tyj Map2k7tm1.1Twad/Map2k7tm1.2Twad
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Map2k7tm1.1Twad mutation (0 available); any Map2k7 mutation (20 available)
Map2k7tm1.2Twad mutation (0 available); any Map2k7 mutation (20 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

neoplasm
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice

cellular
• following adenovirus cre infection, mice exhibit impaired DNA damage response compared with control mice

homeostasis/metabolism
• following adenovirus cre infection, mice exhibit impaired DNA damage response compared with control mice

respiratory system
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice




Genotype
MGI:3836556
cn13
Allelic
Composition
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Tg(MUC1)79.24Gend/0
Genetic
Background
B6.Cg-Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tg(MUC1)79.24Gend mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• pancreatic tumors exhibit lower proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend heterozygotes (J:138959)
• mice exhibit carcinoma in situ in the pancreas (J:234412)
• mice exhibit high-grade PanIN lesions and carcinoma in situ, associated with disorganized glandular epithelium (J:234412)
• mice treated with gemcitabine exhibit normal pancreatic glandular structure 26 weeks after the beginning of treatment (J:234412)
• at 48 weeks, 6 of 10 mice develop metastasis to the lung and liver compared to 4 of 10 metastasis at 34 weeks of age in Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend heterozygotes

endocrine/exocrine glands
• pancreatic tumors exhibit lower proliferation rates than in Krastm4Tyj Ptf1atm1.1(cre)Cvw Tg(MUC1)79.24Gend heterozygotes (J:138959)
• mice exhibit carcinoma in situ in the pancreas (J:234412)
• mice exhibit high-grade PanIN lesions and carcinoma in situ, associated with disorganized glandular epithelium (J:234412)
• mice treated with gemcitabine exhibit normal pancreatic glandular structure 26 weeks after the beginning of treatment (J:234412)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
adenoma DOID:657 J:138959
pancreatic carcinoma DOID:4905 OMIM:260350
J:234412




Genotype
MGI:5752237
cn14
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
B6J.Cg-Tg(Tyr-cre/ERT2)13Bos Cdkn2atm2.1Nesh Krastm4Tyj
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
pigmentation
• mice treated with 4-hydroxytamoxifen (4-OHT) neonatally exhibit the presence of nevi and hyperpigmented regions on the paws and tails

integument
• mice treated with 4-OHT neonatally develop melanoma with 76% penetrance and a median latency of 36.3 weeks
• melanomas contain both spindle-cell and desmoplastic cell types with no overt signs of macrometastatic spread

neoplasm
• mice treated with 4-OHT neonatally develop melanoma with 76% penetrance and a median latency of 36.3 weeks
• melanomas contain both spindle-cell and desmoplastic cell types with no overt signs of macrometastatic spread

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
skin melanoma DOID:8923 OMIM:608035
OMIM:612263
J:220627




Genotype
MGI:5432240
cn15
Allelic
Composition
Apctm2Rak/Apctm2Rak
Krastm4Tyj/Kras+
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Rak mutation (1 available); any Apc mutation (158 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 36% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are carcinomas
• 20% of mutants injected with an adenovirus expressing cre recombinase in the distal colon to inactivate Apc exhibit spontaneous gross liver metastases starting 24 weeks after adenoviral injection; these lesions are adenocarcinomas
• 96% of mutants injected with an adenovirus expressing cre recombinase in the distal colon to inactivate Apc develop distal colonic tumors as little as 3 weeks after viral administration
• rapamycin treatment of mutants with tumors does not result in tumor regression
• 64% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are adenomas

digestive/alimentary system
• 64% of tumors that develop in mutant colons injected with an adenovirus expressing cre recombinase are adenomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
colorectal cancer DOID:9256 OMIM:114500
J:156532




Genotype
MGI:4849444
cn16
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Gfap-cre)77.6Mvs/0
Genetic
Background
involves: 129 * BALB/c * C57BL/6NHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Gfap-cre)77.6Mvs mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mutants do not develop tumors




Genotype
MGI:7736740
cn17
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop pancreatic cancer
• all pancreata of 7-month old mice are replaced by aggressive pancreatic ductal adenocarcinoma with lung and liver metastasis
• circulating pancreatic neoplastic cells are increased in the blood of mice harboring pancreatic adenocarcinoma
• 100% of 3-month old mice exhibit abundant acinar-ductal metaplasia and low- and high-grade pancreatic intraepithelial neoplasia (PanIN) lesions

mortality/aging
• average survival is 5.2 +/- 1.2 months

endocrine/exocrine glands
• mice develop pancreatic cancer
• all pancreata of 7-month old mice are replaced by aggressive pancreatic ductal adenocarcinoma with lung and liver metastasis
• circulating pancreatic neoplastic cells are increased in the blood of mice harboring pancreatic adenocarcinoma
• 100% of 3-month old mice exhibit abundant acinar-ductal metaplasia and low- and high-grade pancreatic intraepithelial neoplasia (PanIN) lesions
• 100% of 3-month old mice exhibit abundant acinar-ductal metaplasia and low- and high-grade pancreatic intraepithelial neoplasia (PanIN) lesions
• circulating pancreatic neoplastic cells are increased in the blood of mice harboring PanI




Genotype
MGI:7736726
cn18
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trim29tm1c(EUCOMM)Wtsi mutation (0 available); any Trim29 mutation (28 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• 73.3% of 3-month old and 75% of 12-month old mice show normal pancreas
• although 26.7% of 3-month old and 25% of 12-month old mice show rare acinar-ductal metaplasia and low-grade pancreatic intraepithelial neoplasia (PanIN1) lesions, these lesions express TRIM29 due to incomplete recombination of the floxed allele

mortality/aging
N
• all mice are alive at 12 months




Genotype
MGI:7736747
cn19
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Trim29tm1c(EUCOMM)Wtsi/Trim29tm1c(EUCOMM)Wtsi
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trim29tm1c(EUCOMM)Wtsi mutation (0 available); any Trim29 mutation (28 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• mice with cerulein-induced acute pancreatitis show reversion of acinar-ductal metaplasia lesions to normal acinar morphology after 7 days of recovery as in wild-type mice
• primary pancreatic acinar cells from 1.5-month-old mice grown in 3D collagen culture show attenuated KRAStm4Tyj-induced acinar cell transdifferentiation and acinar-ductal metaplasia formation

neoplasm
• primary pancreatic acinar cells from 1.5-month-old mice grown in 3D collagen culture show attenuated KRAStm4Tyj-induced acinar cell transdifferentiation and acinar-ductal metaplasia formation




Genotype
MGI:7736746
cn20
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• primary pancreatic acinar cells from 1.5-month-old mice grown in 3D collagen culture undergo acinar-ductal metaplasia, forming large duct-like structures, indicating induction of acinar-to-ductal transdifferentiation
• mice with cerulein-induced acute pancreatitis do not show reversion of acinar-ductal metaplasia lesions to normal acinar morphology as in wild-type mice and show complete replacement of pancreatic tissue with fibrosis, infiltration of inflammatory cells, widespread acinar-ductal metaplasia/ pancreatic intraepithelial neoplasia (PanIN) lesions with loss of amylase-expressing acinar tissue, and maintain a small and persistent fraction of apoptotic cells

immune system
• mice with cerulein-induced acute pancreatitis do not show reversion of acinar-ductal metaplasia lesions to normal acinar morphology as in wild-type mice and show complete replacement of pancreatic tissue with fibrosis, infiltration of inflammatory cells, widespread acinar-ductal metaplasia/ pancreatic intraepithelial neoplasia (PanIN) lesions with loss of amylase-expressing acinar tissue, and maintain a small and persistent fraction of apoptotic cells




Genotype
MGI:5308954
cn21
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop pancreatic tumors with an average latency of 7.2 weeks
• 60% of tumors exhibit anaplastic carcinoma histology
• 40% of tumors exhibit well differentiated ductal adenocarcinoma histology
• 20% of tumors exhibit metastasis

endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 7.2 weeks
• 60% of tumors exhibit anaplastic carcinoma histology
• 40% of tumors exhibit well differentiated ductal adenocarcinoma histology

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:108298




Genotype
MGI:5308963
cn22
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop pancreatic tumors with an average latency of 18.3 weeks
• 100% of tumors are sarcomatoid in histology
• 33% of tumors exhibit metastasis

endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 18.3 weeks
• 100% of tumors are sarcomatoid in histology




Genotype
MGI:5308962
cn23
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop pancreatic tumors with an average latency of 13.1 weeks
• 25% of tumors exhibit sarcomatoid carcinoma histology
• 75% of tumors exhibit well differentiated ductal adenocarcinoma histology
• 25% of tumors exhibit metastasis

endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 13.1 weeks
• 25% of tumors exhibit sarcomatoid carcinoma histology
• 75% of tumors exhibit well differentiated ductal adenocarcinoma histology

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:108298




Genotype
MGI:5308961
cn24
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop pancreatic tumors with an average latency of 14.7 weeks
• 19% of tumors exhibit sarcomatoid differentiation
• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology
• 25% of tumors exhibit metastasis

endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 14.7 weeks
• 19% of tumors exhibit sarcomatoid differentiation
• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology




Genotype
MGI:5308959
cn25
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop pancreatic tumors with an average latency of 21.8 weeks
• 100% of tumors are well differentiated ductal adenocarcinomas
• 33% of tumors exhibit metastasis

endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 21.8 weeks
• 100% of tumors are well differentiated ductal adenocarcinomas




Genotype
MGI:5308946
cn26
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop pancreatic tumors with an average latency of 6.2 weeks
• mutants exhibit rapid pancreatic ductal adenocaracinoma progression, developing lethal tumors by 8 weeks of age
• 100% of tumors are well differentiated ductal adenocarcinomas

endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 6.2 weeks
• mutants exhibit rapid pancreatic ductal adenocaracinoma progression, developing lethal tumors by 8 weeks of age
• 100% of tumors are well differentiated ductal adenocarcinomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:108298




Genotype
MGI:5308951
cn27
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129 * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop pancreatic tumors with an average latency of 6.5 weeks
• 20% of tumors exhibit anaplastic carcinoma histology
• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology

endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 6.5 weeks
• 20% of tumors exhibit anaplastic carcinoma histology
• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:108298




Genotype
MGI:3624415
cn28
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Scgb1a1-cre)1Kkw/?
Genetic
Background
involves: 129 * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Scgb1a1-cre)1Kkw mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• early mortality with a median survival of 8 weeks

neoplasm
• progressive phenotype characterized by cellular atypia, adenoma, and ultimately adenocarcinoma in CC10 positive cells of bronchial epithelia

immune system
• a robust inflammatory response characterized by an abundant infiltration of alveolar macrophages and neutrophils

respiratory system
• progressive phenotype characterized by cellular atypia, adenoma, and ultimately adenocarcinoma in CC10 positive cells of bronchial epithelia




Genotype
MGI:6296000
cn29
Allelic
Composition
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Prdm1tm1Clme/Prdm1tm1Clme
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
Genetic
Background
involves: 129 * C57BL/6NCrl * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (4 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Prdm1tm1Clme mutation (1 available); any Prdm1 mutation (66 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice exhibit a similar overall pancreatic tumor burden as KPCT (Krastm4Tyj/Kras+ Trp53tm2Tyj/Trp53+ Tg(Pdx1-cre)6Tuv/0 Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+) mice
• pancreas contains PanINs and adenocarcinoma that are similar to pancreatic ductal adenocarcinoma (PDAC) in KPCT mice
• only 3 of 14 mice develop metastases, with only half of mice showing peritoneal disseminated tumor cells
• cancer cells exhibit a higher mitotic index than KPCT mice
• pancreas contains PanINs and adenocarcinoma that are similar to PDAC in KPCT mice

mortality/aging
• mice exhibit a shorter survival than KPCT mice

endocrine/exocrine glands
• mice exhibit a similar overall pancreatic tumor burden as KPCT (Krastm4Tyj/Kras+ Trp53tm2Tyj/Trp53+ Tg(Pdx1-cre)6Tuv/0 Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+) mice
• pancreas contains PanINs and adenocarcinoma that are similar to pancreatic ductal adenocarcinoma (PDAC) in KPCT mice
• only 3 of 14 mice develop metastases, with only half of mice showing peritoneal disseminated tumor cells
• cancer cells exhibit a higher mitotic index than KPCT mice
• pancreas contains PanINs and adenocarcinoma that are similar to PDAC in KPCT mice




Genotype
MGI:6296002
cn30
Allelic
Composition
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
Genetic
Background
involves: 129 * C57BL/6NCrl * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (4 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• pancreas contains PanINs and adenocarcinoma
• pancreas contains PanINs and adenocarcinoma

neoplasm
• pancreas contains PanINs and adenocarcinoma
• pancreas contains PanINs and adenocarcinoma
• most mice develop metastases which are numerous and widespread in many different sites, including the lymph nodes, diaphragm, lungs, and liver
• all mice exhibit peritoneal disseminated tumor cells




Genotype
MGI:3695424
cn31
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 12 of 13 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4

mortality/aging
• average tumor-free survival is 14 weeks

neoplasm
• 5 of 13 mice develop intraductal papillary mucinous neoplasms
• tumor fibrosis is increased compared to mice wild-type for Smad4
• 12 of 13 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4




Genotype
MGI:3695421
cn32
Allelic
Composition
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• seen in all mice

mortality/aging
• mice die between 8 and 24 weeks of age
• average tumor-free survival is 15.7 weeks

neoplasm
• 12 of 12 mice develop intraductal papillary mucinous neoplasms
• 2 of 12 mice develop pancreatic ductal adenocarcinoma

endocrine/exocrine glands
• 2 of 12 mice develop pancreatic ductal adenocarcinoma
• seen in all mice




Genotype
MGI:3695428
cn33
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 4 of 4 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4
• tumor fibrosis is increased compared to mice wild-type for Smad4

mortality/aging
• average tumor-free survival is 8.8 weeks

neoplasm
• 4 of 4 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4
• tumor fibrosis is increased compared to mice wild-type for Smad4




Genotype
MGI:6256733
cn34
Allelic
Composition
Albtm1(cre/ERT2)Mtz/Alb+
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Albtm1(cre/ERT2)Mtz mutation (2 available); any Alb mutation (97 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm2Mak mutation (4 available); any Pten mutation (88 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma
• mice injected with tamoxifen at 8 weeks after birth develop multiple liver tumors that are all hepatocellular carcinoma and hepatocellular dysplasia, but not intrahepatic cholangiocarcinoma

liver/biliary system
• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma
• mice injected with tamoxifen at 8 weeks after birth develop multiple liver tumors that are all hepatocellular carcinoma and hepatocellular dysplasia, but not intrahepatic cholangiocarcinoma

endocrine/exocrine glands
• mice injected with tamoxifen at P10 develop liver tumors that are exclusively intrahepatic cholangiocarcinoma




Genotype
MGI:4948964
cn35
Allelic
Composition
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Trp53tm1Tyj/Trp53tm1Tyj
Genetic
Background
involves: 129P2/OlaHsd * 129S2/SvPas * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Map2k7tm1.1Twad mutation (0 available); any Map2k7 mutation (20 available)
Map2k7tm1.2Twad mutation (0 available); any Map2k7 mutation (20 available)
Trp53tm1Tyj mutation (12 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice
• however, tumorigenesis is the same as in Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice
• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice

respiratory system
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice
• however, tumorigenesis is the same as in Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice
• following adenovirus cre infection, mice exhibit more adenocarcinomas than Map2k7tm1.1Twad/Map2k7tm1.2Twad Krastm4Tyj/Kras+ mice




Genotype
MGI:5510702
cn36
Allelic
Composition
Krastm4Tyj/Kras+
Raf1tm2Bacc/Raf1tm2Bacc
Ptf1atm1(cre)Hnak/Ptf1a+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (31 available)
Raf1tm2Bacc mutation (2 available); any Raf1 mutation (117 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• as in Krastm4Tyj Ptf1atm1(cre)Hnak double heterozygotes

endocrine/exocrine glands
• as in Krastm4Tyj Ptf1atm1(cre)Hnak double heterozygotes




Genotype
MGI:3716963
cn37
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following cre-adenovirus treatment, all mice develop primary lung tumors
• following cre-adenovirus treatment, lung tumors resemble those found in Krastm4Tyj heterozygotes
• following cre-adenovirus treatment, tumors occupy 24% of lung space
• at 6 weeks following cre-adenovirus treatment, mice have lesions ranging from atypical adenomatous hyperplasia to small adenomas that are smaller than in Krastm4Tyj Trp53tm1Brn homozygotes

respiratory system
• following cre-adenovirus treatment, all mice develop primary lung tumors
• following cre-adenovirus treatment, lung tumors resemble those found in Krastm4Tyj heterozygotes
• following cre-adenovirus treatment, tumors occupy 24% of lung space
• at 6 weeks following cre-adenovirus treatment, mice have lesions ranging from atypical adenomatous hyperplasia to small adenomas that are smaller than in Krastm4Tyj Trp53tm1Brn homozygotes




Genotype
MGI:3716966
cn38
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• at 19 weeks following cre-adenovirus treatment, sinonasal adenocarninomas develop in 64% of mice
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes

respiratory system
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes




Genotype
MGI:5562914
cn39
Allelic
Composition
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Rnf7Gt(XE423)Byg mutation (0 available); any Rnf7 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of Ad-Cre treated mice is 27.6 weeks, with all mice dying by 33 weeks

neoplasm
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre)
• a few adenocarcinomas develop in mice following Ad-Cre administration

respiratory system
• mice develop lung adenomas with a few adenocarcinomas following intratracheal administration of an adenovirus expressing Cre (Ad-Cre)
• a few adenocarcinomas develop in mice following Ad-Cre administration




Genotype
MGI:3716968
cn40
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following cre-adenovirus treatment, a subset of tumors are highly invasive and grow into the hilus, heart, and overlying pleura
• following cre-adenovirus treatment, lymph node metastases are present in over 50% of mice
• at 19 weeks following cre-adenovirus treatment, sinonasal adenocarninomas develop in 14% of mice
• mice infected with low-titre (5X103) lentiviruses expressing Cre and Nfkbia have either a single lung adenocarcinoma or none at all
• mice infected with high-titre (5X104) lentiviruses expressing Cre and Nfkbia have 6-22 lung adenocarcinomas detected per mouse
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes
• at 6 weeks following cre-adenovirus treatment, mice have lesions ranging from atypical adenomatous hyperplasia to small adenomas that are larger than in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus (J:203686)
• following cre-adenovirus treatment, all mice develop advanced pulmonary adenocarinomas (J:103407)
• following cre-adenovirus treatment, multiple tumors are present ranging from well-defined tumors to advanced highly dysplastic lesions containing large sheets of dysplastic cells, abnormal mitoses, and multinucleated giant cells (J:103407)
• seventeen weeks after infection with low-titre (5X103) cre lentiviruses, an average of 30 lung adenocarcinomas are detected per mouse (J:154041)
• seventeen weeks after infection with high-titre (5X104) cre lentiviruses, 90-131 lung adenocarcinomas are detected per mouse (J:154041)
• mice develop multiple, aggressive adenocarcinomas in the lungs bilaterally following intranasal delivery of an adenovirus expressing Cre recombinase (J:195492)
• tumor growth is reduced to a similar extent following either two 7.3 Gy fractions of radiation therapy or a single 11.6 Gy fraction (J:195492)
• tumors incorporate high levels of BrdU 4 hours after radiation treatment similarly to unirradiated tumors, indicating lack of an intact G1 cell-cycle checkpoint (J:195492)

mortality/aging
• mice do not survive to 26 weeks post cre-adenovirus treatment in contrast to Krastm4Tyj Trp53tm1Brn heterozygous mice

respiratory system
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes
• at 6 weeks following cre-adenovirus treatment, mice have lesions ranging from atypical adenomatous hyperplasia to small adenomas that are larger than in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus (J:203686)
• following cre-adenovirus treatment, all mice develop advanced pulmonary adenocarinomas (J:103407)
• following cre-adenovirus treatment, multiple tumors are present ranging from well-defined tumors to advanced highly dysplastic lesions containing large sheets of dysplastic cells, abnormal mitoses, and multinucleated giant cells (J:103407)
• seventeen weeks after infection with low-titre (5X103) cre lentiviruses, an average of 30 lung adenocarcinomas are detected per mouse (J:154041)
• seventeen weeks after infection with high-titre (5X104) cre lentiviruses, 90-131 lung adenocarcinomas are detected per mouse (J:154041)
• mice develop multiple, aggressive adenocarcinomas in the lungs bilaterally following intranasal delivery of an adenovirus expressing Cre recombinase (J:195492)
• tumor growth is reduced to a similar extent following either two 7.3 Gy fractions of radiation therapy or a single 11.6 Gy fraction (J:195492)
• tumors incorporate high levels of BrdU 4 hours after radiation treatment similarly to unirradiated tumors, indicating lack of an intact G1 cell-cycle checkpoint (J:195492)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:103407 , J:154041 , J:195492 , J:203686




Genotype
MGI:5562910
cn41
Allelic
Composition
Krastm4Tyj/Kras+
Rnf7Gt(XE423)Byg/Rnf7tm1.1Ysun
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Rnf7Gt(XE423)Byg mutation (0 available); any Rnf7 mutation (17 available)
Rnf7tm1.1Ysun mutation (0 available); any Rnf7 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of Ad-Cre treated mice is 37.9 weeks, with most mice dying by 60 weeks

neoplasm
• mice show reduced lung tumor burden following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) compared to single Kras homozygotes, however the number of hyperplastic loci is not affected
• hyperplasia or adenomas from Ad-Cre treated mice show reduced proliferation compared to single Kras homozygotes

respiratory system
• mice show reduced lung tumor burden following intratracheal administration of an adenovirus expressing Cre (Ad-Cre) compared to single Kras homozygotes, however the number of hyperplastic loci is not affected
• hyperplasia or adenomas from Ad-Cre treated mice show reduced proliferation compared to single Kras homozygotes




Genotype
MGI:5510703
cn42
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm2Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (31 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• however, treatment with a potent and selective oral pan class I PI3K inhibitor (GDC 0941) blocks tumor growth

endocrine/exocrine glands
• however, treatment with a potent and selective oral pan class I PI3K inhibitor (GDC 0941) blocks tumor growth




Genotype
MGI:4441491
cn43
Allelic
Composition
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Lyz2tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• the maximum survival is 24 days

respiratory system
• lung weight is 10-fold higher than that in control mice at 3 weeks old

neoplasm

growth/size/body
• lung weight is 10-fold higher than that in control mice at 3 weeks old




Genotype
MGI:6256734
cn44
Allelic
Composition
Krastm4Tyj/Kras+
Krt19tm1(cre/ERT)Ggu/Krt19+
Ptentm2Mak/Ptentm2Mak
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Krt19tm1(cre/ERT)Ggu mutation (1 available); any Krt19 mutation (21 available)
Ptentm2Mak mutation (4 available); any Pten mutation (88 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice administered tamoxifen at 8 weeks of age show a median survival of 30 days after tamoxifen injection

digestive/alimentary system
• colonic serrated epithelial changes in tamoxifen treated mice
• hyperplastic changes of gastric mucosa in tamoxifen treated mice

endocrine/exocrine glands
• extrahepatic bile duct is rigid and dilated in tamoxifen treated mice
• papillary hyperplasia of the extrahepatic biliary tract
• papillary hyperplasia of the gallbladder in tamoxifen treated mice
• gallbladder and cystic duct are rigid and dilated in tamoxifen treated mice
• in tamoxifen treated mice
• PanIN-like lesions and hyperplasia in the pancreatic ducts in tamoxifen treated mice
• however, no obvious tumors are seen in mice administered tamoxifen at 8 weeks of age

immune system
• obstructive pneumonia in tamoxifen treated mice

liver/biliary system
• extrahepatic bile duct is rigid and dilated in tamoxifen treated mice
• papillary hyperplasia of the extrahepatic biliary tract
• papillary hyperplasia of the gallbladder in tamoxifen treated mice
• gallbladder and cystic duct are rigid and dilated in tamoxifen treated mice
• in tamoxifen treated mice
• liver of tamoxifen treated mice shows pre-malignant papillary ductal lesions in periportal areas

neoplasm
• PanIN-like lesions and hyperplasia in the pancreatic ducts in tamoxifen treated mice
• however, no obvious tumors are seen in mice administered tamoxifen at 8 weeks of age

respiratory system
• obstructive pneumonia in tamoxifen treated mice
• papillary hyperplasia of bronchial epithelia in tamoxifen treated mice
• respiratory failure by lung lesions in tamoxifen treated mice




Genotype
MGI:5298088
cn45
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Shhtm2(cre/ERT2)Cjt/Shh+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Shhtm2(cre/ERT2)Cjt mutation (1 available); any Shh mutation (48 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
N
• no macroscopic or microscopic skin tumors are observed up to 4 months after tamoxifen treatment




Genotype
MGI:5298083
cn46
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Krt19tm1(cre/ERT)Ggu/Krt19+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Krt19tm1(cre/ERT)Ggu mutation (1 available); any Krt19 mutation (21 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• tamoxifen treated mice die within 2 months from intestinal cancers before developing skin tumors

digestive/alimentary system
• tamoxifen treated mice develop intestinal cancers

neoplasm
• tamoxifen treated mice develop intestinal cancers
• when back skin from mutant animals is grafted onto back skin of nude mice, all engrafted mice develop skin tumors, including ulcerative lesions (benign and squamous cell carcinomas) within 2 months of tamoxifen administration
• tamoxifen treated mice develop terminal intestinal carcinomas with 2 months of treatment

integument
• when back skin from mutant animals is grafted onto back skin of nude mice, all engrafted mice develop skin tumors, including ulcerative lesions (benign and squamous cell carcinomas) within 2 months of tamoxifen administration




Genotype
MGI:6403693
cn47
Allelic
Composition
Hprt1tm1(CAG-BRF1)Gu/Hprt1+
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hprt1tm1(CAG-BRF1)Gu mutation (0 available); any Hprt1 mutation (1279 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• as in mice lacking the BRF1 knock-in

neoplasm
• as in mice lacking the BRF1 knock-in

homeostasis/metabolism
• tRNA levels are increased in the pancreas

endocrine/exocrine glands
• as in mice lacking the BRF1 knock-in

cellular
• tRNA levels are increased in the pancreas




Genotype
MGI:6377665
cn48
Allelic
Composition
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd9tm1c(EUCOMM)Hmgu mutation (0 available); any Cd9 mutation (104 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele




Genotype
MGI:6377669
cn49
Allelic
Composition
Cd9tm1c(EUCOMM)Hmgu/Cd9tm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd9tm1c(EUCOMM)Hmgu mutation (0 available); any Cd9 mutation (104 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• as severe as in mice wild-type for Cd9




Genotype
MGI:6377664
cn50
Allelic
Composition
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd9tm1c(EUCOMM)Hmgu mutation (0 available); any Cd9 mutation (104 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele

neoplasm
• at 8 weeks, not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele
• increased tumor weight compared to in mice homozygous for a conditional allele
• compared to in mice homozygous for a conditional allele

endocrine/exocrine glands
• at 8 weeks, not as severe as in mice wild-type for Cd9 or homozygous for a conditional allele
• increased tumor weight compared to in mice homozygous for a conditional allele




Genotype
MGI:6377668
cn51
Allelic
Composition
Cd9tm1c(EUCOMM)Hmgu/Cd9tm1c(EUCOMM)Hmgu
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd9tm1c(EUCOMM)Hmgu mutation (0 available); any Cd9 mutation (104 available)
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• as severe as in mice wild-type for Cd9

neoplasm
• at 8 weeks, more severe than in mice heterozygous for the Cd9 conditional allele

endocrine/exocrine glands
• at 8 weeks, more severe than in mice heterozygous for the Cd9 conditional allele




Genotype
MGI:6377671
cn52
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die by 30 weeks of age

neoplasm

endocrine/exocrine glands




Genotype
MGI:6377672
cn53
Allelic
Composition
Gt(ROSA)26Sortm1(EYFP)Cos/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(EYFP)Cos mutation (11 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die by 8 weeks of age




Genotype
MGI:4441490
cn54
Allelic
Composition
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fntbtm1.1Mbrg mutation (0 available); any Fntb mutation (208 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (208 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pggt1btm1.1Mbrg mutation (0 available); any Pggt1b mutation (27 available)
Pggt1btm1Mbrg mutation (0 available); any Pggt1b mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment
• the lung surface of Cre-adenovirus treated mice is nearly indistinguishable from that of control mice
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment
• presence of small adenomas after Cre-adenovirus treatment
• adenocarcinoma in 1 of 11 mice after Cre-adenovirus treatment

respiratory system
• the lung surface of Cre-adenovirus treated mice is nearly indistinguishable from that of control mice
• 76% fewer tumors and 79% smaller lesion area than Krastm4Tyj heterozygous mice after Cre-adenovirus treatment
• presence of small adenomas after Cre-adenovirus treatment
• adenocarcinoma in 1 of 11 mice after Cre-adenovirus treatment
• presence of epithelial hyperplasia after Cre-adenovirus treatment




Genotype
MGI:4441492
cn55
Allelic
Composition
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fntbtm1.1Mbrg mutation (0 available); any Fntb mutation (208 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (208 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Lyz2tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• longer life span than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (>100 days in some cases)

respiratory system
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice but higher than in normal mice

neoplasm
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice

growth/size/body
• lung weight is less than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice but higher than in normal mice




Genotype
MGI:4441486
cn56
Allelic
Composition
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fntbtm1.1Mbrg mutation (0 available); any Fntb mutation (208 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (208 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• Cre-adenovirus treatment results in G2M cell-cycle arrest in embryonic fibroblasts




Genotype
MGI:4441488
cn57
Allelic
Composition
Fntbtm1.1Mbrg/Fntbtm1.2Mbrg
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1.1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * BALB/cJ * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fntbtm1.1Mbrg mutation (0 available); any Fntb mutation (208 available)
Fntbtm1.2Mbrg mutation (0 available); any Fntb mutation (208 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Lyz2tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (40 available)
Pggt1btm1.1Mbrg mutation (0 available); any Pggt1b mutation (27 available)
Pggt1btm1Mbrg mutation (0 available); any Pggt1b mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median life span is 170 days
• longer median life span than Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice (170 vs. 22 days)

neoplasm
• lung weight and histology are indistinguishable from littermate control mice at 3-week old, compare with lung weight is 10-fold higher in Lyz2tm1(cre)Ifo, Krastm4Tyj heterozygous mice
• lung weight and histology are indistinguishable from littermate control mice at 3-week old
• but eventually develop lung tumors at older age

respiratory system
• lung weight and histology are indistinguishable from littermate control mice at 3-week old
• but eventually develop lung tumors at older age




Genotype
MGI:5528686
cn58
Allelic
Composition
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Mapkapk2tm1.1Yaff mutation (1 available); any Mapkapk2 mutation (35 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus
• tumor burden progresses from 11% of lung (6 weeks) to 45% at experimental endpoint (12+ weeks) in the presence of a Cre-recombinase expressing adenovirus
• Mapkap2 expressing tumors (MK2+) represent a higher proportion of tumor burden, however over time the proportion of these tumors decreases and the proportion of Mapkapk2 (MK2-) null tumors increases in the presence of a Cre-recombinase expressing adenovirus
• proportion of total lung tumor burden composed of Mapkapk2 (MK2-) null tumors is reduced from 39% to 11% following cisplatin treatment

respiratory system
• lung adenocarcinomas cover 11% of lung area 6 weeks after administration of a Cre-recombinase expressing adenovirus
• tumor burden progresses from 11% of lung (6 weeks) to 45% at experimental endpoint (12+ weeks) in the presence of a Cre-recombinase expressing adenovirus
• Mapkap2 expressing tumors (MK2+) represent a higher proportion of tumor burden, however over time the proportion of these tumors decreases and the proportion of Mapkapk2 (MK2-) null tumors increases in the presence of a Cre-recombinase expressing adenovirus
• proportion of total lung tumor burden composed of Mapkapk2 (MK2-) null tumors is reduced from 39% to 11% following cisplatin treatment




Genotype
MGI:5559052
cn59
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• extremity sarcomas in mice injected with Ad-Cre invade adjacent skeletal muscle and uterine sarcomas invade the intestinal wall and pancreas
• 20% of mice with large extremity sarcomas develop metastasis to the lungs
• 90% of mice injected intramuscularly with an adenovirus expressing Cre recombinase (Ad-Cre) into the extremities develop soft tissue sarcomas after a median time of 3 months (J:125101)
• high penetrance of soft tissue sarcomas also develops after injection of Ad-Cre into the uterus (J:125101)
• soft tissue sarcomas present as large solitary masses originating at the site of Ad-Cre injection, and are high-grade spindle cell neoplasms (J:125101)
• sarcomas show myofibroblastic differentiation with intracytoplasmic filaments with densities (J:125101)
• gene expression analysis indicates that Ad-Cre induced sarcomas are undifferentiated pleomorphic sarcoma/malignant fibrous histiocytoma (J:155389)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
malignant fibrous histiocytoma DOID:1907 J:155389
sarcoma DOID:1115 J:204376 , J:125101 , J:155389




Genotype
MGI:5547939
cn60
Allelic
Composition
Krastm4Tyj/Kras+
Myod1tm1.1(cre/ERT,TVA)Gcg/Myod1+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Myod1tm1.1(cre/ERT,TVA)Gcg mutation (1 available); any Myod1 mutation (23 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• when mice older than 6 weeks are given systemic tamoxifen treatment by intraperitoneal delivery, mice develop multiple tumors at clinically relevant sites with a median tumor free survival of 153 days (longer latency than Pax7CE mutants
• tamoxifen treated mice develop sarcomas that are exclusively undifferentiated pleomorphic sarcomas (UPS), myogenic or nonmyogenic in type
• tumors can appear in the body wall, the extremities, or the head and neck region




Genotype
MGI:4460775
cn61
Allelic
Composition
Krastm4Tyj/Kras+
Lrrc17tm1Nik/Lrrc17+
Srpk2tm1Nik/Srpk2+
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Lrrc17tm1Nik mutation (0 available); any Lrrc17 mutation (21 available)
Srpk2tm1Nik mutation (0 available); any Srpk2 mutation (47 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in pIpC-treated mice similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice

immune system
• pIpC-treated mice develop myeloproliferative disorder with anemia unlike wild-type mice that is similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice

hematopoietic system
• bone marrow cells from pIpC-treated mice spontaneous form colony forming units-granulocyte and macrophage (CFU-GM) in the absence of cytokines unlike wild-type cells
• in pIpC-treated mice similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice
• pIpC-treated mice develop myeloproliferative disorder with anemia unlike wild-type mice that is similar to in pIpC-treated Krastm4Tyj Tg(Mx1-cre)1Cgn mice




Genotype
MGI:4948965
cn62
Allelic
Composition
Krastm4Tyj/Kras+
Map2k7tm1.1Twad/Map2k7tm1.2Twad
Tg(Trp53)bSrn/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Map2k7tm1.1Twad mutation (0 available); any Map2k7 mutation (20 available)
Map2k7tm1.2Twad mutation (0 available); any Map2k7 mutation (20 available)
Tg(Trp53)bSrn mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• following adenovirus cre infection, mice exhibit the same tumor burden as in control mice




Genotype
MGI:5428898
cn63
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival is 52 weeks of age

neoplasm
• mutants develop intrahepatic cholangiocarcinoma as early as 32 weeks of age
• intrahepatic cholangiocarcinoma recapitulates the histologic and molecular features of multistage progression of human intrahepatic cholangiocarcinoma
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor
• tumors are highly metastatic, with tumors showing invasion into adjacent organs such as the diaphragm, bowel, pancreas and stomach or distant metastasis to the lymph nodes, spleen, lungs, or peritoneal cavity
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas

cardiovascular system
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis

liver/biliary system
• mutants develop intrahepatic cholangiocarcinoma as early as 32 weeks of age
• intrahepatic cholangiocarcinoma recapitulates the histologic and molecular features of multistage progression of human intrahepatic cholangiocarcinoma
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor

endocrine/exocrine glands
• mutants develop intrahepatic cholangiocarcinoma as early as 32 weeks of age
• intrahepatic cholangiocarcinoma recapitulates the histologic and molecular features of multistage progression of human intrahepatic cholangiocarcinoma
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:184949




Genotype
MGI:4819844
cn64
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Yap1tm1.1Dupa/Yap1tm1.1Dupa
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
Yap1tm1.1Dupa mutation (2 available); any Yap1 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm

liver/biliary system




Genotype
MGI:5428907
cn65
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival is 19 weeks of age

neoplasm
• mutants develop intrahepatic cholangiocarcinoma as early as 9 weeks of age
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor
• tumors are highly metastatic, with 75% of mutants having tumors showing invasion into adjacent organs such as the diaphragm, bowel, pancreas and stomach or distant metastasis to the lymph nodes, spleen, lungs, or peritoneal cavity
• intrahepatic cholangiocarcinoma is associated with biliary hamartomas

cardiovascular system
• hepatic lesions frequently show hemorrhage into the peritoneal cavity and exhibit evidence of tumor necrosis

liver/biliary system
• mutants develop intrahepatic cholangiocarcinoma as early as 9 weeks of age
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor

endocrine/exocrine glands
• mutants develop intrahepatic cholangiocarcinoma as early as 9 weeks of age
• intrahepatic cholangiocarcinoma is associated with intraductal papillary neoplasms of the bile ducts and Von Meyenburg complexes, or biliary hamartomas
• intrahepatic cholangiocarcinoma is characterized by elevated levels of autophagy
• different grades of differentiation are seen in the same tumor

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:184949




Genotype
MGI:6256730
cn66
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm2Mak/Ptentm2Mak
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm2Mak mutation (4 available); any Pten mutation (88 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival is 46 days

growth/size/body
• seen in 5 month old mice
• all mice start to show abdominal distension at about 5 weeks of age, frequently accompanied by jaundice and weight loss
• distension is due to hepatic enlargement and/or hemorrhagic ascites

neoplasm
• tumors primarily show glandular morphology that resembles well-differentiated human cholangiocarcinoma and marker analysis indicates that tumors are intrahepatic cholangiocarcinoma
• in some cases, regions of moderately differentiated tumor with a cribriform appearance are seen
• no metastasis or invasion to other organs is seen
• tumors are frequently surrounded by dense fibrous stroma, indicating accumulation of fibrillar collagens
• stellate cells are activated and acquire a myofibroblast-like phenotype
• tumor cells show mucin production, a characteristic of epithelial cells in the bile duct
• multiple solid tumors with various sizes are seen throughout the liver
• invasive tumors are apparent after 7 weeks of age, with abundant desmoplastic stroma or desmoplasia

endocrine/exocrine glands
• various degrees of hyperplasia are seen in the bile ducts, characterized by increase in number and size and change in morphology, at 4 weeks of age
• at 5 weeks, a part of the hyperplastic ductal lesions at the hilum become enlarged and show a pattern of papillary growth
• tumors primarily show glandular morphology that resembles well-differentiated human cholangiocarcinoma and marker analysis indicates that tumors are intrahepatic cholangiocarcinoma
• in some cases, regions of moderately differentiated tumor with a cribriform appearance are seen
• no metastasis or invasion to other organs is seen
• tumors are frequently surrounded by dense fibrous stroma, indicating accumulation of fibrillar collagens
• stellate cells are activated and acquire a myofibroblast-like phenotype
• tumor cells show mucin production, a characteristic of epithelial cells in the bile duct

homeostasis/metabolism

liver/biliary system
• various degrees of hyperplasia are seen in the bile ducts, characterized by increase in number and size and change in morphology, at 4 weeks of age
• at 5 weeks, a part of the hyperplastic ductal lesions at the hilum become enlarged and show a pattern of papillary growth
• tumors primarily show glandular morphology that resembles well-differentiated human cholangiocarcinoma and marker analysis indicates that tumors are intrahepatic cholangiocarcinoma
• in some cases, regions of moderately differentiated tumor with a cribriform appearance are seen
• no metastasis or invasion to other organs is seen
• tumors are frequently surrounded by dense fibrous stroma, indicating accumulation of fibrillar collagens
• stellate cells are activated and acquire a myofibroblast-like phenotype
• tumor cells show mucin production, a characteristic of epithelial cells in the bile duct
• multiple solid tumors with various sizes are seen throughout the liver
• invasive tumors are apparent after 7 weeks of age, with abundant desmoplastic stroma or desmoplasia
• seen in 5 month old mice

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:254370




Genotype
MGI:6256732
cn67
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm2Mak/Pten+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm2Mak mutation (4 available); any Pten mutation (88 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• some lesions are diagnosed as intrahepatic cholangiocarcinoma by the appearance of adenocarcinoma showing tubular and/or papillary structures with a fibrous stroma; these tumor cells show loss of Pten expression
• mice develop liver tumors at 6 months of age, showing obvious symptoms after 7 months with abdominal distension due to multiple tumors at later stages
• mice develop liver tumors with both hepatocyte and cholangiocyte differentiation
• majority of large nodules are hepatocellular dysplasia, a precursor lesion of hepatocellular carcinoma

liver/biliary system
• some lesions are diagnosed as intrahepatic cholangiocarcinoma by the appearance of adenocarcinoma showing tubular and/or papillary structures with a fibrous stroma; these tumor cells show loss of Pten expression
• mice develop liver tumors at 6 months of age, showing obvious symptoms after 7 months with abdominal distension due to multiple tumors at later stages
• mice develop liver tumors with both hepatocyte and cholangiocyte differentiation
• majority of large nodules are hepatocellular dysplasia, a precursor lesion of hepatocellular carcinoma

endocrine/exocrine glands
• some lesions are diagnosed as intrahepatic cholangiocarcinoma by the appearance of adenocarcinoma showing tubular and/or papillary structures with a fibrous stroma; these tumor cells show loss of Pten expression




Genotype
MGI:5486065
cn68
Allelic
Composition
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Sftpctm1.1(cre/ERT2)Ptch mutation (0 available); any Sftpc mutation (24 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• many mice do not survive to 13 weeks after tamoxifen treatment due to high tumor burden
• mice display leaky cre expression without tamoxifen treatment and survive a few months longer than tamoxifen-treated animals

neoplasm
• after tamoxifen treatment, mice show a more severe phenotype than animals with wild-type Trp53 (greater tumor size, tumor growth and tumor grade); by 3-4 weeks after tamoxifen treatment, several small adenomas of papillary nature are observed in alveoli
• at 10 weeks after tamoxifen injection, many alveoli have large tumors; tumors exhibit enlarged pleomorphic nuclei, aberrant mitosis; tumor giant cells are present
• mice surviving to 13 weeks after tamoxifen treatment have adenocarcinomas in the alveoli of the lungs
• without tamoxifen treatment, mice develop invasive lung adenocarcinomas localized to the alveoli
• bronchioalveolar duct junctions (BADJs) appear normal ( in mice with or without tamoxifen treatment)

respiratory system
• after tamoxifen treatment, mice show a more severe phenotype than animals with wild-type Trp53 (greater tumor size, tumor growth and tumor grade); by 3-4 weeks after tamoxifen treatment, several small adenomas of papillary nature are observed in alveoli
• at 10 weeks after tamoxifen injection, many alveoli have large tumors; tumors exhibit enlarged pleomorphic nuclei, aberrant mitosis; tumor giant cells are present
• mice surviving to 13 weeks after tamoxifen treatment have adenocarcinomas in the alveoli of the lungs
• without tamoxifen treatment, mice develop invasive lung adenocarcinomas localized to the alveoli
• bronchioalveolar duct junctions (BADJs) appear normal ( in mice with or without tamoxifen treatment)
• 8 days after tamoxifen treatment, extensive type II cell proliferation is observed compared to wild-type; however, proliferating bronchioalveolar stem cells (BASCs) are rarely observed (at 8 days, 3, 6, 10 and 13 weeks after tamoxifen treatment)
• tumor cells express type II cell markers and are highly proliferative, even without tamoxifen treatment




Genotype
MGI:4835045
cn69
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2a+
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen-treated mice develop melanomas with spindle-like morphology
• 3 of 7 (43%) mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology at a median latency greater than 52 weeks compared with Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos mice whose median latency is 14 weeks

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:4835041
cn70
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice treated with tamoxifen neonatally die within 14 weeks of treatment due to aggressive melanomas with spindle-like morphology unlike control mice in which only one mouse develops melanoma over a period of 60 weeks

neoplasm
• tumor growth is more aggressive than in Cdkn2atm1Rdp/Cdkn2atm1Rdp Tg(Tyr-HRAS)60Lc mice
• tamoxifen-treated mice develop melanomas with spindle-like morphology
• all mice treated with tamoxifen neonatally die within 14 weeks of treatment due to aggressive melanomas with spindle-like morphology unlike control mice in which only one mouse develops melanoma over a period of 60 weeks
• tumors in tamoxifen-treated mice occur on the flank, ear, and tail
• the number of tumors in tamoxifen-treated mice is greater than in similarly treated Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Tg(Tyr-cre/ERT2)13Bos mice or Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos mice
• by 15 weeks, 17 of 27 adult mice treated with tamoxifen develop melanomas at the site of application and depilation
• however, no uveal tumors are observed

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:5604750
cn71
Allelic
Composition
Krastm4Tyj/Kras+
Tg(CAG-Bgeo,-tsA58T)T26Ichi/0
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(CAG-Bgeo,-tsA58T)T26Ichi mutation (0 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice do not survive beyond P21

neoplasm
• mice develop highly aggressive adenocarcinoma with a ductal cell phenotype and inflammation resembling human pancreatic ductal adenocarcinoma within a short period (5 and 10 days after birth) and die within 3 weeks
• at P16, pancreatic ductal adenocarcinoma progresses to occupy the whole pancreas and to invade the muscular wall of the duodenum
• PanIN-3 are detected in the pancreas with inflammation at P3 and P4

endocrine/exocrine glands
• mice develop highly aggressive adenocarcinoma with a ductal cell phenotype and inflammation resembling human pancreatic ductal adenocarcinoma within a short period (5 and 10 days after birth) and die within 3 weeks
• at P16, pancreatic ductal adenocarcinoma progresses to occupy the whole pancreas and to invade the muscular wall of the duodenum
• PanIN-3 are detected in the pancreas with inflammation at P3 and P4
• invasive features of pancreatic ductal adenocarcinoma are seen containing acinoductal metaplasia at P5-P10

homeostasis/metabolism
• hemorrhagic ascites are seen by P16

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:214846




Genotype
MGI:3776026
cn72
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• large, prominent goblet cells develop in the colon
• mice develop widespread hyperplasia throughout the colonic epithelium
• colonic epithelium has a larger transit amplifying cell zone than wild-type; cells in the colonic epithelium have a higher mitotic index than in wild-type
• hyperplasia is typified by extreme lengthening of the crypts

endocrine/exocrine glands
• hyperplasia is typified by extreme lengthening of the crypts

cellular
• large, prominent goblet cells develop in the colon




Genotype
MGI:5635880
cn73
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Gev/Trp53tm1Gev
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Gev mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice exhibit rapid development of pancreatic tumors within 8 weeks with features typical of human pancreatic adenocarcinoma
• tumors treated with ibrutinib show a reduction in proliferation rate and tumor fibrosis, inhibition of mast cell degranulation, and reduction in CD11b+ and F4/80+ macrophages and mice show increased survival
• mice treated with both ibrutinib and gemcitabine show extended survival compared to treatment with gemcitabine alone
• mice treated with a daily injection of cromolyn, a blocker of mast cell degranulation and inflammogen release, starting at 8 weeks of age show a reduction in F4/80+ cells and CD11b+ cells in the tumor stroma

endocrine/exocrine glands
• mice exhibit rapid development of pancreatic tumors within 8 weeks with features typical of human pancreatic adenocarcinoma
• tumors treated with ibrutinib show a reduction in proliferation rate and tumor fibrosis, inhibition of mast cell degranulation, and reduction in CD11b+ and F4/80+ macrophages and mice show increased survival
• mice treated with both ibrutinib and gemcitabine show extended survival compared to treatment with gemcitabine alone
• mice treated with a daily injection of cromolyn, a blocker of mast cell degranulation and inflammogen release, starting at 8 weeks of age show a reduction in F4/80+ cells and CD11b+ cells in the tumor stroma

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:220300




Genotype
MGI:5659893
cn74
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a mean survival of 14 weeks after ad-cre inoculation

neoplasm
• 4 of 9 (44%) ad-cre inoculated mice exhibit metastasis
• mice inoculated ad-cre by inhalation develop lung adenocarcinomas with high multiplicity

respiratory system
• mice inoculated ad-cre by inhalation develop lung adenocarcinomas with high multiplicity




Genotype
MGI:6377667
cn75
Allelic
Composition
Cd9tm1c(EUCOMM)Hmgu/Cd9+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm1Brn/Trp53+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6N * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cd9tm1c(EUCOMM)Hmgu mutation (0 available); any Cd9 mutation (104 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• reduced glutamate uptake and intracellular levels in organoids derived from tumor initiating cells




Genotype
MGI:5298084
cn76
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT14-cre/ERT)20Efu/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * CD-1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(KRT14-cre/ERT)20Efu mutation (3 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• lesions are squamous cell carcinomas (SCCs)characterized by fibroblast-like shaped cells and disruption of basal lamina
• numerous microscopic and small invasive SCCs are observed in the dermis of the back skin in addition to the macroscopic lesions

integument
• within 2 months of tamoxifen treatment, animals develop rapidly growing ulcerative skin lesions in the back skin
• lesions are squamous cell carcinomas (SCCs)characterized by fibroblast-like shaped cells and disruption of basal lamina
• numerous microscopic and small invasive SCCs are observed in the dermis of the back skin in addition to the macroscopic lesions

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
squamous cell carcinoma DOID:1749 J:172048




Genotype
MGI:3776028
cn77
Allelic
Composition
Apctm2.1Cip/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2.1Cip mutation (2 available); any Apc mutation (158 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• animals have greatly reduced life-span compared to mutants expressing wild-type Kras

neoplasm
• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio
• mice have more tumors than mutants expressing wild-type Kras
• terminally differentiated cells are absent from tumors

digestive/alimentary system
• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio
• mice have more tumors than mutants expressing wild-type Kras
• terminally differentiated cells are absent from tumors




Genotype
MGI:4835046
cn78
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen-treated mice develop melanomas with spindle-like morphology
• 5 of 11 mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology at a longer latency (median latency 31 weeks) than in Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1BrnTg(Tyr-cre/ERT2)13Bos mice (median latency 14 weeks)

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:5484548
cn79
Allelic
Composition
Cdkn2atm2Brn/Cdkn2atm2Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2Brn mutation (2 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• after 5 days in culture, pancreatic explants exhibit irregular branching and disorganization with increased proliferation, pseudostratification, nuclear crowding and elongation resembling precancerous lesions
• however, no cysts develop

cellular
• after 5 days in culture, pancreatic explants exhibit irregular branching with increased proliferation




Genotype
MGI:3716399
cn80
Allelic
Composition
Krastm4Tyj/Kras+
Spry2tm1.1Mrt/Spry2tm1.1Mrt
Meox2tm1(cre)Sor/Meox2+
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJaeSor * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Meox2tm1(cre)Sor mutation (3 available); any Meox2 mutation (18 available)
Spry2tm1.1Mrt mutation (1 available); any Spry2 mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• lungs at E12.5 show increased branching compared to Kras; Meox2-cre, Spry2-wild-type lungs; bronchi number is increased, but is still less than age-matched wild-type




Genotype
MGI:4940096
cn81
Allelic
Composition
Brca2tm1Brn/Brca2tm1Cam
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (5 available); any Brca2 mutation (132 available)
Brca2tm1Cam mutation (0 available); any Brca2 mutation (132 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm3Tyj mutation (3 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• about 18% of assessable tumor cases develop an acinar-cell carcinoma component of pancreatic tumors
• high penetrance (29 of 30 mutants) of pancreatic ductal adenocarcinomas

mortality/aging
• average survival time is 84 days, with a range of 48-110 days

endocrine/exocrine glands
• about 18% of assessable tumor cases develop an acinar-cell carcinoma component of pancreatic tumors
• high penetrance (29 of 30 mutants) of pancreatic ductal adenocarcinomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:166678




Genotype
MGI:4940102
cn82
Allelic
Composition
Brca2tm1Cam/Brca2tm1Brn
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (5 available); any Brca2 mutation (132 available)
Brca2tm1Cam mutation (0 available); any Brca2 mutation (132 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• pancreatic insufficiency; spectrum of anomalies are seen from isolated paucity of the islets of Langerhans to complete fibro-inflammatory or cystic degeneration of both the endocrine and exocrine pancreas

endocrine/exocrine glands
• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls
• pancreatic insufficiency; spectrum of anomalies are seen from isolated paucity of the islets of Langerhans to complete fibro-inflammatory or cystic degeneration of both the endocrine and exocrine pancreas
• mutants not succumbing to pancreatic insufficiency later develop pancreatic ductal adenocarcinomas with a moderate latency and incomplete penetrance (6 of 32 mutants)

mortality/aging
• mutants exhibit shortened pancreatic ductal adenocarcinoma-free survival

neoplasm
• mutants not succumbing to pancreatic insufficiency later develop pancreatic ductal adenocarcinomas with a moderate latency and incomplete penetrance (6 of 32 mutants)

cellular
• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls




Genotype
MGI:5486056
cn83
Allelic
Composition
Krastm4Tyj/Kras+
Sftpctm1.1(cre/ERT2)Ptch/Sftpc+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Sftpctm1.1(cre/ERT2)Ptch mutation (0 available); any Sftpc mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• by 18 weeks after tamoxifen treatment, numerous adenomas develop in alveoli; small numbers of cells with features of malignant transformation are observed in some lung sections
• tumors are usually found in proximity to the airways, bronchioalveolar duct junctions (BADJs), or surface of the lung, but lesions are not found in the BADJs
• tumor cells are highly proliferative
• airways and BADJs retain normal architecture

respiratory system
• by 18 weeks after tamoxifen treatment, numerous adenomas develop in alveoli; small numbers of cells with features of malignant transformation are observed in some lung sections
• tumors are usually found in proximity to the airways, bronchioalveolar duct junctions (BADJs), or surface of the lung, but lesions are not found in the BADJs
• tumor cells are highly proliferative
• airways and BADJs retain normal architecture




Genotype
MGI:3695431
cn84
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average tumor-free survival is 8.6 weeks

neoplasm
• 6 of 6 mice develop pancreatic ductal adenocarcinoma

endocrine/exocrine glands
• 6 of 6 mice develop pancreatic ductal adenocarcinoma




Genotype
MGI:3695432
cn85
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average tumor-free survival is 38 weeks

neoplasm
• 6 of 10 mice develop pancreatic ductal adenocarcinoma

endocrine/exocrine glands
• 6 of 10 mice develop pancreatic ductal adenocarcinoma




Genotype
MGI:3821739
cn86
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Bhlha15tm3(cre/ERT2)Skz/Bhlha15+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bhlha15tm3(cre/ERT2)Skz mutation (1 available); any Bhlha15 mutation (15 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 2 months after injection with tamoxifen, mice exhibit focal low grade pancreatic intraepithelial neoplasia (PanIN) originating from acinar cells that progresses to carcinoma in situ in some cases by 4 to 12 months following injection with tamoxifen
• tamoxifen treated mice exhibit lesions that progress from normal acinar parenchyma to acinar-ductal metaplastic structures to PanIN with biphenotypic exocrine differentiation
• tamoxifen treated mice exhibit highly proliferative acinar derived PanIN

endocrine/exocrine glands
• 2 months after injection with tamoxifen, mice exhibit focal low grade pancreatic intraepithelial neoplasia (PanIN) originating from acinar cells that progresses to carcinoma in situ in some cases by 4 to 12 months following injection with tamoxifen
• tamoxifen treated mice exhibit lesions that progress from normal acinar parenchyma to acinar-ductal metaplastic structures to PanIN with biphenotypic exocrine differentiation
• tamoxifen treated mice exhibit highly proliferative acinar derived PanIN




Genotype
MGI:4839216
cn87
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Scgb1a1tm1.1(cre)Fjd mutation (0 available); any Scgb1a1 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival is 8 weeks

immune system
• increase in inflammation in lesions compared to single Kras mutants, with an increase in neutrophil and endothelial cell infiltration; infiltration of these cells increases with malignant progression

respiratory system
• increase in inflammation in lesions compared to single Kras mutants, with an increase in neutrophil and endothelial cell infiltration; infiltration of these cells increases with malignant progression
• mutants have higher numbers of lesions and more extensive tumors than single Kras mutants
• mutants develop distinct bronchial and alveolar tumors
• mutants develop lung lesions as early as 4 weeks of age including proliferative atypical adenomatous hyperplasia lesions
• mutants develop lung lesions as early as 4 weeks of age that includes atypical papillary bronchiolar proliferation
• mucinous bronchioloalveolar cell carcinoma-like lesions, a subtype of lung adenocarcinoma
• by 2 months of age, mutants exhibit tachypnea

neoplasm
• mutants have higher numbers of lesions and more extensive tumors than single Kras mutants
• mutants develop distinct bronchial and alveolar tumors
• mutants develop lung lesions as early as 4 weeks of age including proliferative atypical adenomatous hyperplasia lesions
• mutants develop lung lesions as early as 4 weeks of age that includes atypical papillary bronchiolar proliferation
• mucinous bronchioloalveolar cell carcinoma-like lesions, a subtype of lung adenocarcinoma

growth/size/body
• by 2 months of age, mutants exhibit weight loss




Genotype
MGI:3032576
cn88
Allelic
Composition
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• pancreatic ductal adenocarcinomas (J:87973)
• transitions of epithelium from cuboid to columnar as early as 2 weeks (J:87973)
• extra pancreatic tumors are rare (J:87973)
• number and extent of lesions increases with age (J:87973)
• by 7-10 months occasional animals with invasive and metastatic adenocarcinomas (J:87973)
• lesions eventually found in liver diaphragm and lungs (J:87973)
• average cancer free survival is greater than 52 weeks and 2 of 9 mice develop pancreatic ductal adenocarcinoma (J:116130)
• pancreatic intraepithelial neoplasia (PanIN)-1 lesions are distributed widely throughout the pancreas, whereas PanIN-2 or -3 lesions are rarely seen

digestive/alimentary system
• 6 month old mice exhibit mild acinar cell loss

endocrine/exocrine glands
• 6 month old mice exhibit mild acinar cell loss
• pancreatic ductal adenocarcinomas (J:87973)
• transitions of epithelium from cuboid to columnar as early as 2 weeks (J:87973)
• extra pancreatic tumors are rare (J:87973)
• number and extent of lesions increases with age (J:87973)
• by 7-10 months occasional animals with invasive and metastatic adenocarcinomas (J:87973)
• lesions eventually found in liver diaphragm and lungs (J:87973)
• average cancer free survival is greater than 52 weeks and 2 of 9 mice develop pancreatic ductal adenocarcinoma (J:116130)
• pancreatic intraepithelial neoplasia (PanIN)-1 lesions are distributed widely throughout the pancreas, whereas PanIN-2 or -3 lesions are rarely seen

growth/size/body

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:87973




Genotype
MGI:4839215
cn89
Allelic
Composition
Krastm4Tyj/Kras+
Scgb1a1tm1.1(cre)Fjd/Scgb1a1+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Scgb1a1tm1.1(cre)Fjd mutation (0 available); any Scgb1a1 mutation (29 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average survival is 24 weeks

respiratory system
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site
• however, no carcinomas are seen by 24 weeks of age
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site
• atypical adenomatous hyperplasia lesions and adenomas

neoplasm
• mutants develop lung lesions that are first detected at 12 weeks of age in alveoli and bronchioles
• mutants develop epithelial lesions termed atypical papillary bronchiolar proliferation that has papillary proliferations of the bronchiolar epithelium located at the bronchiolar terminal site
• atypical adenomatous hyperplasia lesions and adenomas




Genotype
MGI:5559061
cn90
Allelic
Composition
Bak1tm1Thsn/Bak1tm1Thsn
Baxtm1Sjk/Baxtm2Sjk
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Bak1tm1Thsn mutation (2 available); any Bak1 mutation (25 available)
Baxtm1Sjk mutation (1 available); any Bax mutation (24 available)
Baxtm2Sjk mutation (1 available); any Bax mutation (24 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• intranasal instillation of an adenovirus expressing Cre recombinase (Ad-Cre) results in the development of sinonasal adenocarcinomas
• however, mice injected intramuscularly with Ad-Cre into the extremities or uterus do not develop soft tissue sarcomas




Genotype
MGI:6273518
cn91
Allelic
Composition
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo/Gt(ROSA)26Sor+
Tg(Flt3-cre)#Ccb/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm4(ACTB-tdTomato,-EGFP)Luo mutation (10 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Flt3-cre)#Ccb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die at a median age of 26 days

growth/size/body
• mice show progressive weight loss after 2 weeks of age
• mice show hepatosplenomegaly after 2 weeks of age

endocrine/exocrine glands
• mice exhibit an atrophied thymus

hematopoietic system
• mice exhibit an atrophied thymus
• mice show hepatosplenomegaly after 2 weeks of age
• mice show anemia after 2 weeks of age
• mice show thrombocytopenia after 2 weeks of age
• mice show an increase in the frequency of CD11c+dendritic cells in the bone marrow and spleen, with expansion particularly in the atrophied thymus
• mice show histiocytic infiltrate in the spleen, liver, lung and intestines and an increase in frequency of CD11b+Gr1+ cells in the blood, bone marrow, liver, and spleen
• frequency of B220+ B lymphocytes is decreased
• frequency of CD3+ T lymphocytes is decreased
• atrophied thymus shows a deficit of CD4-CD8-CD25+ committed T cell progenitors
• atrophied thymus shows a deficit of CD4+CD8+ double-positive cells
• mice show leukocytosis after 2 weeks of age
• mice show monocytosis after 2 weeks of age
• moribund mice show a reduction hematopoietic stem cells (LSK CD150+CD48-) and multipotent progenitors (LSK CD150-CD48+) in the bone marrow and spleen

immune system
• mice exhibit an atrophied thymus
• mice show hepatosplenomegaly after 2 weeks of age
• mice show an increase in the frequency of CD11c+dendritic cells in the bone marrow and spleen, with expansion particularly in the atrophied thymus
• mice show histiocytic infiltrate in the spleen, liver, lung and intestines and an increase in frequency of CD11b+Gr1+ cells in the blood, bone marrow, liver, and spleen
• frequency of B220+ B lymphocytes is decreased
• frequency of CD3+ T lymphocytes is decreased
• atrophied thymus shows a deficit of CD4-CD8-CD25+ committed T cell progenitors
• atrophied thymus shows a deficit of CD4+CD8+ double-positive cells
• mice show leukocytosis after 2 weeks of age
• mice show monocytosis after 2 weeks of age

neoplasm
• mice develop a juvenile myelomonocytic leukemia-like disease

liver/biliary system
• mice show hepatosplenomegaly after 2 weeks of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
juvenile myelomonocytic leukemia DOID:0050458 OMIM:607785
J:247853




Genotype
MGI:5468269
cn92
Allelic
Composition
Gfi1tm5.1(GFI1*)Tmo/Gfi1tm5.1(GFI1*)Tmo
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gfi1tm5.1(GFI1*)Tmo mutation (0 available); any Gfi1 mutation (31 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• of all pIpC-treated mice faster than control mice

hematopoietic system
• all pIpC-treated mice die of myeloproliferative disorder accompanied by an expansion of myeloid cells in the bone marrow, an infiltration of myeloid cells in the spleen, and the appearance of blast cells in the blood faster than control mice

immune system
• all pIpC-treated mice die of myeloproliferative disorder accompanied by an expansion of myeloid cells in the bone marrow, an infiltration of myeloid cells in the spleen, and the appearance of blast cells in the blood faster than control mice




Genotype
MGI:5468270
cn93
Allelic
Composition
Gfi1tm5.1(GFI1*)Tmo/Gfi1+
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gfi1tm5.1(GFI1*)Tmo mutation (0 available); any Gfi1 mutation (31 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• of all pIpC-treated mice faster than control mice

hematopoietic system
• all pIpC-treated mice die of myeloproliferative disorder accompanied by an expansion of myeloid cells in the bone marrow, an infiltration of myeloid cells in the spleen, and the appearance of blast cells in the blood faster than control mice

immune system
• all pIpC-treated mice die of myeloproliferative disorder accompanied by an expansion of myeloid cells in the bone marrow, an infiltration of myeloid cells in the spleen, and the appearance of blast cells in the blood faster than control mice




Genotype
MGI:5468271
cn94
Allelic
Composition
Gfi1tm6.1(GFI1)Tmo/Gfi1tm6.1(GFI1)Tmo
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gfi1tm6.1(GFI1)Tmo mutation (0 available); any Gfi1 mutation (31 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• of all pIpC-treated mice

hematopoietic system
• all pIpC-treated mice die of myeloproliferative disorder accompanied by an expansion of myeloid cells in the bone marrow, an infiltration of myeloid cells in the spleen, and the appearance of blast cells in the blood faster

immune system
• all pIpC-treated mice die of myeloproliferative disorder accompanied by an expansion of myeloid cells in the bone marrow, an infiltration of myeloid cells in the spleen, and the appearance of blast cells in the blood faster




Genotype
MGI:3695569
cn95
Allelic
Composition
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tgfbr2tm1.2Hlm mutation (0 available); any Tgfbr2 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• exhibit reduced survival than controls after 200 days of age, with a median survival of 347 days

neoplasm
• pancreatic tumors examined demonstrate a dominant sarcomatoid histology (50% or more) as well as the ductal adenocarcinoma
• at 200 days of age or later, show well-differentiated ductal adenocarcinoma in the pancreas head region
• develop pancreatic intraepithelial neoplasia (mPanIN) lesions predominantly in the pancreas tail region
• tumors frequently show gross metastasis to the liver and lung, direct invasion to the duodenum, and also peritoneal dissemination
• frequency of metastasis or invasion is much higher (about 50%) than in similar mutants with homozygous, instead of heterozygous, loss of Tgfbr2

endocrine/exocrine glands
• pancreatic tumors examined demonstrate a dominant sarcomatoid histology (50% or more) as well as the ductal adenocarcinoma
• at 200 days of age or later, show well-differentiated ductal adenocarcinoma in the pancreas head region
• develop pancreatic intraepithelial neoplasia (mPanIN) lesions predominantly in the pancreas tail region




Genotype
MGI:3695567
cn96
Allelic
Composition
Krastm4Tyj/Kras+
Tgfbr2tm1.2Hlm/Tgfbr2tm1.2Hlm
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tgfbr2tm1.2Hlm mutation (0 available); any Tgfbr2 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• some die suddenly with a median survival of 59 days

growth/size/body
• begin to demonstrate abdominal distension at around 6-7 weeks of age due to pancreatic tumor
• seen frequently

neoplasm
• 100% penetrance of pancreatic tumors
• progressive development of pancreatic ductal adenocarcinoma; tumor uniformly occupies the whole pancreas and is irregularly shaped and results in almost complete loss of normal pancreatic tissue
• carcinoma cells frequently show nuclear atypia and invasion beyond the basement membrane
• stromal expansion starts in the early tumorigenesis stages and tumors do not show sarcomatoid architecture
• 100% penetrance and tumors are always accompanied by a whole panel of pancreatic intraepithelial neoplasia (mPanIN) lesions and acinar-ductal metaplasia lesions
• tumors are always accompanied by a whole panel of pancreatic intraepithelial neoplasia (mPanIN) lesions and acinar-ductal metaplasia lesions
• although no distant metastasis is seen at 7-10 weeks of age, the few mutants that survive up to 24-27 weeks, show prominent desmoplasia and liver metastasis, lung metastasis, diaphragmatic and duodenal invasion and peritoneal dissemination

liver/biliary system
• duodenum loop is compressed by the tumor, resulting in duodenal and gallbladder dilatation
• at late-stage tumor burden, exhibit multiple necrotic areas in the distal liver parenchyma
• observed sometimes

homeostasis/metabolism
• at late-stage tumor burden (7-10 weeks of age), 32% exhibit portal vein thrombosis; the main trunk of the portal vein is completely obstructed with thrombus
• frequently display bloody ascites

hematopoietic system
• seen frequently

immune system
• seen frequently

behavior/neurological
• a few mutants exhibit paraplegia, most likely because of circulation failure due to oppression of large vessels by the growing tumor

digestive/alimentary system
• duodenum loop is compressed by the tumor, resulting in duodenal and gallbladder dilatation

endocrine/exocrine glands
• duodenum loop is compressed by the tumor, resulting in duodenal and gallbladder dilatation
• 100% penetrance of pancreatic tumors
• progressive development of pancreatic ductal adenocarcinoma; tumor uniformly occupies the whole pancreas and is irregularly shaped and results in almost complete loss of normal pancreatic tissue
• carcinoma cells frequently show nuclear atypia and invasion beyond the basement membrane
• stromal expansion starts in the early tumorigenesis stages and tumors do not show sarcomatoid architecture
• 100% penetrance and tumors are always accompanied by a whole panel of pancreatic intraepithelial neoplasia (mPanIN) lesions and acinar-ductal metaplasia lesions
• tumors are always accompanied by a whole panel of pancreatic intraepithelial neoplasia (mPanIN) lesions and acinar-ductal metaplasia lesions

cardiovascular system
• at late-stage tumor burden (7-10 weeks of age), 32% exhibit portal vein thrombosis; the main trunk of the portal vein is completely obstructed with thrombus




Genotype
MGI:6192639
cn97
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Erbb2*)#Maed/0
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
Tg(Erbb2*)#Maed mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 6 month old mice exhibit severe acinar cell loss

endocrine/exocrine glands
• 6 month old mice exhibit severe acinar cell loss
• mice show accelerated pancreatic intraepithelial neoplasia (PanIN) lesions with severe acinar cell loss, with majority of lesions being PanIN-1 but having some PanIN-2 and -3 lesions

neoplasm
• mice show accelerated pancreatic intraepithelial neoplasia (PanIN) lesions with severe acinar cell loss, with majority of lesions being PanIN-1 but having some PanIN-2 and -3 lesions




Genotype
MGI:6384017
cn98
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Ptpn11tm1Gsf/Ptpn11tm1Gsf
Tg(Six3-cre)69Frty/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptpn11tm1Gsf mutation (0 available); any Ptpn11 mutation (46 available)
Tg(Six3-cre)69Frty mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
vision/eye
N
• normal retina morphology at age P21 and P120
• normal optic nerve morphology at age P21 and P120
• with scotopic ERG using very bright flashes at age 3 months, but not as severe as mice with wildtype Kras allele
• with scotopic ERG using dim flashes at age 3 months, but not as severe as mice with wildtype Kras allele
• with photopic ERG using double flashes at age 3 months, but not as severe as mice with wildtype Kras allele
• reduced b wave amplitude with photopic ERG using double flashes at age 3 months, but not as severe as mice with wildtype Kras allele
• reduced saturated a wave amplitude with scotopic ERG using very bright flashes at age 3 months, but not as severe as mice with wildtype Kras allele
• reduced b wave amplitude with scotopic ERG using dim flashes at age 3 months, but not as severe as mice with wildtype Kras allele




Genotype
MGI:3695568
cn99
Allelic
Composition
Krastm4Tyj/Kras+
Ptf1atm1.1(cre)Cvw/Ptf1a+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1.1(cre)Cvw mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• develop pancreatic intraepithelial neoplasia (mPanIN) lesions within a large amount of normal pancreas

endocrine/exocrine glands
• develop pancreatic intraepithelial neoplasia (mPanIN) lesions within a large amount of normal pancreas




Genotype
MGI:4355873
cn100
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Trim33tm1Los/Trim33tm1Los
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
Trim33tm1Los mutation (0 available); any Trim33 mutation (71 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Pancreatic tumors in Krastm4Tyj/Krastm4Tyj Trim33tm1Los/Trim33tm1Los Tg(Pdx1-cre)89.1Dam/0 and Krastm4Tyj/Krastm4Tyj Cdkn2atm4Rdp/Cdkn2atm4Rdp Tg(Pdx1-cre)89.1Dam/0 mice

endocrine/exocrine glands
• over time endocrine and exocrine components are replaced with abnormal ductal structures
• as early as 3 weeks, mice develop enlarged and dilated ductal structures resembling budding cysts unlike in wild-type mice
• with age, islets become disorganized
• as early 7 weeks
• mice develop pancreatic intraepithelial neoplasia and tumors reminiscent of human intraductal papillary mucinous neoplasm
• however, mice do not exhibit macroscopic evidence of invasive carcinoma
• as early as 3 weeks, mice develop pancreatic intraepithelial neoplasias
• as early 7 weeks, mice exhibit multifocal cystic lesions unlike wild-type mice
• all mice develop cysts that at 6 weeks occupy 50% of the pancreatic area unlike in wild-type mice
• cysts are composed of epithelial cells with cuboidal or cylindrical morphologies that form numerous papillary projections into the cysts
• papillary projections contain masses of small monomorphic cells with an endocrine morphology
• as early as 3 weeks, mice develop acute inflammation of the pancreas unlike wild-type mice

neoplasm
• mice develop pancreatic intraepithelial neoplasia and tumors reminiscent of human intraductal papillary mucinous neoplasm
• however, mice do not exhibit macroscopic evidence of invasive carcinoma
• as early as 3 weeks, mice develop pancreatic intraepithelial neoplasias

immune system
• as early as 3 weeks, mice develop acute inflammation of the pancreas unlike wild-type mice

digestive/alimentary system
• as early as 3 weeks, mice develop enlarged and dilated ductal structures resembling budding cysts unlike in wild-type mice

growth/size/body
• as early 7 weeks
• as early 7 weeks, mice exhibit multifocal cystic lesions unlike wild-type mice
• all mice develop cysts that at 6 weeks occupy 50% of the pancreatic area unlike in wild-type mice
• cysts are composed of epithelial cells with cuboidal or cylindrical morphologies that form numerous papillary projections into the cysts
• papillary projections contain masses of small monomorphic cells with an endocrine morphology




Genotype
MGI:5638045
cn101
Allelic
Composition
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scribtm1.1Phum
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Scribtm1.1Phum mutation (0 available); any Scrib mutation (54 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 100% of mice develop lung lesions at 6 weeks post intranasal adenoviral cre (AdCre) administration, ranging from grades 1 to 3
• mice show accelerated lung tumorigenesis, with more advanced and higher-grade tumors post intranasal AdCre administration compared to single Kras heterozygotes
• a 2.9-fold increase in tumor burden compared to single Kras heterozygotes at 12 weeks post intranasal AdCre administration
• lung tumors from intranasally AdCre treated mice show enhanced stromal reactivity and inflammation

respiratory system
• 100% of mice develop lung lesions at 6 weeks post intranasal adenoviral cre (AdCre) administration, ranging from grades 1 to 3
• mice show accelerated lung tumorigenesis, with more advanced and higher-grade tumors post intranasal AdCre administration compared to single Kras heterozygotes
• a 2.9-fold increase in tumor burden compared to single Kras heterozygotes at 12 weeks post intranasal AdCre administration
• lung tumors from intranasally AdCre treated mice show enhanced stromal reactivity and inflammation

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:216266




Genotype
MGI:5638047
cn102
Allelic
Composition
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scrib+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Scribtm1.1Phum mutation (0 available); any Scrib mutation (54 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 83% of mice develop tumors ranging from grades 1 to 3 at 6 weeks post intranasal adenoviral cre (AdCre) administration

respiratory system
• 83% of mice develop tumors ranging from grades 1 to 3 at 6 weeks post intranasal adenoviral cre (AdCre) administration
• 100% of mice show epithelial hyperplasia at 6 weeks post intranasal AdCre administration

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:216266




Genotype
MGI:3716965
cn103
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)
• following cre-adenovirus treatment, tumors occupy 27% of lung space (J:103407)
• mice treated with intratracheal delivery of cre-expressing adenovirus develop lung cancer (J:191425)
• mice infected with higher doses of cre expressing adenovirus present with clinical signs of lung cancer by 15 weeks of treatment while lower dosed animals show signs of disease around 37 weeks (J:191425)
• a subset of tumors from mice treated with intratracheal delivery of cre-expressing adenovirus show loss of heterozygosity of Trp53 (J:191425)
• treatment of mice treated with intratracheal delivery of cre-expressing adenovirus with an miR-34 expressing lentilvirus almost completely abrogates tumor formation (J:191425)
• treatment of mice that have already formed lung tumors following intratracheal delivery of cre-expressing adenovirus with an miR-34 expressing lentilvirus prevents further progression of tumors (J:191425)
• mice treated with intratracheal delivery of cre-expressing adenovirus show evidence that high-grade adenocarcinomas acquire metastatic characteristics of non-small cell lung cancer
• tumors of mice treated with intratracheal delivery of cre-expressing adenovirus are adenocarcinomas and some evidence that high-grade adenocarcinomas acquire metastatic characteristics

immune system
• mice treated with intratracheal delivery of cre-expressing adenovirus exhibit large lungs filled with tumors and inflammation
• the inflammation that develops in the lungs of mice treated with intratracheal delivery of cre-expressing adenovirus occurs after initial nodules develop

behavior/neurological
• mice treated with intratracheal delivery of cre-expressing adenovirus develop a hunched posture in the most severe cases

growth/size/body
• mice treated with intratracheal delivery of cre-expressing adenovirus exhibit a decline in weight

respiratory system
• mice treated with intratracheal delivery of cre-expressing adenovirus exhibit large lungs filled with tumors and inflammation
• the inflammation that develops in the lungs of mice treated with intratracheal delivery of cre-expressing adenovirus occurs after initial nodules develop
• following cre-adenovirus treatment, all mice develop primary lung tumors that are similar to those found in Krastm4Tyj Trp53tm1Brn heterozygotes (J:103407)
• following cre-adenovirus treatment, tumors occupy 27% of lung space (J:103407)
• mice treated with intratracheal delivery of cre-expressing adenovirus develop lung cancer (J:191425)
• mice infected with higher doses of cre expressing adenovirus present with clinical signs of lung cancer by 15 weeks of treatment while lower dosed animals show signs of disease around 37 weeks (J:191425)
• a subset of tumors from mice treated with intratracheal delivery of cre-expressing adenovirus show loss of heterozygosity of Trp53 (J:191425)
• treatment of mice treated with intratracheal delivery of cre-expressing adenovirus with an miR-34 expressing lentilvirus almost completely abrogates tumor formation (J:191425)
• treatment of mice that have already formed lung tumors following intratracheal delivery of cre-expressing adenovirus with an miR-34 expressing lentilvirus prevents further progression of tumors (J:191425)
• mice treated with intratracheal delivery of cre-expressing adenovirus show evidence that high-grade adenocarcinomas acquire metastatic characteristics of non-small cell lung cancer
• tumors of mice treated with intratracheal delivery of cre-expressing adenovirus are adenocarcinomas and some evidence that high-grade adenocarcinomas acquire metastatic characteristics
• mice treated with intratracheal delivery of cre-expressing adenovirus exhibit labored breathing

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:191425




Genotype
MGI:3842378
cn104
Allelic
Composition
Krastm4Tyj/Kras+
Rbl2tm2Tyj/Rbl2tm2Tyj
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Rbl2tm2Tyj mutation (2 available); any Rbl2 mutation (52 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median life span of cre adenovirus-treated mice is 25 weeks

neoplasm
• tumors from cre adenovirus-treated mice exhibit lower cell proliferation rates compared to in tumors from Krastm4Tyj heterozygotes and Krastm4Tyj/Kras+ Rb1tm3Tyj/Rb1tm3Tyj mice
• cre adenovirus-treated mice develop larger tumors than in cre adenovirus-treated Krastm4Tyj heterozygotes and Krastm4Tyj/Kras+ Rb1tm3Tyj/Rb1tm3Tyj mice
• mice treated with adenovirus cre develop lung lesions in 4 to 6 months
• cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia
• in cre adenovirus-treated mice

respiratory system
• mice treated with adenovirus cre develop lung lesions in 4 to 6 months
• cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas and bronchiolar hyperplasia and dysplasia
• in cre adenovirus-treated mice
• in cre-adenovirus-treated mice
• cre adenovirus-treated mice develop bronchiolar hyperplasia and dysplasia unlike wild-type mice




Genotype
MGI:7710917
cn105
Allelic
Composition
Krastm4Tyj/Kras+
Ube2sem1Ysun/Ube2sem1Ysun
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ube2sem1Ysun mutation (0 available); any Ube2s mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice intratracheally administered an adenovirus expressing cre recombinase (Ad-cre) develop lung tumors with a survival rate similar to single mutant Kras homozygous mice

respiratory system
• mice intratracheally administered an adenovirus expressing cre recombinase (Ad-cre) develop lung tumors with a survival rate similar to single mutant Kras homozygous mice

mortality/aging
• mice intratracheally administered Ad-cre have a median survival time as single mutant Kras homozygous mice




Genotype
MGI:6502114
cn106
Allelic
Composition
Dhx33em1Yazh/Dhx33+
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dhx33em1Yazh mutation (0 available); any Dhx33 mutation (22 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 5 of 14 mice delivered with an adenovirus expressing cre recombinase through nasal inhalation at 8 weeks of age develop lung tumors compared to single Krastm4Tyj mice in which all mice develop tumors, indicating reduced tumor development

respiratory system
• 5 of 14 mice delivered with an adenovirus expressing cre recombinase through nasal inhalation at 8 weeks of age develop lung tumors compared to single Krastm4Tyj mice in which all mice develop tumors, indicating reduced tumor development




Genotype
MGI:6502111
cn107
Allelic
Composition
Dhx33em1Yazh/Dhx33em1Yazh
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Dhx33em1Yazh mutation (0 available); any Dhx33 mutation (22 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• most mice delivered with an adenovirus expressing cre recombinase through nasal inhalation at 8 weeks of age show normal lungs and do not develop lung tumors, and show only small neoplastic regions, indicating inhibition of tumor development that is seen in single Krastm4Tyj mice

respiratory system
• most mice delivered with an adenovirus expressing cre recombinase through nasal inhalation at 8 weeks of age show normal lungs and do not develop lung tumors, and show only small neoplastic regions, indicating inhibition of tumor development that is seen in single Krastm4Tyj mice




Genotype
MGI:3842377
cn108
Allelic
Composition
Krastm4Tyj/Kras+
Rb1tm3Tyj/Rb1tm3Tyj
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Rb1tm3Tyj mutation (10 available); any Rb1 mutation (111 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median life span of cre adenovirus-treated mice is 20 weeks

neoplasm
• tumors from cre adenovirus-treated mice exhibit lower cell proliferation rates compared to in tumors from Krastm4Tyj heterozygotes
• mice treated with adenovirus cre develop lung lesions in 4 to 6 months
• cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas, and bronchiolar hyperplasia and dysplasia
• at end stage, 25% of cre adenovirus-treated mice develop grade 5 tumors, defined by stromal desmoplasia
• cre adenovirus-treated mice develop more numerous tumors than in cre adenovirus-treated Krastm4Tyj heterozygotes and Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice
• in cre adenovirus-treated mice

respiratory system
• mice treated with adenovirus cre develop lung lesions in 4 to 6 months
• cre adenovirus-treated mice develop lung adenocarcinomas, papillary adenomas, and bronchiolar hyperplasia and dysplasia
• at end stage, 25% of cre adenovirus-treated mice develop grade 5 tumors, defined by stromal desmoplasia
• cre adenovirus-treated mice develop more numerous tumors than in cre adenovirus-treated Krastm4Tyj heterozygotes and Krastm4Tyj/Kras+ Rbl2tm2Tyj/Rbl2tm2Tyj mice
• in cre adenovirus-treated mice
• cre adenovirus-treated mice develop bronchiolar hyperplasia and dysplasia unlike wild-type mice




Genotype
MGI:5014515
cn109
Allelic
Composition
Fastm1Ach/Fastm1Ach
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fastm1Ach mutation (0 available); any Fas mutation (82 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• triple mutants injected with an adenoviral Cre into the right ovarian bursa to induce recombination are protected from developing ovarian cancer, with only 1 of 11 mice developing cancer compared to 9 of 12 double Kras and Pten mutants

endocrine/exocrine glands
• triple mutants injected with an adenoviral Cre into the right ovarian bursa to induce recombination are protected from developing ovarian cancer, with only 1 of 11 mice developing cancer compared to 9 of 12 double Kras and Pten mutants

reproductive system
• triple mutants injected with an adenoviral Cre into the right ovarian bursa to induce recombination are protected from developing ovarian cancer, with only 1 of 11 mice developing cancer compared to 9 of 12 double Kras and Pten mutants




Genotype
MGI:5014516
cn110
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants injected with an adenoviral Cre into the right ovarian bursa to induce recombination develop ovarian cancer eight weeks after injection

reproductive system
• mutants injected with an adenoviral Cre into the right ovarian bursa to induce recombination develop ovarian cancer eight weeks after injection

endocrine/exocrine glands
• mutants injected with an adenoviral Cre into the right ovarian bursa to induce recombination develop ovarian cancer eight weeks after injection

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
ovarian cancer DOID:2394 OMIM:167000
OMIM:607893
J:161953




Genotype
MGI:5140101
cn111
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm4Att/Trp53tm4Att
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm4Att mutation (1 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• after treatment with adenoviral cre, mice develop a significantly increased lung tumor burden unlike mice having mutations in only one of the two transactivation domains with normal tumor levels




Genotype
MGI:4818400
cn112
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Ptf1atm1(cre)Hnak/Ptf1a+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:3821750
cn113
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Tg(Cela1-cre/ERT)1Dam/0
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Cela1-cre/ERT)1Dam mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen treated and untreated mice develop pancreatic intraepithelial neoplasia (PanIN) that develops from acinar cells

endocrine/exocrine glands
• tamoxifen treated and untreated mice develop pancreatic intraepithelial neoplasia (PanIN) that develops from acinar cells




Genotype
MGI:3818747
cn114
Allelic
Composition
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm3(CAG-luc)Tyj/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm3(CAG-luc)Tyj mutation (2 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following induction of expression using an adenoviral cre, mice develop lung tumors as in Krastm4Tyj

respiratory system
• following induction of expression using an adenoviral cre, mice develop lung tumors as in Krastm4Tyj




Genotype
MGI:3716392
cn115
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Prm-cre)58Og/0
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Prm-cre)58Og mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

embryo
• at E9.5 vasculature is poorly developed; vasculature has a primitive honeycomb-like network lacking branching vitelline vessels, while large vitelline vessels are absent
• at death, embryos exhibit widespread apoptosis
• embryos show developmental arrest
• marked defect in inner labyrinth layer is observed at E9.5
• fetal blood vessels underlying inner labyrinth layer are absent
• at E9.5, yolk sacs are pale and roughened

cellular
• at death, embryos exhibit widespread apoptosis

cardiovascular system
• fetal blood vessels underlying inner labyrinth layer are absent
• at E9.5 vasculature is poorly developed; vasculature has a primitive honeycomb-like network lacking branching vitelline vessels, while large vitelline vessels are absent




Genotype
MGI:4368025
cn116
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(Scgb1a1-rtTA)1Jaw/0
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Scgb1a1-rtTA)1Jaw mutation (3 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• infiltrating inflammatory cells recruited to tumors in which NF-kB has been inhibited
• tumorigenesis is initiated by infection with lentiviruses expressing Cre and Nfkbia lentiviruses
• doxycycline (Dox)-mediated induction of Nfkbia expression specifically in the tumor cells starting at 16 weeks after tumor initiation results in a significantly diminished tumour growth rate
• tumorigenesis is initiated by infection with lentiviruses expressing Cre and Nfkbia lentiviruses
• doxycycline (Dox)-mediated induction of Nfkbia expression specifically in the tumor cells leads to a significant impairment of tumour development
• tumorigenesis is initiated by infection with lentiviruses expressing Cre and Nfkbia lentiviruses




Genotype
MGI:5437472
cn117
Allelic
Composition
Gt(ROSA)26Sortm1(RAC1*)Jkis/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(RAC1*)Jkis mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice treated with a cre-expressing adenovirus exhibit increased tumor burden due to increased lung cancer cell proliferation compared with Krastm4Tyj heterozygotes treated with a cre-expressing adenovirus
• in mice treated with a cre-expressing adenovirus

respiratory system
• in mice treated with a cre-expressing adenovirus




Genotype
MGI:5441555
cn118
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Lejo/Trp53tm1Lejo
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm1Lejo mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following infection with adenovirus-FLPe/IRES/Cre (Ad-FIC)
• following infection with Ad-FIC

respiratory system
• following infection with adenovirus-FLPe/IRES/Cre (Ad-FIC)
• following infection with Ad-FIC

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:187012




Genotype
MGI:5491219
cn119
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop multiple, aggressive adenocarcinomas in the lungs bilaterally following intranasal delivery of an adenovirus expressing Cre recombinase
• tumor growth is reduced more following two 7.3 Gy fractions of radiation therapy than a single 11.6 Gy fraction
• tumors have decreased BrdU uptake 4 hours after radiation treatment compared to unirradiated tumors, indicating the presence of an intact G1 cell-cycle checkpoint

respiratory system
• mice develop multiple, aggressive adenocarcinomas in the lungs bilaterally following intranasal delivery of an adenovirus expressing Cre recombinase
• tumor growth is reduced more following two 7.3 Gy fractions of radiation therapy than a single 11.6 Gy fraction
• tumors have decreased BrdU uptake 4 hours after radiation treatment compared to unirradiated tumors, indicating the presence of an intact G1 cell-cycle checkpoint

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung cancer DOID:1324 OMIM:211980
OMIM:608935
OMIM:612571
OMIM:612593
OMIM:614210
J:195492




Genotype
MGI:5510699
cn120
Allelic
Composition
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Tg(Cela1-cre/ERT)1Dam/0
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pdpk1tm1Mlw mutation (0 available); any Pdpk1 mutation (138 available)
Tg(Cela1-cre/ERT)1Dam mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mice do not develop pancreatic tumors unlike Krastm4Tyj/Kras+ Tg(Ela1-cre/ERT)1Dam mice

respiratory system




Genotype
MGI:5510700
cn121
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Cela1-cre/ERT)1Dam/0
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Cela1-cre/ERT)1Dam mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype



Genotype
MGI:5510701
cn122
Allelic
Composition
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Ptf1atm1(cre)Hnak/Ptf1a+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pdpk1tm1Mlw mutation (0 available); any Pdpk1 mutation (138 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• pancreas of older mice exhibit some areas of fatty degeneration
• however, acinar to ductal metaplasia observed in acini from Krastm4Tyj Ptf1atm1(cre)Hnak double heterozygotes is rescued in an in vitro assay

neoplasm
N
• pancreatic intraepithelial neoplasia and pancreatic ductal adenocarcinoma observed in Krastm4Tyj Ptf1atm1(cre)Hnak double heterozygotes is rescued




Genotype
MGI:3776023
cn123
Allelic
Composition
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm1(cre/ERT2)Tyj/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(cre/ERT2)Tyj mutation (3 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• adult mice develop widespread hyperplasia throughout the colonic epithelium
• hyperplasia is typified by lengthening of the crypts in adult mice
• large, prominent goblet cells develop in the colon in adult mice

endocrine/exocrine glands
• hyperplasia is typified by lengthening of the crypts in adult mice
• large, prominent goblet cells develop in the colon in adult mice

cellular
• large, prominent goblet cells develop in the colon in adult mice




Genotype
MGI:3716967
cn124
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJae
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm3Tyj mutation (3 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following cre-adenovirus treatment, all mice develop primary lung tumors that are shifted towards more lower grade tumor types
• following cre-adenovirus treatment, tumors occupy 36% of lung space

respiratory system
• following cre-adenovirus treatment, all mice develop primary lung tumors that are shifted towards more lower grade tumor types
• following cre-adenovirus treatment, tumors occupy 36% of lung space




Genotype
MGI:5543250
cn125
Allelic
Composition
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Pms2tm2(cre)Lisk/Pms2tm2(cre)Lisk
Genetic
Background
involves: 129S4/SvJae * 129S4/SvJaeSor
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pms2tm2(cre)Lisk mutation (0 available); any Pms2 mutation (53 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• numbers of stained spots in intestines is not increased compared to mice without the Kras allele, but size of stained patches increases suggesting sporadic cre activation of Kras which might have a selective advantage for mutant stem cells resulting in clonal expansion and crypt fission

neoplasm
• animals become moribund at 5 weeks of age due to high lung tumor burden

cellular
• numbers of stained spots in intestines is not increased compared to mice without the Kras allele, but size of stained patches increases suggesting sporadic cre activation of Kras which might have a selective advantage for mutant stem cells resulting in clonal expansion and crypt fission

respiratory system
• animals become moribund at 5 weeks of age due to high lung tumor burden




Genotype
MGI:3716398
cn126
Allelic
Composition
Krastm4Tyj/Kras+
Meox2tm1(cre)Sor/Meox2+
Genetic
Background
involves: 129S4/SvJae * 129S4/SvJaeSor
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Meox2tm1(cre)Sor mutation (3 available); any Meox2 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• embryos are recovered at a lower frequency (15% vs expected 25%) at E13.5

embryo
N
• mutants show normal vascularization of the yolk sac and placental labyrinth
• fetal-derived hematopoietic progenitors form larger CFU-E (colony-forming unit-erythroid) and BFU-E (burst-forming unit-erythroid) colonies compared with controls

cardiovascular system
• excess cushion tissue often leads to obstructed outflow tract
• at E13.5, embryos frequently show double outlet right ventricle
• atrioventricular valve malformations
• all embryonic hearts have prominent septal defects
• heart defects lead to heart failure and death in embryos by ~E14.5
• embryos appear normal at E12.5, but rapidly develop peripheral hemorrhages by E13.5, consistent with heart failure

hematopoietic system
• red blood cells appear immature compared to wild-type and occasionally highly atypical, consisten with a block in erythroid differentiation
• fetal-derived hematopoietic progenitors form larger CFU-E (colony-forming unit-erythroid) and BFU-E (burst-forming unit-erythroid) colonies compared with controls

respiratory system
• defects in lung branching are apparent by E11.5 compared to controls in vivo and in cultured lungs
• decrease in branching is associated with formation of large, fluid-filled sacs rather than normal terminal branches
• at E12.5, mutant lungs exhibit large dilated bronchi whereas wild-type lungs show secondary and tertiary bronchi
• at E14.5, mutants lungs display dilated bronchi and only a few terminal bronchi
• at E14.5, mutants lungs display only a few terminal bronchioles
• at E12.5, lungs exhibit large dilated bronchi; defect is more pronounced at E14.5
• at E12.5, lungs exhibit large dilated bronchi; defect is more pronounced at E14.5

liver/biliary system
• at E12.5 fetal livers show large areas of apoptosis
• at E12.5, fetal livers appear hypocellular

homeostasis/metabolism
• embryos appear normal at E12.5, but rapidly develop edema by E13.5, consistent with heart failure

integument
• embryos appear normal at E12.5, but rapidly develop pallor by E13.5, consistent with heart failure

cellular
• at E12.5 fetal livers show large areas of apoptosis




Genotype
MGI:3821751
cn127
Allelic
Composition
Gt(ROSA)26Sortm1(Notch1)Dam/Gt(ROSA)26Sor+
Krastm4Tyj/Krastm4Tyj
Tg(Cela1-cre/ERT)1Dam/0
Genetic
Background
involves: 129S4/SvJae * 129S4/SvJaeSor
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Notch1)Dam mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Cela1-cre/ERT)1Dam mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• acinar-ductal metaplasia precedes PanIN
• tamoxifen treated and untreated mice develop widespread pancreatic intraepithelial neoplasia (PanIN) that develops from acinar cells
• PanINs proceed to more severe stages than in Krastm4Tyj/Krastm4Tyj Tg(Ela1-cre/ESR1)1Dam mice

endocrine/exocrine glands
• tamoxifen treated and untreated mice develop widespread pancreatic intraepithelial neoplasia (PanIN) that develops from acinar cells
• PanINs proceed to more severe stages than in Krastm4Tyj/Krastm4Tyj Tg(Ela1-cre/ESR1)1Dam mice
• acinar-ductal metaplasia precedes PanIN




Genotype
MGI:3821752
cn128
Allelic
Composition
Gt(ROSA)26Sortm1(Notch1)Dam/Gt(ROSA)26Sor+
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
Genetic
Background
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Notch1)Dam mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre/Esr1*)35.10Dam mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice treated with tamoxifen staring at E10.5 exhibit pancreatic intraepithelial neoplasia (PanIN) that overtakes nearly all of the organ
• mice not treated with tamoxifen develop focal PanIN that are more numerous than in Krastm4Tyj/Krastm4Tyj Tg(Ipf1-cre/Esr1)35.10Dam mice
• acinar-ductal metaplasia precedes PanIN

endocrine/exocrine glands
• mice treated with tamoxifen staring at E10.5 exhibit pancreatic intraepithelial neoplasia (PanIN) that overtakes nearly all of the organ
• mice not treated with tamoxifen develop focal PanIN that are more numerous than in Krastm4Tyj/Krastm4Tyj Tg(Ipf1-cre/Esr1)35.10Dam mice
• acinar-ductal metaplasia precedes PanIN




Genotype
MGI:5502380
cn129
Allelic
Composition
Cdkn2atm1.1Gsu/Cdkn2atm1.1Gsu
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * 129S4/SvJaeSor * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1.1Gsu mutation (1 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival 25.5 weeks

neoplasm
• starting between 6 and 24 weeks with metastasis
• adenocarcinomas in 9 of 9 invasive carcinomas in the pancreas
• adenocarcinomas in 9 of 9 invasive carcinomas in the pancreas

growth/size/body
• starting between 6 and 24 weeks
• increased girth starting between 6 and 24 weeks

liver/biliary system
• starting between 6 and 24 weeks

homeostasis/metabolism
• starting between 6 and 24 weeks

endocrine/exocrine glands
• starting between 6 and 24 weeks with metastasis
• adenocarcinomas in 9 of 9 invasive carcinomas in the pancreas




Genotype
MGI:5298082
cn130
Allelic
Composition
Krastm4Tyj/Kras+
Krt19tm1(cre/ERT)Ggu/Krt19+
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Krt19tm1(cre/ERT)Ggu mutation (1 available); any Krt19 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 2-4 months after tamoxifen treatment, lip tumors develop in 78% of treated mice
• 2-4 months after tamoxifen treatment, tumors develop in the back skin in 33% of treated mice
• skin tumors are benign papillomas with no sign of malignant transformation seen up to 4 months after treatment with tamoxifen

craniofacial
• 2-4 months after tamoxifen treatment, lip tumors develop in 78% of treated mice

growth/size/body
• 2-4 months after tamoxifen treatment, lip tumors develop in 78% of treated mice

integument
• sebaceous cyst formation is observed as result of bulge stem cell proliferation and abnormal hair follicle (HF) differentiation
• 1 month after tamoxifen treatment, Kras activation results in the enlargement of the majority of sebaceous glands
• 1 month after tamoxifen treatment, Kras activation results in transient increase in hair follicle bulge stem cell (SC) proliferation
• hyperproliferative bulge SCs can still undergo terminal differentiation
• 2-4 months after tamoxifen treatment, tumors develop in the back skin in 33% of treated mice
• skin tumors are benign papillomas with no sign of malignant transformation seen up to 4 months after treatment with tamoxifen

endocrine/exocrine glands
• sebaceous cyst formation is observed as result of bulge stem cell proliferation and abnormal hair follicle (HF) differentiation
• 1 month after tamoxifen treatment, Kras activation results in the enlargement of the majority of sebaceous glands

cellular
• 1 month after tamoxifen treatment, Kras activation results in transient increase in hair follicle bulge stem cell (SC) proliferation




Genotype
MGI:5298087
cn131
Allelic
Composition
Krastm4Tyj/Kras+
Shhtm2(cre/ERT2)Cjt/Shh+
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Shhtm2(cre/ERT2)Cjt mutation (1 available); any Shh mutation (48 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
N
• no epidermal defects or tumor formation are observed with tamoxifen treatment at day 28 (during period of up to 4 months after cre induction) when hair follicles are in full anlagen




Genotype
MGI:5515885
cn132
Allelic
Composition
Krastm4Tyj/Kras+
Stk11tm1.2Rdp/Stk11tm1.2Rdp
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Stk11tm1.2Rdp mutation (0 available); any Stk11 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• in the lungs of mice treated with cre-expressing adenovirus

immune system
• in the lungs of mice treated with cre-expressing adenovirus




Genotype
MGI:5510696
cn133
Allelic
Composition
Gt(ROSA)26Sortm2(Pik3ca*)Dsa/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Pdpk1tm1Mlw/Pdpk1tm1Mlw
Ptf1atm1(cre)Hnak/Ptf1a+
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(Pik3ca*)Dsa mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pdpk1tm1Mlw mutation (0 available); any Pdpk1 mutation (138 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• mice do not develop acinar to ductal metaplasia

neoplasm
N
• mice do not develop pancreatic intraepithelial neoplasia or pancreatic ductal adenocarcinoma




Genotype
MGI:3834444
cn134
Allelic
Composition
Krastm4Tyj/Kras+
Pik3r2tm1Lca/Pik3r2tm1Lca
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pik3r2tm1Lca mutation (1 available); any Pik3r2 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following administration of inhaled adenovirus cre

respiratory system
• following administration of inhaled adenovirus cre




Genotype
MGI:3834445
cn135
Allelic
Composition
Krastm4Tyj/Kras+
Pik3r1tm1Lca/Pik3r1+
Pik3r2tm1Lca/Pik3r2tm1Lca
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pik3r1tm1Lca mutation (1 available); any Pik3r1 mutation (56 available)
Pik3r2tm1Lca mutation (1 available); any Pik3r2 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following administration of inhaled adenovirus cre

respiratory system
• following administration of inhaled adenovirus cre




Genotype
MGI:3834443
cn136
Allelic
Composition
Krastm4Tyj/Kras+
Pik3r1tm1Lca/Pik3r1tm1Lca
Pik3r2tm1Lca/Pik3r2tm1Lca
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pik3r1tm1Lca mutation (1 available); any Pik3r1 mutation (56 available)
Pik3r2tm1Lca mutation (1 available); any Pik3r2 mutation (38 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following administration of inhaled adenovirus cre, mice develop fewer lung tumors than in Krastm4Tyj/Kras+ Pik3r2tm1Lca/Pik3r2tm1Lca or Krastm4Tyj/Kras+ Pik3r2tm1Lca/Pik3r2tm1Lca Pik3r1tm1Lca/Pik3r1+ mice

respiratory system
• following administration of inhaled adenovirus cre, mice develop fewer lung tumors than in Krastm4Tyj/Kras+ Pik3r2tm1Lca/Pik3r2tm1Lca or Krastm4Tyj/Kras+ Pik3r2tm1Lca/Pik3r2tm1Lca Pik3r1tm1Lca/Pik3r1+ mice




Genotype
MGI:4999988
cn137
Allelic
Composition
Col1a1tm5(tetO-GFP/RNAi:Cdkn2a)Slowe/Col1a1+
Gt(ROSA)26Sortm1(Luc)Kael/Gt(ROSA)26Sortm1(rtTA*M2)Jae
Krastm4Tyj/Kras+
Tg(Scgb1a1-rtTA)1Jaw/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Col1a1tm5(tetO-GFP/RNAi:Cdkn2a)Slowe mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(Luc)Kael mutation (3 available); any Gt(ROSA)26Sor mutation (993 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (30 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Scgb1a1-rtTA)1Jaw mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit reduced survival compared with control mice

neoplasm
• mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit increased tumor incidence (size and number) in the lungs with rare noninvasive lung adenomas compared with control mice
• however, mice treated with a cre-expressing adenovirus and treated with doxycycline exhibit tumor regression after doxycycline removal
• in mice treated with a cre-expressing adenovirus and treated with doxycycline

respiratory system
• in mice treated with a cre-expressing adenovirus and treated with doxycycline
• rapid shallow breathing in mice treated with a cre-expressing adenovirus and treated with doxycycline

growth/size/body
• in mice treated with a cre-expressing adenovirus and treated with doxycycline




Genotype
MGI:5556259
cn138
Allelic
Composition
Krastm4Tyj/Kras+
Smad4tm2.1Cxd/Smad4tm2.1Cxd
Tg(Krt1-15-cre/PGR*)22Cot/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Smad4tm2.1Cxd mutation (2 available); any Smad4 mutation (48 available)
Tg(Krt1-15-cre/PGR*)22Cot mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice rapidly develop skin tumors beginning 1 month after induction with topical application of RU486 to the back of the skin with 100% penetrance
• tumors that develop after RU486 induction are well-to-moderately differentiated squamous cell carcinomas with an epidermal lineage or basaloid squamous cell carcinomas of unknown stem cell origin
• a subset of benign or locally invasive tumors form adjacent to the squamous cell carcinoma precursor lesions, which are of hair follicle (trichoepitheliomas, basaloid squamous cell carcinoma) or sebaceous gland origin (sebaceous adenomas) after induction with topical application of RU486
• metastases develop between 8 and 18 weeks after induction with RU486, with 28% of tumor-bearing mice developing lung metastasis and 1 of 18 mice showing lymph node metastasis
• a subset of benign or locally invasive tumors form adjacent to the squamous cell carcinoma precursor lesions, which are of hair follicle (trichoepitheliomas, basaloid squamous cell carcinoma) or sebaceous gland origin (sebaceous adenomas) after induction with topical application of RU486
• a few benign papillomas are seen after induction with topical application of RU486

integument
• mice rapidly develop skin tumors beginning 1 month after induction with topical application of RU486 to the back of the skin with 100% penetrance
• tumors that develop after RU486 induction are well-to-moderately differentiated squamous cell carcinomas with an epidermal lineage or basaloid squamous cell carcinomas of unknown stem cell origin
• a subset of benign or locally invasive tumors form adjacent to the squamous cell carcinoma precursor lesions, which are of hair follicle (trichoepitheliomas, basaloid squamous cell carcinoma) or sebaceous gland origin (sebaceous adenomas) after induction with topical application of RU486

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
squamous cell carcinoma DOID:1749 J:203922




Genotype
MGI:6295996
cn139
Allelic
Composition
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Hmga2tm1.1Mmw/Hmga2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm2Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6NCrl * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm9(CAG-tdTomato)Hze mutation (4 available); any Gt(ROSA)26Sor mutation (993 available)
Hmga2tm1.1Mmw mutation (1 available); any Hmga2 mutation (12 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice develop pancreatic ductal adenocarcinoma (PDAC)

neoplasm
• mice develop pancreatic ductal adenocarcinoma (PDAC)
• GFP+ PDAC cells form tumors form more metastases than GFP- PDAC cells when transplanted into recipient mice
• the highly metastatic PDAC subpopulation is enriched for hypoxia-induced genes

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:245611




Genotype
MGI:5013409
cn140
Allelic
Composition
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Tg(Vil1-cre)20Syr/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm2(Rnf187)Jhai mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Vil1-cre)20Syr mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice exhibit increased cell proliferation in the colonic crypt compared with wild-type mice

cellular
• mice exhibit increased cell proliferation in the colonic crypt compared with wild-type mice




Genotype
MGI:5659881
cn141
Allelic
Composition
Krastm4Tyj/Kras+
Stk11tm1.1Rdp/Stk11tm1.2Rdp
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Stk11tm1.1Rdp mutation (0 available); any Stk11 mutation (35 available)
Stk11tm1.2Rdp mutation (0 available); any Stk11 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a mean survival of 9 weeks after ad-cre inoculation

neoplasm
• regional lymph-node metastases and axial skeleton metastases are seen in 61% of ad-cre inoculated mice
• mice inoculated with ad-cre develop lung tumors; tumor burden is increased at early time points and larger lesions at later time points are seen than in single Kras mutants
• adenocarcinoma is seen in all metastatic lesions
• 2 of 27 ad-cre treated mice show large cell carcinoma
• 56% of ad-cre treated mice develop squamous cell carcinomas (SCCs) or adenosquamous carcinomas
• squamous tumors do not express pro-surfactant protein, but express pan-keratin and p63, markers of SCC

respiratory system
• mice inoculated with ad-cre develop lung tumors; tumor burden is increased at early time points and larger lesions at later time points are seen than in single Kras mutants
• adenocarcinoma is seen in all metastatic lesions
• 2 of 27 ad-cre treated mice show large cell carcinoma
• 56% of ad-cre treated mice develop squamous cell carcinomas (SCCs) or adenosquamous carcinomas
• squamous tumors do not express pro-surfactant protein, but express pan-keratin and p63, markers of SCC

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung non-small cell carcinoma DOID:3908 J:124682




Genotype
MGI:5659896
cn142
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a median survival of 24 weeks after ad-cre inoculation

neoplasm
• 3 of 15 (20%) ad-cre inoculated mice exhibit metastasis
• mice inoculated with ad-cre by inhalation develop infrequent highly lethal tumors; all tumors are adenocarcinomas

respiratory system
• mice inoculated with ad-cre by inhalation develop infrequent highly lethal tumors; all tumors are adenocarcinomas




Genotype
MGI:5659880
cn143
Allelic
Composition
Krastm4Tyj/Kras+
Stk11tm1.1Rdp/Stk11tm1.1Rdp
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Stk11tm1.1Rdp mutation (0 available); any Stk11 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a median survival of 9 weeks after ad-cre inoculation

neoplasm
• regional lymph-node metastases and axial skeleton metastases are seen in 61% of ad-cre inoculated mice
• mice inoculated with ad-cre develop lung tumors; tumor burden is increased at early time points and larger lesions at later time points are seen than in single Kras mutants
• adenocarcinoma is seen in all metastatic lesions
• 2 of 27 ad-cre treated mice show large cell carcinoma
• 56% of ad-cre treated mice develop squamous cell carcinomas (SCCs) or adenosquamous carcinomas
• squamous tumors do not express pro-surfactant protein, but express pan-keratin and p63, markers of SCC

respiratory system
• mice inoculated with ad-cre develop lung tumors; tumor burden is increased at early time points and larger lesions at later time points are seen than in single Kras mutants
• adenocarcinoma is seen in all metastatic lesions
• 2 of 27 ad-cre treated mice show large cell carcinoma
• 56% of ad-cre treated mice develop squamous cell carcinomas (SCCs) or adenosquamous carcinomas
• squamous tumors do not express pro-surfactant protein, but express pan-keratin and p63, markers of SCC

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
lung non-small cell carcinoma DOID:3908 J:124682




Genotype
MGI:3814193
cn144
Allelic
Composition
Gt(ROSA)26Sortm1(Tva)Dsa/Gt(ROSA)26Sor+
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Tva)Dsa mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival of mice infected with RCASBP(A)-shTP53, which knocks down Trp53 expression, is only 151 days compared to 485 days for controls

neoplasm
• mice infected with RCASBP(A)-shTP53, which knocks down Trp53 expression, display a significantly shorter latency of pancreatic ductal adenocarcinoma development
• all infected mice develop invasive pancreatic ductal adenocarcinoma within 10 months

endocrine/exocrine glands
• mice infected with RCASBP(A)-shTP53, which knocks down Trp53 expression, display a significantly shorter latency of pancreatic ductal adenocarcinoma development
• all infected mice develop invasive pancreatic ductal adenocarcinoma within 10 months




Genotype
MGI:7435431
cn145
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Cdh5-cre/ERT2)1Rha/0
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6NCrl * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm14(CAG-tdTomato)Hze mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Cdh5-cre/ERT2)1Rha mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice administered tamoxifen at P1 show early lethality beginning at P12

cardiovascular system
N
• mice administered tamoxifen at P1fail to show frequent cranial hemorrhage or cortical brain arteriovenous malformations (bAVMs) at P14 or P21




Genotype
MGI:5502381
cn146
Allelic
Composition
Cdkn2atm2.1Rdp/Cdkn2atm2.1Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Rdp mutation (2 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival 15.5 weeks

neoplasm
• starting between 6 and 24 weeks with metastasis
• adenocarcinomas in 21 of 22 invasive carcinomas in the pancreas
• adenocarcinomas in 21 of 22 invasive carcinomas in the pancreas

growth/size/body
• starting between 6 and 24 weeks
• increased girth starting between 6 and 24 weeks

liver/biliary system
• starting between 6 and 24 weeks

homeostasis/metabolism
• starting between 6 and 24 weeks

endocrine/exocrine glands
• starting between 6 and 24 weeks with metastasis
• adenocarcinomas in 21 of 22 invasive carcinomas in the pancreas




Genotype
MGI:5141739
cn147
Allelic
Composition
Fgfr3tm4Cxd/Fgfr3+
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fgfr3tm4Cxd mutation (0 available); any Fgfr3 mutation (54 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Upk2-cre)6Xrw mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• by 1 year of age, 44% of mutants develop skin papilloma, with tumors reaching 1 cm in diameter by a median of 220 days

mortality/aging
• shorter survival due to skin papillomas, with a survival time between 100-400 days

neoplasm
N
• mice aged to 12 month do not develop urothelial hyperplasia or urothelial carcinoma or lung tumors
• by 1 year of age, 44% of mutants develop skin papilloma, with tumors reaching 1 cm in diameter by a median of 220 days




Genotype
MGI:5438089
cn148
Allelic
Composition
Krastm4Tyj/Kras+
Gt(ROSA)26Sortm1(sb13)Tuv/Gt(ROSA)26Sor+
Tg(Pdx1-cre)6Tuv/0
TgTn(sb-T2/Onc)#Dla/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(sb13)Tuv mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
TgTn(sb-T2/Onc)#Dla mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice succumb to invasive pancreatic neoplasms

neoplasm
• rapid progression, multi-focal and invasive
• pancreatic ductal adenocarcinoma or invasive cystic neoplasms with metastasis to the liver and lungs

endocrine/exocrine glands
• rapid progression, multi-focal and invasive
• pancreatic ductal adenocarcinoma or invasive cystic neoplasms with metastasis to the liver and lungs




Genotype
MGI:5432231
cn149
Allelic
Composition
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Amhr2tm3(cre)Bhr/Amhr2+
Genetic
Background
involves: 129S4/SvJae * 129S7/SvEvBrd * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Amhr2tm3(cre)Bhr mutation (1 available); any Amhr2 mutation (29 available)
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (49 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• female mutants develop granulosa cell tumors by 12-14 weeks of age
• male mutants develop granulosa cell tumors of the testis by 4-5 months of age; tumors do not spread or metastasize

reproductive system
• female mutants develop granulosa cell tumors by 12-14 weeks of age
• seminiferous tubule degeneration is seen by 4 weeks of age
• male mutants develop granulosa cell tumors of the testis by 4-5 months of age; tumors do not spread or metastasize

endocrine/exocrine glands
• female mutants develop granulosa cell tumors by 12-14 weeks of age
• seminiferous tubule degeneration is seen by 4 weeks of age
• male mutants develop granulosa cell tumors of the testis by 4-5 months of age; tumors do not spread or metastasize




Genotype
MGI:6403690
cn150
Allelic
Composition
Brf1tm1Arte/Brf1tm1Arte
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * 129S7/SvEvBrd * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brf1tm1Arte mutation (0 available); any Brf1 mutation (23 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• extended survival compared to control mice with normal Brf1

neoplasm
• at a reduced rate and with extended survival compared to control mice with normal Brf1
• however, tumors that do form lack recombined Brf1

endocrine/exocrine glands
• at a reduced rate and with extended survival compared to control mice with normal Brf1
• however, tumors that do form lack recombined Brf1




Genotype
MGI:5432224
cn151
Allelic
Composition
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Tg(CYP19A1-cre)1Jri/0
Genetic
Background
involves: 129S4/SvJae * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (49 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(CYP19A1-cre)1Jri mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mutants die within 3.5-5.5 months of age

neoplasm
• female mutants exhibit precancerous lesions in the ovaries at between 4 and 5 weeks of age
• female mutants develop bilateral granulosa cell tumors by 3 months of age

endocrine/exocrine glands
• marker analysis indicates that at 6 weeks of age granulosa cell differentiation is blocked
• female mutants exhibit precancerous lesions in the ovaries at between 4 and 5 weeks of age
• female mutants develop bilateral granulosa cell tumors by 3 months of age

reproductive system
• marker analysis indicates that at 6 weeks of age granulosa cell differentiation is blocked
• female mutants exhibit precancerous lesions in the ovaries at between 4 and 5 weeks of age
• female mutants develop bilateral granulosa cell tumors by 3 months of age

homeostasis/metabolism
• at 6 weeks of age in females
• at 6 weeks of age in females
• at 6 weeks of age in females

cellular
• marker analysis indicates that at 6 weeks of age granulosa cell differentiation is blocked

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
granulosa cell tumor DOID:2999 J:186144
ovarian cancer DOID:2394 OMIM:167000
OMIM:607893
J:186144




Genotype
MGI:5790500
cn152
Allelic
Composition
Ctnnb1tm1Mmt/Ctnnb1tm1Mmt
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
Genetic
Background
involves: 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (49 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Upk2-cre)6Xrw mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mean survival of 185 days and median survival of 200 days

neoplasm
• mice rapidly develop bladder tumors resembling urothelial cell carcinoma

renal/urinary system
• mice rapidly develop bladder tumors resembling urothelial cell carcinoma

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
urinary bladder cancer DOID:11054 OMIM:109800
J:234236




Genotype
MGI:5141743
cn153
Allelic
Composition
Ctnnb1tm1Mmt/Ctnnb1+
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
Genetic
Background
involves: 129S4/SvJae * 129X1/SvJ * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (49 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Upk2-cre)6Xrw mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm

respiratory system




Genotype
MGI:5013916
cn154
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants exhibit accelerated development of acinar-to-ductal metaplasia, malignant pancreatic intraepithelial neoplasia and pancreatic ductal adenocarcinoma compared to single heterozygous Kras mutants, with almost 100% of mutants succumbing to cancer by 12 months of age
• 21 of 25 mice alive past 2 months of age develop well-to-moderately differentiated invasive ductal cancers
• rare metastasis to lungs is seen
• at 3 months of age, 8 of 12 mutants show development of pancreatic ductal adenocarcinoma (PDAC), and all mice show PDAC by 6 months of age
• loss of Pten heterozygosity is seen during pancreatic ductal adenocarcinoma progression but not in mPanIN lesions
• mutants show malignant pancreatic intraepithelial neoplasia (mPanIN) development starting at 1 month of age, and all show mPanIN by 3 months of age

mortality/aging
• median survival time is about 3.5 months

endocrine/exocrine glands
• mutants exhibit accelerated development of acinar-to-ductal metaplasia, malignant pancreatic intraepithelial neoplasia and pancreatic ductal adenocarcinoma compared to single heterozygous Kras mutants, with almost 100% of mutants succumbing to cancer by 12 months of age
• 21 of 25 mice alive past 2 months of age develop well-to-moderately differentiated invasive ductal cancers
• rare metastasis to lungs is seen
• at 3 months of age, 8 of 12 mutants show development of pancreatic ductal adenocarcinoma (PDAC), and all mice show PDAC by 6 months of age
• loss of Pten heterozygosity is seen during pancreatic ductal adenocarcinoma progression but not in mPanIN lesions
• mutants show malignant pancreatic intraepithelial neoplasia (mPanIN) development starting at 1 month of age, and all show mPanIN by 3 months of age
• acinar-to-ductal metaplasia is seen at 1-3 months of age, concentrated in the transition zone between morphologically normal pancreatic structures and mPanIN and PDAC lesions
• acinar-to-ductal metaplasia development precedes mPanIN formation
• metaplastic lesions show an increase in CD44+ cells

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:164210




Genotype
MGI:3035835
cn155
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• survival for around 35 days after pI-pC treatment
• survival of around 58 days even without pI-pC treatment

neoplasm
• 7 of 25 mice injected with pIpC develop thymic T cell lymphoblastic lymphomas
• 2 of 6 non pIpC treated mice show thymic lymphomas
• 10 of 17 mice injected with pIpC exhibit multiple nodules in the lungs consisting of proliferating type II penumocytes
• 5 of 6 non pIpC treated mice show pulmonary adenomas
• squamous papillomas
• 8 of 25 mice injected with pIpC develop squamous papillomas involving the oral mucosa
• 2 of 6 non-pIpC treated mice show oral squamous papillomas
• 8 of 22 mice injected with pIpC develop squamous papillomas involving the esophageal mucosa
• 12 of 19 mice injected with pIpC develop squamous papillomas involving the anal and vulvo-vaginal skin and 8 of 22 mice develop squamous papillomas involving the ear
• 2 of 6 non-pIpC treated mice show ear squamous papillomas

growth/size/body
• 8 of 25 mice injected with pIpC develop squamous papillomas involving the oral mucosa
• 2 of 6 non-pIpC treated mice show oral squamous papillomas
• becoming emaciated
• mice injected with pIpC develop moderate to severe splenomegaly

hematopoietic system
• 7 of 25 mice injected with pIpC develop thymic T cell lymphoblastic lymphomas
• 2 of 6 non pIpC treated mice show thymic lymphomas
• mice injected with pIpC develop moderate to severe splenomegaly
• develop lethal hematopoietic disease
• 4-7 week old mice injected with pIpC develop a myeloproliferative disorder
• bone marrow of mice injected with pIpC shows myelomonocytic expansion
• all mice that are not treated with pIpC also develop a hematopoietic disease, however these mice exhibit expression of the mutant Kras, indicating that most likely endogenous IFN expression is sufficient to induce the cre transgene
• bone marrow cells from pIpC injected mice readily form colonies, predominately monocyte colony-forming units (M-CFUs) in a growth factor-independent manner unlike controls
• myeloproliferative phenotype
• myeloid hyperplasia of bone marrow
• expansion of red pulp in spleen by granulocyte/monocyte lineages in 11 out of 16 cases
• erythroid expansion was seen in red pulp of spleen in 5 of 16 cases
• the liver shows perivascular and periportal infiltration by myeloid and erythroid cell populations
• mice injected with pIpC become anemic
• mice injected with pIpC have a mean hematocrit of 27% compared with 45% in controls
• leukocytosis, usually involving increases in granulocytes, in both pIpC and non-pIpC treated mice
• leukocytosis in mice injected with pIpC is mainly due to an increase in granulocyte population
• mice injected with pIpC show expansion of the red pulp by varying degrees of granulocytic

immune system
• 7 of 25 mice injected with pIpC develop thymic T cell lymphoblastic lymphomas
• 2 of 6 non pIpC treated mice show thymic lymphomas
• mice injected with pIpC develop moderate to severe splenomegaly
• 4-7 week old mice injected with pIpC develop a myeloproliferative disorder
• bone marrow of mice injected with pIpC shows myelomonocytic expansion
• all mice that are not treated with pIpC also develop a hematopoietic disease, however these mice exhibit expression of the mutant Kras, indicating that most likely endogenous IFN expression is sufficient to induce the cre transgene
• bone marrow cells from pIpC injected mice readily form colonies, predominately monocyte colony-forming units (M-CFUs) in a growth factor-independent manner unlike controls
• myeloproliferative phenotype
• myeloid hyperplasia of bone marrow
• leukocytosis, usually involving increases in granulocytes, in both pIpC and non-pIpC treated mice
• leukocytosis in mice injected with pIpC is mainly due to an increase in granulocyte population
• mice injected with pIpC show expansion of the red pulp by varying degrees of granulocytic
• 6 of 17 mice injected with pIpC develop nodal lymphoid hyperplasia

liver/biliary system
• perivascular and periportal infiltration in liver by myeloid and erythroid cells similar to what is seen in spleen

integument
• ruffled fur
• 12 of 19 mice injected with pIpC develop squamous papillomas involving the anal and vulvo-vaginal skin and 8 of 22 mice develop squamous papillomas involving the ear
• 2 of 6 non-pIpC treated mice show ear squamous papillomas

digestive/alimentary system
• 8 of 22 mice injected with pIpC develop squamous papillomas involving the esophageal mucosa

endocrine/exocrine glands
• 7 of 25 mice injected with pIpC develop thymic T cell lymphoblastic lymphomas
• 2 of 6 non pIpC treated mice show thymic lymphomas

respiratory system
• 10 of 17 mice injected with pIpC exhibit multiple nodules in the lungs consisting of proliferating type II penumocytes
• 5 of 6 non pIpC treated mice show pulmonary adenomas

craniofacial
• 8 of 25 mice injected with pIpC develop squamous papillomas involving the oral mucosa
• 2 of 6 non-pIpC treated mice show oral squamous papillomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
juvenile myelomonocytic leukemia DOID:0050458 OMIM:607785
J:88163




Genotype
MGI:5013917
cn156
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• all mutants develop pancreatic ductal adenocarcinoma by 3 weeks of age

endocrine/exocrine glands
• mutants show severe exocrine pancreatic atrophy and edema along with the presence of mPanINs, metaplasias, and ducto-insular complexes and pancreatic ductal adenocarcinoma at P17
• all mutants develop pancreatic ductal adenocarcinoma by 3 weeks of age
• mutants exhibit acinar-to-ductal metaplasia

homeostasis/metabolism
• pancreas at P1-P17 shows edema

mortality/aging
• mutants are moribound by weaning, with a median survival of about 17 days

digestive/alimentary system
• mutants show severe exocrine pancreatic atrophy and edema along with the presence of mPanINs, metaplasias, and ducto-insular complexes and pancreatic ductal adenocarcinoma at P17

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:164210




Genotype
MGI:4849441
cn157
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Gfap-cre)77.6Mvs/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL/6NHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Gfap-cre)77.6Mvs mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• survival is on average 22 weeks

neoplasm
• mutants develop multiple visible subcutaneous tumors with 100% penetrance, starting from 4 months of age
• majority of tumors are located on the back and sides
• each mutant has more than one lesion with features of human neurofibroma and malignant peripheral nerve sheath tumor
• progressive development of malignant peripheral nerve sheath tumors (MPNST) from neurofibroma, with 100% of mutants showing MPNST when followed for 7 months
• Pten loss of heterozygosity in mutants correlates with MPNST transformation from neurofibromas

nervous system
• each mutant has more than one lesion with features of human neurofibroma and malignant peripheral nerve sheath tumor
• progressive development of malignant peripheral nerve sheath tumors (MPNST) from neurofibroma, with 100% of mutants showing MPNST when followed for 7 months
• Pten loss of heterozygosity in mutants correlates with MPNST transformation from neurofibromas




Genotype
MGI:3716393
cn158
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Tek-cre)12Flv/0
Genetic
Background
involves: 129S4/SvJae * C3H * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Tek-cre)12Flv mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryo
N
• mutants show normal vascularization of the yolk sac and placental labyrinth




Genotype
MGI:4943568
cn159
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Scgb1a1-cre)1Tauc/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Scgb1a1-cre)1Tauc mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
respiratory system
• bronchioles exhibit clusters of CCSP+SPC+ cells (indicators of BASCs) as early as 4 weeks of age that are not seen in controls
• mutants exhibit expansion of bronchioalveolar stem cells (BASCs) in terminal bronchi
• small bronchi exhibit clusters of CCSP+SPC+ cells (indicators of BASCs) as early as 4 weeks of age that are not seen in controls




Genotype
MGI:5659853
cn160
Allelic
Composition
Krastm4Tyj/Kras+
Siva1tm1.1Att/Siva1tm1.2Att
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Siva1tm1.1Att mutation (1 available); any Siva1 mutation (17 available)
Siva1tm1.2Att mutation (0 available); any Siva1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice exhibit reduced numbers of both adenomas and adenocarcinomas as compared to controls following intratracheal injection of Cre expressing adenovirus (Ad-Cre)
• mice exhibit lower tumor burden (% of lung area comprising tumors) as compared to controls following intratracheal injection of Ad-Cre

respiratory system
• mice exhibit reduced numbers of both adenomas and adenocarcinomas as compared to controls following intratracheal injection of Cre expressing adenovirus (Ad-Cre)
• mice exhibit lower tumor burden (% of lung area comprising tumors) as compared to controls following intratracheal injection of Ad-Cre
• mice exhibit reduced numbers of hyperplastic lesions as compared to controls following intratracheal injection of Ad-Cre




Genotype
MGI:4411919
cn161
Allelic
Composition
Krastm4Tyj/Kras+
Tg(MUC1)79.24Gend/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(MUC1)79.24Gend mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• following injection of a cre adenovirus in the ovarian bursa, all mice develop ovarian lesions consisting of endometrial glandular epithelium unlike un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice

immune system
• following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice
• following injection of a cre adenovirus in the ovarian bursa, mice exhibit an increase in the anti-MUC1 IgG response compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice
• following injection of a cre adenovirus in the ovarian bursa, mice exhibit an increase in MUC1-specific IgM unlike un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice and similarly treated Tg(MUC1)79.24Gend mice
• following injection of a cre adenovirus in the ovarian bursa, T cells in the spleen and regional lymph nodes exhibit decreased IFN-gamma in response to polyclonal stimulation compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice

hematopoietic system
• following injection of a cre adenovirus in the ovarian bursa, mice with endometriosis also exhibit an increase in spleen and regional lymph nodes T regulatory cells compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice
• following injection of a cre adenovirus in the ovarian bursa, mice exhibit an increase in the anti-MUC1 IgG response compared with un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice
• following injection of a cre adenovirus in the ovarian bursa, mice exhibit an increase in MUC1-specific IgM unlike un-injected Krastm4Tyj Tg(MUC1)79.24Gend mice and similarly treated Tg(MUC1)79.24Gend mice




Genotype
MGI:5659856
cn162
Allelic
Composition
Krastm4Tyj/Kras+
Siva1tm1.2Att/Siva1+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Siva1tm1.2Att mutation (0 available); any Siva1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice exhibit reduced numbers of both adenomas and adenocarcinomas as compared to controls following intratracheal injection of Cre expressing adenovirus (Ad-Cre)
• mice exhibit lower tumor burden (% of lung area comprising tumors) as compared to controls following intratracheal injection of Ad-Cre

respiratory system
• mice exhibit reduced numbers of both adenomas and adenocarcinomas as compared to controls following intratracheal injection of Cre expressing adenovirus (Ad-Cre)
• mice exhibit lower tumor burden (% of lung area comprising tumors) as compared to controls following intratracheal injection of Ad-Cre
• mice exhibit reduced numbers of hyperplastic lesions as compared to controls following intratracheal injection of Ad-Cre




Genotype
MGI:5607955
cn163
Allelic
Composition
Krastm4Tyj/Kras+
Plcl1tm1.1Matk/Plcl1tm1.1Matk
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Plcl1tm1.1Matk mutation (0 available); any Plcl1 mutation (54 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• lung tumor incidence in ad-cre infected mice is similar to Kras mutant mice wild-type for Plcl1




Genotype
MGI:5559056
cn164
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice injected intramuscularly with an adenovirus expressing Cre recombinase into the extremities or into the uterus develop soft tissue sarcomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
sarcoma DOID:1115 J:125101




Genotype
MGI:5528687
cn165
Allelic
Composition
Krastm4Tyj/Kras+
Mapkapk2tm1.1Yaff/Mapkapk2tm1.1Yaff
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Mapkapk2tm1.1Yaff mutation (1 available); any Mapkapk2 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• lung adenocarcinomas cover 9% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus
• tumor burden progresses from 9% of lung (6 weeks) to 28% at experimental endpoint (12+ weeks) in the presence of a Cre-recombinase expressing adenovirus
• Mapkap2 expressing tumors (MK2+) represent a higher proportion of tumor burden in relation to Mapkapk2 (MK2-) null tumors in the presence of a Cre-recombinase expressing adenovirus adenovirus

respiratory system
• lung adenocarcinomas cover 9% of lung area 9 weeks after administration of a Cre-recombinase expressing adenovirus
• tumor burden progresses from 9% of lung (6 weeks) to 28% at experimental endpoint (12+ weeks) in the presence of a Cre-recombinase expressing adenovirus
• Mapkap2 expressing tumors (MK2+) represent a higher proportion of tumor burden in relation to Mapkapk2 (MK2-) null tumors in the presence of a Cre-recombinase expressing adenovirus adenovirus




Genotype
MGI:5298090
cn166
Allelic
Composition
Krastm4Tyj/Kras+
Tg(IVL-cre/ERT2)1Blpn/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(IVL-cre/ERT2)1Blpn mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 2-4 months following tamoxifen treatment, tumors develop in the face in 40% of treated mutants
• 100% of animals develop lip tumors 2-4 months after tamoxifen treatment
• 2-4 months following RU486 treatment, tumors develop in the back skin in 80% of treated mice
• tumors have hallmarks of benign papillomas with signs of squamous differentiation
• no animals develop invasive carcinoma within 4 months of tamoxifen treatment

craniofacial
• 2-4 months following tamoxifen treatment, tumors develop in the face in 40% of treated mutants
• 100% of animals develop lip tumors 2-4 months after tamoxifen treatment

integument
• hyperplasia of the interfollicular epidermis in TAM treated mice
• after tamoxifen treatment, hyperthickening of the interfollicular epidermis (IFE) is observed, indicating that hyperproliferation of IFE cells and hyperplasia of the IFE results from Kras LSL-G12D activation
• 2-4 months following RU486 treatment, tumors develop in the back skin in 80% of treated mice
• tumors have hallmarks of benign papillomas with signs of squamous differentiation
• no animals develop invasive carcinoma within 4 months of tamoxifen treatment

growth/size/body
• 2-4 months following tamoxifen treatment, tumors develop in the face in 40% of treated mutants
• 100% of animals develop lip tumors 2-4 months after tamoxifen treatment




Genotype
MGI:5440071
cn167
Allelic
Composition
Braftm2Cpri/Braf+
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm2Cpri mutation (0 available); any Braf mutation (60 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• in primary mouse embryonic fibroblasts treated with adenovirus-cre compared with wild-type cells although not as much as in cells heterozygous for Krastm4Tyj

neoplasm
• in mice infected with adenovirus cre
• however, mice do not exhibit increased lung tumor incidence compared with Krastm4Tyj heterozygotes

respiratory system
• in mice infected with adenovirus cre
• however, mice do not exhibit increased lung tumor incidence compared with Krastm4Tyj heterozygotes




Genotype
MGI:7738284
cn168
Allelic
Composition
Diras2em1Gpt/Diras2em1Gpt
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
Ube2ftm1c(EUCOMM)Hmgu/Ube2ftm1c(EUCOMM)Hmgu
Genetic
Background
involves: 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Diras2em1Gpt mutation (0 available); any Diras2 mutation (20 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (31 available)
Ube2ftm1c(EUCOMM)Hmgu mutation (0 available); any Ube2f mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• relative to mutant mice wild-type for Diras2
• incidence of pancreatic tumors is similar to mutant mice wild-type for both Diras2 and Ube2f but with fewer stage I and more stage II and III tumors

neoplasm
• relative to mutant mice wild-type for Diras2
• incidence of pancreatic tumors is similar to mutant mice wild-type for both Diras2 and Ube2f but with fewer stage I and more stage II and III tumors




Genotype
MGI:5505293
cn169
Allelic
Composition
Krastm4Tyj/Kras+
Ralatm1.2Cjm/Ralatm1.2Cjm
Ralbtm1.1Cjm/Ralbtm1.2Cjm
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ralatm1.2Cjm mutation (2 available); any Rala mutation (28 available)
Ralbtm1.1Cjm mutation (0 available); any Ralb mutation (47 available)
Ralbtm1.2Cjm mutation (2 available); any Ralb mutation (47 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• in a model of non-small cell lung carcinoma, mice exposed to a cre-expressing adenovirus exhibit fewer tumors and smaller tumor area compared with Krastm4Tyj/Kras+ Ralatm1.2Cjm/Rala+ Ralbtm1.1Cjm/Ralbtm1.2Cjm control mice




Genotype
MGI:6505552
cn170
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• pIpC-induced mice die earlier than induced conditional Krastm1.1Khai mice

hematopoietic system
• mice induced with polyinosinic:polycytidylic acid (pIpC) develop a myelodysplastic syndrome/myeloproliferative neoplasm that is qualitatively similar to that seen in conditional Krastm1.1Khai mice, but with a faster onset
• dying pIpC-induced mice show splenomegaly
• dying pIpC-induced mice show severe anemia
• expansion of immature myeloid cells in the bone marrow and spleen in pIpC-induced mice
• expansion of immature myeloid cells in the bone marrow of pIpC-induced mice

immune system
• dying pIpC-induced mice show splenomegaly

growth/size/body
• dying pIpC-induced mice show splenomegaly




Genotype
MGI:5556244
cn171
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Krt1-15-cre/PGR*)22Cot/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Krt1-15-cre/PGR*)22Cot mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop benign papillomas without progressing to malignancy following topical application of RU486 to the back of skin at 3 weeks of age for 5 days




Genotype
MGI:6157296
cn172
Allelic
Composition
Fbxw7tm1Iken/Fbxw7tm1Iken
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fbxw7tm1Iken mutation (0 available); any Fbxw7 mutation (84 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• all mice develop cholangiocarcinoma-like lesions composed of dysplastic dust-like structures surrounded by fibrosis within 2 months of birth

neoplasm
• all mice develop cholangiocarcinoma-like lesions composed of dysplastic dust-like structures surrounded by fibrosis within 2 months of birth

endocrine/exocrine glands
• all mice develop cholangiocarcinoma-like lesions composed of dysplastic dust-like structures surrounded by fibrosis within 2 months of birth




Genotype
MGI:6157295
cn173
Allelic
Composition
Fbxw7tm1Iken/Fbxw7+
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6N * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Fbxw7tm1Iken mutation (0 available); any Fbxw7 mutation (84 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• bile duct hyperplasia is seen in some mice at 8 months of age
• bile duct dilation is seen in some mice at 8 months of age

liver/biliary system
• bile duct hyperplasia is seen in some mice at 8 months of age
• bile duct dilation is seen in some mice at 8 months of age




Genotype
MGI:5441554
cn174
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• invasive ductal adenocarcinomas with extensive regional and distant metastases

endocrine/exocrine glands
• invasive ductal adenocarcinomas with extensive regional and distant metastases

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:187012




Genotype
MGI:3821753
cn175
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre/Esr1*)35.10Dam mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice treated with tamoxifen staring at E10.5 exhibit focal pancreatic intraepithelial neoplasia
• mice not treated with tamoxifen develop focal PanIN that are not as numerous as in Gt(ROSA)26Sortm1(Notch1)Dam/Gt(ROSA)26Sor+ Krastm4Tyj/Krastm4Tyj Tg(Ipf1-cre/Esr1)35.10Dam mice
• acinar-ductal metaplasia precedes PanIN

endocrine/exocrine glands
• mice treated with tamoxifen staring at E10.5 exhibit focal pancreatic intraepithelial neoplasia
• mice not treated with tamoxifen develop focal PanIN that are not as numerous as in Gt(ROSA)26Sortm1(Notch1)Dam/Gt(ROSA)26Sor+ Krastm4Tyj/Krastm4Tyj Tg(Ipf1-cre/Esr1)35.10Dam mice
• acinar-ductal metaplasia precedes PanIN




Genotype
MGI:2687206
cn176
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• average cancer free survival is greater than 52 weeks and 2 of 9 mice develop pancreatic ductal adenocarcinoma (J:116130)
• 2 of 11 mutants show evidence of pancreatic ductal adenocarcinoma at 6 months of age, but not at earlier times (J:164210)
• pancreatic ductal lesions are seen at 9, 12, 18, and 26 weeks of are, similar to human pancreatic intraepithelial neoplasias (PanINs) (J:87196)
• PanINs increase in number and size with age, however no invasive tumors are seen up to 30 weeks of age (J:87196)
• no evidence of neoplasia in the acinar cell compartment, however focal reactive metaplastic changes are seen (J:87196)
• low-grade mPanIN lesions are seen in 3 month old mutants and by 6 months of age, most mice exhibit mPanIN lesions (J:164210)

endocrine/exocrine glands
• pancreatic islets are moderately enlarged but do not show evidence of neoplasia
• average cancer free survival is greater than 52 weeks and 2 of 9 mice develop pancreatic ductal adenocarcinoma (J:116130)
• 2 of 11 mutants show evidence of pancreatic ductal adenocarcinoma at 6 months of age, but not at earlier times (J:164210)
• pancreatic ductal lesions are seen at 9, 12, 18, and 26 weeks of are, similar to human pancreatic intraepithelial neoplasias (PanINs) (J:87196)
• PanINs increase in number and size with age, however no invasive tumors are seen up to 30 weeks of age (J:87196)
• no evidence of neoplasia in the acinar cell compartment, however focal reactive metaplastic changes are seen (J:87196)
• low-grade mPanIN lesions are seen in 3 month old mutants and by 6 months of age, most mice exhibit mPanIN lesions (J:164210)
• acinar-to-ductal metaplasia is seen at 1 week of age

growth/size/body
• most mutants exhibit abdominal distention due to ascites fluid and pancreatic enlargement

homeostasis/metabolism




Genotype
MGI:3810650
cn177
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Fabp7-cre,-lacZ)3Gtm/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp7-cre,-lacZ)3Gtm mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• unlike mice homozygous for Nf1tm1Par and hemizygous for Tg(Fabp7-cre)2Gtm , mice are viable with no reduction in life span

nervous system
N
• unlike mice homozygous for Nf1tm1Par and hemizygous for Tg(Fabp7-cre)2Gtm no change in pyramidal neuron apical dendrite length or neuritic development are detected
• increase in the number of Olig2+ progenitor cells
• an increase in proliferating cells is seen in the CA2/3 region
• expansion of glial cells similar to that in mice homozygous for Nf1tm1Par and hemizygous for Tg(Fabp7-cre)2Gtm
• increase in the number of GFAP+ astrocytes in the brain

growth/size/body
N
(J:138868)
• unlike mice homozygous for Nf1tm1Par and hemizygous for Tg(Fabp7-cre)2Gtm , no growth retardation is seen (J:139866)

endocrine/exocrine glands
N
• unlike mice homozygous for Nf1tm1Par and hemizygous for Tg(Fabp7-cre)2Gtm , no impairment in pituitary gland development is detected




Genotype
MGI:5582314
cn178
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive for a median of 84 days after pIpC injection

hematopoietic system
• increase in the number of proliferating splenocytes in pIpC treated mice; most of these proliferating cells are Mac1+/Gr1 lo or Ter119+
• spleens of pIpC-treated moribund mice are massively enlarged (J:87429)
• in pIpC treated mice (J:115071)
• mice treated with pIpC show large numbers of proliferating splenic Ter199+ cells, indicating that erythropoiesis is ineffective (J:87429)
• the erythroid progenitor compartment is massively expanded in the spleen of pIpC treated mice (J:115071)
• pIpC treated mice show normal numbers of early erythroid cells in the bone marrow but a paucity of all the more mature TER119 hi populations, indicating an inefficient transition from TER119- to TER119 hi stages of erythropoiesis (J:115071)
• bone marrow from pIpC treated mice forms abnormally large BFU-E colonies characterized by both erythropoietin-independent growth and hypersensitivity to erythropoietin (J:115071)
• spleen of pIpC treated mice contains increase of immature CD71 hi TER119-/lo cells and large numbers of TER119 hi erythroblasts (J:115071)
• pIpC injected mice develop a myeloproliferative disease with excess monocytes
• bone marrow mononuclear cells from pIpC treated mice form significant numbers of colony-forming unit granulocyte-macrophage (CFU-GM) colonies in the absence of exogenous cytokines while wild-type cells do not
• CFU-GM shows an increased proliferative response without added cytokines (9-fold) or to GM-CSF (19-fold increase) or IL-3 (37-fold increase)
• mice show abundant myeloid cells at various stages of differentiation after pIpC injection
• pups injected with pIpC develop anemia (J:87429)
• however, normal platelet counts are seen in pIpC injected mice (J:87429)
• in pIpC treated mice
• in pIpC treated mice
• in pIpC treated mice
• pups injected with pIpC at 21 days of age develop progressive leukocytosis that is evident 3 weeks after pIpC injection
• mice show an expanded population of Mac-1+, Gr-1 lo cells, indicating an expansion of immature monocytic cells
• in pIpC treated mice

immune system
• increase in the number of proliferating splenocytes in pIpC treated mice; most of these proliferating cells are Mac1+/Gr1 lo or Ter119+
• spleens of pIpC-treated moribund mice are massively enlarged (J:87429)
• in pIpC treated mice (J:115071)
• pIpC injected mice develop a myeloproliferative disease with excess monocytes
• bone marrow mononuclear cells from pIpC treated mice form significant numbers of colony-forming unit granulocyte-macrophage (CFU-GM) colonies in the absence of exogenous cytokines while wild-type cells do not
• CFU-GM shows an increased proliferative response without added cytokines (9-fold) or to GM-CSF (19-fold increase) or IL-3 (37-fold increase)
• mice show abundant myeloid cells at various stages of differentiation after pIpC injection
• pups injected with pIpC at 21 days of age develop progressive leukocytosis that is evident 3 weeks after pIpC injection
• mice show an expanded population of Mac-1+, Gr-1 lo cells, indicating an expansion of immature monocytic cells

liver/biliary system
• pIpC injected mice show moderate hepatomegaly with myeloid infiltration, particularly in periportal areas

cellular
• increase in the number of proliferating splenocytes in pIpC treated mice; most of these proliferating cells are Mac1+/Gr1 lo or Ter119+

homeostasis/metabolism
• serum erythropoietin levels are increased in proportion to anemia in pIpC treated mice

growth/size/body
• pIpC injected mice show moderate hepatomegaly with myeloid infiltration, particularly in periportal areas
• spleens of pIpC-treated moribund mice are massively enlarged (J:87429)
• in pIpC treated mice (J:115071)




Genotype
MGI:3695430
cn179
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average tumor-free survival is 38 weeks

neoplasm
• 6 of 10 mice develop pancreatic ductal adenocarcinoma

endocrine/exocrine glands
• 6 of 10 mice develop pancreatic ductal adenocarcinoma




Genotype
MGI:2687217
cn180
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• complete penetrance of death due to invasive and metastic cancer by 11 weeks of age (J:87196)
• average tumor-free survival is 8.6 weeks (J:116130)

neoplasm
• solid pancreatic tumors, frequently adhering to adjacent organs and the retroperitoneum (J:87196)
• tumors are highly invasive, frequently involving the duodenum, stomach, liver and/or spleen and occasionally obstructing the common bile duct (J:87196)
• 26% of tumors exhibit anaplastic carcinoma histology (J:108298)
• 26% of tumors exhibit sarcomatoid differentiation (J:108298)
• tumors exhibit pathologic features of human pancreatic ductal adenocarcinomas (J:87196)
• 48% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)
• 6 of 6 mice develop pancreatic ductal adenocarcinoma (J:116130)
• earlier onset (3-4 weeks of age) of local premalignant ductal lesions (pancreatic intraepithelial neoplasia) than in mice just expressing the oncogenic form KRAS2 and not deficient for Cdkn2a expression
• pancreatic ductal lesions progress rapidly to invasive pancreatic adenocarcinoma
• neoplasms frequently invade the lymphatic and vascular system, indicating metastatic invasion (J:87196)
• 11% of tumors exhibit metastasis (J:108298)
• neoplasms rapidly progressed to become invasive and metastatic tumors

endocrine/exocrine glands
• solid pancreatic tumors, frequently adhering to adjacent organs and the retroperitoneum (J:87196)
• tumors are highly invasive, frequently involving the duodenum, stomach, liver and/or spleen and occasionally obstructing the common bile duct (J:87196)
• 26% of tumors exhibit anaplastic carcinoma histology (J:108298)
• 26% of tumors exhibit sarcomatoid differentiation (J:108298)
• tumors exhibit pathologic features of human pancreatic ductal adenocarcinomas (J:87196)
• 48% of tumors exhibit well differentiated ductal adenocarcinoma histology (J:108298)
• 6 of 6 mice develop pancreatic ductal adenocarcinoma (J:116130)
• earlier onset (3-4 weeks of age) of local premalignant ductal lesions (pancreatic intraepithelial neoplasia) than in mice just expressing the oncogenic form KRAS2 and not deficient for Cdkn2a expression
• pancreatic ductal lesions progress rapidly to invasive pancreatic adenocarcinoma

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:87196 , J:108298




Genotype
MGI:5308806
cn181
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop pancreatic tumors with an average latency of 34.2 weeks
• 43% of tumors exhibit sarcomatoid differentiation
• 57% of tumors exhibit well differentiated ductal adenocarcinoma histology
• 69% of tumors exhibit metastasis

endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 34.2 weeks
• 43% of tumors exhibit sarcomatoid differentiation
• 57% of tumors exhibit well differentiated ductal adenocarcinoma histology




Genotype
MGI:5308964
cn182
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop pancreatic tumors with an average latency of 57 weeks
• 100% of tumors exhibit sarcomatoid carcinoma histology
• 67% of tumors exhibit metastasis

endocrine/exocrine glands
• mutants develop pancreatic tumors with an average latency of 57 weeks
• 100% of tumors exhibit sarcomatoid carcinoma histology




Genotype
MGI:5659911
cn183
Allelic
Composition
Krastm4Tyj/Kras+
Tg(KRT14-cre/ERT)20Efu/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(KRT14-cre/ERT)20Efu mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen treated mice develop oral tumors

craniofacial
• tamoxifen treated mice develop oral tumors

growth/size/body
• tamoxifen treated mice develop oral tumors




Genotype
MGI:5659910
cn184
Allelic
Composition
Krastm4Tyj/Kras+
Tg(CAG-HPV16E6E7,-luc)#Mspi/0
Tg(KRT14-cre/ERT)20Efu/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * CD-1 * FVB/N * FVB/NJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(CAG-HPV16E6E7,-luc)#Mspi mutation (0 available)
Tg(KRT14-cre/ERT)20Efu mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen treated mice develop oral tumors; tumors grow faster than in single conditional Kras mutants
• oral tumors of tamoxifen treated mice are papillomas that express HPV-biomarkers p16 and MCM7
• 14 days after tamoxifen treatment, mice treated with rapamycin for 3 days exhibit a transient decrease in tumor growth with regrowth after rapamycin is removed
• 14 days after tamoxifen treatment, mice that are treated with image-guided radiotherapy show regression of tumors

craniofacial
• tamoxifen treated mice develop oral tumors; tumors grow faster than in single conditional Kras mutants
• oral tumors of tamoxifen treated mice are papillomas that express HPV-biomarkers p16 and MCM7
• 14 days after tamoxifen treatment, mice treated with rapamycin for 3 days exhibit a transient decrease in tumor growth with regrowth after rapamycin is removed
• 14 days after tamoxifen treatment, mice that are treated with image-guided radiotherapy show regression of tumors

growth/size/body
• tamoxifen treated mice develop oral tumors; tumors grow faster than in single conditional Kras mutants
• oral tumors of tamoxifen treated mice are papillomas that express HPV-biomarkers p16 and MCM7
• 14 days after tamoxifen treatment, mice treated with rapamycin for 3 days exhibit a transient decrease in tumor growth with regrowth after rapamycin is removed
• 14 days after tamoxifen treatment, mice that are treated with image-guided radiotherapy show regression of tumors

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
oral cavity cancer DOID:8618 J:210533




Genotype
MGI:5428897
cn185
Allelic
Composition
Krastm4Tyj/Kras+
Speer6-ps1Tg(Alb-cre)21Mgn/Speer6-ps1+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Speer6-ps1Tg(Alb-cre)21Mgn mutation (6 available); any Speer6-ps1 mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mutants develop invasive intrahepatic cholangiocarcinoma with low penetrance (1 of 8 mutants) and long latency (at 36 weeks of age)
• mice develop liver tumors at 12 months of age and do not show obvious symptoms up to 18 months of age
• tumors resemble hepatocellular dysplasia

liver/biliary system
• mutants develop invasive intrahepatic cholangiocarcinoma with low penetrance (1 of 8 mutants) and long latency (at 36 weeks of age)
• mice develop liver tumors at 12 months of age and do not show obvious symptoms up to 18 months of age
• tumors resemble hepatocellular dysplasia

endocrine/exocrine glands
• mutants develop invasive intrahepatic cholangiocarcinoma with low penetrance (1 of 8 mutants) and long latency (at 36 weeks of age)

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
intrahepatic cholangiocarcinoma DOID:4928 J:184949




Genotype
MGI:4355874
cn186
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Pancreatic tumors in Krastm4Tyj/Krastm4Tyj Trim33tm1Los/Trim33tm1Los Tg(Pdx1-cre)89.1Dam/0 and Krastm4Tyj/Krastm4Tyj Cdkn2atm4Rdp/Cdkn2atm4Rdp Tg(Pdx1-cre)89.1Dam/0 mice

endocrine/exocrine glands
• mice develop invasive pancreatic masses that are firm and homogeneous unlike in wild-type mice

neoplasm
• mice develop invasive pancreatic masses that are firm and homogeneous unlike in wild-type mice

homeostasis/metabolism
• PET scans detected abnormal metabolic activity in the abdomen unlike in wild-type mice

growth/size/body




Genotype
MGI:4355875
cn187
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Accelerated pancreatic neoplasia in Krastm4Tyj/Krastm4Tyj Trim33tm1Los/Trim33tm1Los Tg(Pdx1-cre)89.1Dam/0 mice compared to Krastm4Tyj/Krastm4Tyj Tg(Pdx1-cre)89.1Dam/0 mice

endocrine/exocrine glands
• at 6 weeks, cysts occupy 20% of the pancreatic space unlike in wild-type mice

neoplasm

growth/size/body
• at 6 weeks, cysts occupy 20% of the pancreatic space unlike in wild-type mice




Genotype
MGI:4458349
cn188
Allelic
Composition
Braftm1Rima/Braf+
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)1Lru/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Braftm1Rima mutation (0 available); any Braf mutation (60 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Tyr-cre/ERT2)1Lru mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• within 6 months, tamoxifen-treated mice develop large, rapid growing oligo-pigmented tumors with ulceration unlike wild-type mice
• tumors in tamoxifen-treated mice are largely composed of spindle cells with malignancy features

pigmentation
• within 2 to 3 months, tamoxifen-treated mice exhibit a darkening of the tails, ears, and paws compared with wild-type mice




Genotype
MGI:5705321
cn189
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop invasive carcinoma in both the dorsolateral and anterior lobes of the prostate as early as 4 weeks with poorly differentiated carcinoma by 10 weeks
• marker analysis indicates that prostatic epithelial cells undergo epithelial-to-mesenchymal transition and that tumors exhibit a human metastatic prostate cancer signature
• mice develop macrometastatic lesions in the lung and liver with 100% penetrance

mortality/aging
• early lethality, with mice dying between around 10 and 30 weeks of age

endocrine/exocrine glands
• prostates show an expansion of the leukemia stem cell (LSC)high subpopulation of stem/progenitor cells
• both the LSChigh (basal cell population) and LSClow (luminal cell population) subpopulations show enhanced sphere-forming in vitro
• mice develop invasive carcinoma in both the dorsolateral and anterior lobes of the prostate as early as 4 weeks with poorly differentiated carcinoma by 10 weeks
• marker analysis indicates that prostatic epithelial cells undergo epithelial-to-mesenchymal transition and that tumors exhibit a human metastatic prostate cancer signature

reproductive system
• prostates show an expansion of the leukemia stem cell (LSC)high subpopulation of stem/progenitor cells
• both the LSChigh (basal cell population) and LSClow (luminal cell population) subpopulations show enhanced sphere-forming in vitro
• mice develop invasive carcinoma in both the dorsolateral and anterior lobes of the prostate as early as 4 weeks with poorly differentiated carcinoma by 10 weeks
• marker analysis indicates that prostatic epithelial cells undergo epithelial-to-mesenchymal transition and that tumors exhibit a human metastatic prostate cancer signature




Genotype
MGI:5705328
cn190
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• lethality around 40 weeks of age

neoplasm
• mice develop focal neoplastic expansions in the prostate by 10 weeks and invasive carcinoma by 20 weeks
• mice develop macrometastatic lesions in the lung and liver with 100% penetrance

endocrine/exocrine glands
• mice develop focal neoplastic expansions in the prostate by 10 weeks and invasive carcinoma by 20 weeks

reproductive system
• mice develop focal neoplastic expansions in the prostate by 10 weeks and invasive carcinoma by 20 weeks




Genotype
MGI:7435433
cn191
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Slco1c1-icre/ERT2)1Mash/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * DBA/2 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Slco1c1-icre/ERT2)1Mash mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• vasculature surrounding brain arteriovenous malformations is abnormal in tamoxifen-administered mice, with vessels appearing tortuous and dilated, similar to niduses associated with these lesions in human patients
• mice administered tamoxifen at P1 show presence of brain arteriovenous malformations at 8 weeks of age occurring in the cortex, just anterior to the cerebellum, as well as near the olfactory bulb
• mice administered tamoxifen at P1 only rarely show intracranial hemorrhage (1 of 28 mice) at 8 weeks of age

nervous system
• vasculature surrounding brain arteriovenous malformations is abnormal in tamoxifen-administered mice, with vessels appearing tortuous and dilated, similar to niduses associated with these lesions in human patients
• mice administered tamoxifen at P1 only rarely show intracranial hemorrhage (1 of 28 mice) at 8 weeks of age

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
arteriovenous malformations of the brain DOID:0060688 OMIM:108010
J:312482




Genotype
MGI:4835044
cn192
Allelic
Composition
Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm2.1Nesh mutation (4 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• tamoxifen-treated mice develop melanomas with spindle-like morphology
• 8 of 11 (73%) mice treated with tamoxifen neonatally develop melanomas with spindle-like morphology formation at a longer latency (median latency 24 weeks) than in Cdkn2atm2.1Nesh/Cdkn2atm2.1Nesh Krastm4Tyj/Kras+ Trp53tm1Brn/Trp53tm1Brn Tg(Tyr-cre/ERT2)13Bos mice (median latency 14 weeks)

pigmentation
• tamoxifen-treated mice exhibit melanocyte proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:6505560
cn193
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm3.1Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm3.1Tyj mutation (2 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• all mice develop pancreatic tumors; all cancers are invasive pancreatic ductal adenocarcinoma

mortality/aging
• median lifespan is approximately 70 days, with all mice dying around 120 days

endocrine/exocrine glands
• all mice develop pancreatic tumors; all cancers are invasive pancreatic ductal adenocarcinoma

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:276349




Genotype
MGI:5494465
cn194
Allelic
Composition
Brca1tm1Thl/Brca1tm2Rjbr
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Thl mutation (1 available); any Brca1 mutation (114 available)
Brca1tm2Rjbr mutation (1 available); any Brca1 mutation (114 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 45 days compared with 68 days in Krastm4Tyj/Kras+ Tg(Ipf1-cre)6Tuv Trp53tm1Thl/Trp53tm1Thl
• however, latency is similar to in Brca1tm1Thl/Brca1tm1Thl Krastm4Tyj/Kras+ Tg(Ipf1-cre)6Tuv Trp53tm1Thl/Trp53tm1Thl




Genotype
MGI:5494464
cn195
Allelic
Composition
Brca1tm1Thl/Brca1tm1Thl
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Thl mutation (1 available); any Brca1 mutation (114 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice succumb to pancreatic tumors with an average latency of 68 days




Genotype
MGI:5494462
cn196
Allelic
Composition
Brca1tm1Thl/Brca1tm3.1Rjbr
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca1tm1Thl mutation (1 available); any Brca1 mutation (114 available)
Brca1tm3.1Rjbr mutation (1 available); any Brca1 mutation (114 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• as in Krastm4Tyj/Kras+ Tg(Ipf1-cre)6Tuv Trp53tm1Thl/Trp53tm1Thlmice succumb to pancreatic tumors with an average latency of 65 days




Genotype
MGI:3821936
cn197
Allelic
Composition
Gt(ROSA)26Sortm1(MYC/ERT2)Gev/Gt(ROSA)26Sortm1(MYC/ERT2)Gev
Krastm4Tyj/Krastm4Tyj
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(MYC/ERT2)Gev mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following intranasal treatment with adenovirus cre only, mice exhibit hyperplastic and dysplastic bronchiolar lesions unlike similarly treated wild-type mice but similar to in cre-activated Krastm4Tyj homozygotes
• 6 weeks following intranasal exposure to adenovirus cre and treatment with tamoxifen, mice develop large and numerous papillary adenomas that are poorly differentiated and grow in small tumor clusters with individual cells embedded within desmoplastic stroma
• 6 weeks following intranasal exposure to adenovirus cre and treatment with tamoxifen

respiratory system
• following intranasal treatment with adenovirus cre only, mice exhibit hyperplastic and dysplastic bronchiolar lesions unlike similarly treated wild-type mice but similar to in cre-activated Krastm4Tyj homozygotes
• 6 weeks following intranasal exposure to adenovirus cre and treatment with tamoxifen, mice develop large and numerous papillary adenomas that are poorly differentiated and grow in small tumor clusters with individual cells embedded within desmoplastic stroma
• 6 weeks following intranasal exposure to adenovirus cre and treatment with tamoxifen




Genotype
MGI:4941337
cn198
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• PanIN-1 and PanIN-2, but not PanIN-3 or pancreatic ductal adenocarcinoma, are seen at 22 weeks after birth (J:214846)
• mice develop intraepithelial neoplasia (PanIN) by 8 weeks of age (J:276349)
• mice show accelerated PanIN development when treated with cerulein to induce acute pancreatitis (J:276349)

digestive/alimentary system
• mice develop a varying number of ductal cell proliferation foci in the pancreas from 9 weeks after birth

endocrine/exocrine glands
• mice develop a varying number of ductal cell proliferation foci in the pancreas from 9 weeks after birth
• PanIN-1 and PanIN-2, but not PanIN-3 or pancreatic ductal adenocarcinoma, are seen at 22 weeks after birth (J:214846)
• mice develop intraepithelial neoplasia (PanIN) by 8 weeks of age (J:276349)
• mice show accelerated PanIN development when treated with cerulein to induce acute pancreatitis (J:276349)




Genotype
MGI:4941336
cn199
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

neoplasm
• all but one mouse, develop large, firm, fibrotic head of the pancreas tumors
• metastatic foci spread to the surface of the liver, lungs, diaphragm, and adrenals with occasional metastasis to the peripancreatic, mesenteric, and retroperitoneal lymph nodes
• mice exhibit the full spectrum of preinvasive lesions
• some tumors are minor, poorly differentiated, or undifferentiated with anaplastic or sarcomatoid features
• some mice exhibit esophageal papillomas and hyperplasias or papillomatosis of the biliary tree unlike control mice

liver/biliary system

homeostasis/metabolism
• hemorrhagic

cellular
• in tumor cells

growth/size/body

digestive/alimentary system
• mice frequently exhibit small bowel obstructions unlike control mice

endocrine/exocrine glands
• all but one mouse, develop large, firm, fibrotic head of the pancreas tumors
• metastatic foci spread to the surface of the liver, lungs, diaphragm, and adrenals with occasional metastasis to the peripancreatic, mesenteric, and retroperitoneal lymph nodes
• mice exhibit the full spectrum of preinvasive lesions
• some tumors are minor, poorly differentiated, or undifferentiated with anaplastic or sarcomatoid features

immune system

hematopoietic system

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:98936




Genotype
MGI:6505545
cn200
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice show colon epithelium crypt hyperplasia that is greater than seen in conditional Krastm1.1Khai mice
• Paneth cells are absent in colons
• mice treated with trametinib show restoration of Paneth cell differentiation in colons
• colons show a greater hyperproliferative phenotype than in conditional Krastm1.1Khai mice

endocrine/exocrine glands
• mice show colon epithelium crypt hyperplasia that is greater than seen in conditional Krastm1.1Khai mice
• Paneth cells are absent in colons
• mice treated with trametinib show restoration of Paneth cell differentiation in colons




Genotype
MGI:4940098
cn201
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Trp53tm3Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm3Tyj mutation (3 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 24 of 30 mutants develop pancreatic ductal adenocarcinomas

mortality/aging
• average survival time is 168 days, with a range of 60-254 days

endocrine/exocrine glands
• 24 of 30 mutants develop pancreatic ductal adenocarcinomas




Genotype
MGI:7711290
cn202
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm2Tyj/Trp53+
Zdhhc20em1Jdo/Zdhhc20em1Jdo
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2Tyj mutation (4 available); any Trp53 mutation (240 available)
Zdhhc20em1Jdo mutation (0 available); any Zdhhc20 mutation (41 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• survival is similar to mutant mice wild-type for Zdhhc20

neoplasm
• liver metastases are found in 40% of mice compared to 93% of mutant mice wild-type for Zdhhc20
• a similar trend is seen for lung metastases
• both total liver lesion area and number are profoundly reduced




Genotype
MGI:6505558
cn203
Allelic
Composition
Apctm2Rak/Apc+
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm2Rak mutation (1 available); any Apc mutation (158 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

mortality/aging
• mice show 100% lethality before 150 days of age

digestive/alimentary system
• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
colorectal cancer DOID:9256 OMIM:114500
J:276349




Genotype
MGI:7710915
cn204
Allelic
Composition
Krastm4Tyj/Kras+
Ube2cem1Gpt/Ube2cem1Gpt
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ube2cem1Gpt mutation (0 available); any Ube2c mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice intratracheally administered an adenovirus expressing cre recombinase (Ad-cre) show reduced lung tumor burden compared to single mutant Kras homozygous mice

mortality/aging
• mice intratracheally administered Ad-cre have a median survival time of approximately 150 days and 100% death by 210 days compared to single mutant Kras homozygous mice which have a survival time of approximately 130 days with 100% death by 175 days, indicating increased survival

respiratory system
• mice intratracheally administered an adenovirus expressing cre recombinase (Ad-cre) show reduced lung tumor burden compared to single mutant Kras homozygous mice




Genotype
MGI:7261333
cn205
Allelic
Composition
Ggctem1.2Smoc/Ggctem1.2Smoc
Krastm4Tyj/Kras+
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ggctem1.2Smoc mutation (0 available); any Ggct mutation (10 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• completely blocked in vitro proliferation of embryonic fibroblasts from mice treated with a cre-expressing adenovirus

neoplasm
• in 3-months-old mice after cre-expressing adenovirus




Genotype
MGI:4836596
cn206
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• survival of majority of mice is 10-20 weeks after intrabursal injection of an adenovirus expressing Cre

neoplasm
• 43% of ovarian tumors metastasize to the lungs
• 7 weeks after intrabursal injection through the infundibulum of an adenovirus expressing Cre, mice, mutants develop endometrioid ovarian cancer
• primary tumor is located in the ovary
• tumors are solid and cystic and diagnosed as ovarian edometrioid adenocarcinomas

reproductive system
• 7 weeks after intrabursal injection through the infundibulum of an adenovirus expressing Cre, mice, mutants develop endometrioid ovarian cancer
• primary tumor is located in the ovary
• tumors are solid and cystic and diagnosed as ovarian edometrioid adenocarcinomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
ovarian cancer DOID:2394 OMIM:167000
OMIM:607893
J:96296




Genotype
MGI:7710919
cn207
Allelic
Composition
Deptortm1.2Ysun/Deptortm1.2Ysun
Krastm4Tyj/Kras+
Ube2cem1Gpt/Ube2cem1Gpt
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Deptortm1.2Ysun mutation (0 available); any Deptor mutation (29 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ube2cem1Gpt mutation (0 available); any Ube2c mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice intratracheally administered an adenovirus expressing cre recombinase (Ad-cre) develop lung tumor burden similar to single mutant Kras homozygous mice indicating rescue of the suppression of lung tumorigenesis by Ube2c

respiratory system
• mice intratracheally administered an adenovirus expressing cre recombinase (Ad-cre) develop lung tumor burden similar to single mutant Kras homozygous mice indicating rescue of the suppression of lung tumorigenesis by Ube2c




Genotype
MGI:7738283
cn208
Allelic
Composition
Diras2em1Gpt/Diras2em1Gpt
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
Genetic
Background
involves: 129S4/SvJae * C57BL/6J * C57BL/6JGpt
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Diras2em1Gpt mutation (0 available); any Diras2 mutation (20 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• more aggressive neoplastic progression with increased population of stage III neoplasia and decreased populations of acinar cells, acinar-to-ductal metaplasia, and stage I neoplasia compared to mutant mice wild-type for Diras2

neoplasm
• more aggressive neoplastic progression with increased population of stage III neoplasia and decreased populations of acinar cells, acinar-to-ductal metaplasia, and stage I neoplasia compared to mutant mice wild-type for Diras2




Genotype
MGI:7738261
cn209
Allelic
Composition
Krastm4Tyj/Kras+
Ptf1atm1(cre)Hnak/Ptf1a+
Ube2ftm1c(EUCOMM)Hmgu/Ube2ftm1c(EUCOMM)Hmgu
Genetic
Background
involves: 129S4/SvJae * C57BL/6J * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptf1atm1(cre)Hnak mutation (1 available); any Ptf1a mutation (31 available)
Ube2ftm1c(EUCOMM)Hmgu mutation (0 available); any Ube2f mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• relative to mutant mice wild-type for Ube2f indicating improved growth

neoplasm
• decrease in pancreatic intraepithelial neoplasia at all 3 stages relative to mutant mice wild-type for Ube2f at 4, 6, and 9 months of age
• by 12 months of age there is an increase in stage I but decrease in stage II and III lesions in the pancreas indicating a delay in pancreatic tumor progression

endocrine/exocrine glands
• relative to mutant mice wild-type for Ube2f
• decrease in disruption of acinar cell population in cerulein-induced pancreatitis
• fewer infiltrations of leukocytes and neutrophils at 3d after cerulein treatment




Genotype
MGI:6267351
cn210
Allelic
Composition
Chaf1btm2c(EUCOMM)Hmgu/Chaf1b+
Krastm4Tyj/Kras+
Tg(Mx1-cre)1Cgn/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6J * C57BL/6N * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Chaf1btm2c(EUCOMM)Hmgu mutation (0 available); any Chaf1b mutation (37 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Mx1-cre)1Cgn mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• in pIpC-treated mice but not as severe as when Chaf1b alleles are wild-type

hematopoietic system
N
• pIpC-treated mice exhibit normal numbers of red blood cells and platelets
• in pIpC-treated mice

immune system
• in pIpC-treated mice




Genotype
MGI:5298086
cn211
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Krt1-15-cre/PGR*)22Cot/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6J * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Krt1-15-cre/PGR*)22Cot mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 2-4 months following RU486 treatment, tumors develop in the face in 35% of treated mutants
• 2-4 months following RU486 treatment, lip tumors develop in 57% of treated mice
• 2-4 months following RU486 treatment, tumors develop in the back skin in 14% of treated mice
• skin tumors are benign papillomas with no sign of malignant transformtion seen up to 4 months after treatment with RU486
• double mutants not treated with tamoxifen develop some papillomas but with increased latency (>6 months)

integument
• 2-4 months following RU486 treatment, tumors develop in the back skin in 14% of treated mice
• skin tumors are benign papillomas with no sign of malignant transformtion seen up to 4 months after treatment with RU486
• double mutants not treated with tamoxifen develop some papillomas but with increased latency (>6 months)

growth/size/body
• 2-4 months following RU486 treatment, tumors develop in the face in 35% of treated mutants
• 2-4 months following RU486 treatment, lip tumors develop in 57% of treated mice

craniofacial
• 2-4 months following RU486 treatment, tumors develop in the face in 35% of treated mutants
• 2-4 months following RU486 treatment, lip tumors develop in 57% of treated mice




Genotype
MGI:5484547
cn212
Allelic
Composition
Krastm4Tyj/Kras+
Stk11tm1.1Gne/Stk11tm1.1Gne
Genetic
Background
involves: 129S4/SvJae * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Stk11tm1.1Gne mutation (0 available); any Stk11 mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• in pancreatic explants treated with 1NMPP1 and infected with a cre-expressing adenovirus without loss of intrinsic cell polarity

growth/size/body
• in pancreatic explants treated with 1NMPP1 and infected with a cre-expressing adenovirus without loss of intrinsic cell polarity




Genotype
MGI:3821737
cn213
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Tg(Cela1-cre/ERT2)1Stof/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Cela1-cre/ERT2)1Stof mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 2 months after injection with tamoxifen, 50% of mice exhibit focal low grade pancreatic intraepithelial neoplasia (PanIN) that progresses to carcinoma in situ by 4 to 12 months following injection with tamoxifen
• tamoxifen treated mice exhibit lesions that progress from normal acinar parenchyma to acinar-ductal metaplastic structures to PanIN with biphenotypic exocrine differentiation
• tamoxifen treated mice exhibit highly proliferative acinar derived PanIN

endocrine/exocrine glands
• 2 months after injection with tamoxifen, 50% of mice exhibit focal low grade pancreatic intraepithelial neoplasia (PanIN) that progresses to carcinoma in situ by 4 to 12 months following injection with tamoxifen
• tamoxifen treated mice exhibit lesions that progress from normal acinar parenchyma to acinar-ductal metaplastic structures to PanIN with biphenotypic exocrine differentiation
• tamoxifen treated mice exhibit highly proliferative acinar derived PanIN




Genotype
MGI:3821738
cn214
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Tg(Pdx1-cre/Esr1*)35.10Dam/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre/Esr1*)35.10Dam mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mice treated with tamoxifen as adults do not develop pancreatic intraepithelial neoplasia




Genotype
MGI:3044680
cn215
Allelic
Composition
Krastm4Tyj/Kras+
Tg(MMTV-cre)4Mam/0
Genetic
Background
involves: 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(MMTV-cre)4Mam mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• submandibular gland hyperplasia is seen in mutant mice

digestive/alimentary system
• submandibular gland hyperplasia is seen in mutant mice




Genotype
MGI:7435429
cn216
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Cdh5-cre/ERT2)1Rha/0
Genetic
Background
involves: 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Cdh5-cre/ERT2)1Rha mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice administered tamoxifen at P1 show lethality beginning at P12
• lethality is not due to failure to thrive
• however, mice treated with tamoxifen between 2 and 4 months of age show no effect on overall survival up to 8 weeks later and show no differences in viability up to 36 weeks later

cardiovascular system
• mice treated with tamoxifen at P1 show thin and fragile appearing cerebral vessels
• however, vessel density within the brain at P21 is normal
• more than 50% of mice treated with tamoxifen between 2 and 4 months develop brain arteriovenous malformations within 8 weeks of treatment
• however, mice treated with tamoxifen at P1 do not exhibit cortical brain arteriovenous malformations and cerebral vessels do not appear dilated
• mice administered tamoxifen at P1 that survive to P21 show an incompletely penetrant (11 of 32 mice) phenotype of focal intracranial hemorrhage
• however, mice treated with tamoxifen at P1 do not show hemorrhage in the intestines, lung, or liver at P14
• however, mice treated with tamoxifen between 2 and 4 months do not show hemorrhage 8 weeks after treatment

nervous system
• mice treated with tamoxifen at P1 show thin and fragile appearing cerebral vessels
• however, vessel density within the brain at P21 is normal
• mice administered tamoxifen at P1 that survive to P21 show an incompletely penetrant (11 of 32 mice) phenotype of focal intracranial hemorrhage
• however, mice treated with tamoxifen at P1 do not show hemorrhage in the intestines, lung, or liver at P14
• however, mice treated with tamoxifen between 2 and 4 months do not show hemorrhage 8 weeks after treatment

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
arteriovenous malformations of the brain DOID:0060688 OMIM:108010
J:312482




Genotype
MGI:4835047
cn217
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Tyr-cre/ERT2)13Bos/0
Genetic
Background
involves: 129S4/SvJae * FVB
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Tyr-cre/ERT2)13Bos mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 1 in 14 tamoxifen treated mice develops melanoma with a median tumor latency greater than 52 weeks

pigmentation
• tamoxifen-treated mice exhibit melanocytic proliferation unlike wild-type mice
• tamoxifen-treated mice develop pigmented macules in the paws and tail unlike wild-type mice




Genotype
MGI:6113915
cn218
Allelic
Composition
Krastm4Tyj/Kras+
Rab11fip1tm1.1Jicn/Rab11fip1tm1.1Jicn
Tg(Pdx1-cre)6Tuv/0
Trp53tm2.1Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Rab11fip1tm1.1Jicn mutation (0 available); any Rab11fip1 mutation (41 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2.1Tyj mutation (2 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• phenotypes are relative to the control KPC (KrasG12D/+, p53R172H/+, Pdx1-Cre) PDAC (pancreatic adenocarcinoma) model mice
• size of PDAC primary tumors same as control
• significantly reduced number of detectable PDAC metastases to liver, lung and other tissues
• reduced migration of PDAC cells in vitro

mortality/aging
N
• survival same as control




Genotype
MGI:5438091
cn219
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Usp9x+
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Usp9xtm1Tuv mutation (0 available); any Usp9x mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• due to local or metastatic pancreatic cancer or aggressive oral papillomas

neoplasm
• aggressive oral papillomas
• within 3 months, mice develop pancreatic intraepithelial neoplasia and microinvasive neoplasms
• in the face and urogenital area at 3 months

integument
• in the face and urogenital area at 3 months

endocrine/exocrine glands
• within 3 months, mice develop pancreatic intraepithelial neoplasia and microinvasive neoplasms

craniofacial
• aggressive oral papillomas

growth/size/body
• aggressive oral papillomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:186717




Genotype
MGI:5438090
cn220
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Usp9xtm1Tuv/Y
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Usp9xtm1Tuv mutation (0 available); any Usp9x mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• due to local or metastatic pancreatic cancer or aggressive oral papillomas

neoplasm
• aggressive oral papillomas
• within 3 months, mice develop pancreatic intraepithelial neoplasia and microinvasive neoplasms
• in the face and urogenital area at 3 months

integument
• in the face and urogenital area at 3 months

endocrine/exocrine glands
• within 3 months, mice develop pancreatic intraepithelial neoplasia and microinvasive neoplasms

craniofacial
• aggressive oral papillomas

growth/size/body
• aggressive oral papillomas

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic ductal adenocarcinoma DOID:3498 J:186717




Genotype
MGI:5494463
cn221
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Thl/Trp53tm1Thl
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice succumb to pancreatic tumors with an average latency of 68 days




Genotype
MGI:3032575
cn222
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/?
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• transitions of epithelium from cuboid to columnar as early as 2 weeks
• number and extent of lesions increases with age
• by 7-10 months occasional animals with invasive and metastatic adenocarcinomas
• lesions eventually found in liver diaphragm and lungs

endocrine/exocrine glands
• transitions of epithelium from cuboid to columnar as early as 2 weeks
• number and extent of lesions increases with age
• by 7-10 months occasional animals with invasive and metastatic adenocarcinomas
• lesions eventually found in liver diaphragm and lungs

growth/size/body

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
pancreatic carcinoma DOID:4905 OMIM:260350
J:87973




Genotype
MGI:5141742
cn223
Allelic
Composition
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Upk2-cre)6Xrw/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Upk2-cre)6Xrw mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• 42% of mutants develop skin papillomas

neoplasm
• 42% of mutants develop skin papillomas




Genotype
MGI:3044567
cn224
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• diffuse hyperplasia and dysplasia of the colonic crypts is seen by 4 weeks of age
• increased proliferation of the hyperplastic and dysplastic colonic epithelium is seen in mutants




Genotype
MGI:5141740
cn225
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Upk2-cre)6Xrw/0
Genetic
Background
involves: 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Upk2-cre)6Xrw mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• mutants aged up to 18 months do not develop skin papillomas, bladder tumors or lung tumors (J:174242)
(J:234236)

renal/urinary system
N
• mice do not develop urothelium hyperplasia or bladder tumors




Genotype
MGI:5780080
cn226
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Tg-cre/ERT2)#Mmcm/0
Genetic
Background
involves: 129S4/SvJae * FVB/NCr
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Tg-cre/ERT2)#Mmcm mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• tamoxifen treated mice do not exhibit thyroid size abnormalities or abnormal levels of TSH or T4




Genotype
MGI:5300204
cn227
Allelic
Composition
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scribtm1.1Phum
Tg(Pbsn-cre)20Fwan/0
Genetic
Background
involves: 129S4/SvJae * FVB/NCrl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Scribtm1.1Phum mutation (0 available); any Scrib mutation (54 available)
Tg(Pbsn-cre)20Fwan mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 3 of 10 mice exhibit signs of illness and were sacrificed prior to 400 days

reproductive system
• well-differentiated adenocarcinomas in 20% of mice
• increased cell proliferation and apoptosis compared to in Tg(Pbsn-cre)20Fwan mice

neoplasm
• 3 of 15 mice develop poorly differentiated invasive carcinoma
• well-differentiated adenocarcinomas in 20% of mice

digestive/alimentary system
• focal intestinal metaplasia

endocrine/exocrine glands
• well-differentiated adenocarcinomas in 20% of mice
• increased cell proliferation and apoptosis compared to in Tg(Pbsn-cre)20Fwan mice




Genotype
MGI:5300203
cn228
Allelic
Composition
Krastm4Tyj/Kras+
Tg(Pbsn-cre)20Fwan/0
Genetic
Background
involves: 129S4/SvJae * FVB/NCrl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pbsn-cre)20Fwan mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• low-grade in 73% of mice
• high-grade in 18% of mice
• increased cell proliferation and apoptosis compared to in Tg(Pbsn-cre)20Fwan mice

neoplasm

digestive/alimentary system
• focal intestinal metaplasia

endocrine/exocrine glands
• low-grade in 73% of mice
• high-grade in 18% of mice
• increased cell proliferation and apoptosis compared to in Tg(Pbsn-cre)20Fwan mice




Genotype
MGI:5300205
cn229
Allelic
Composition
Krastm4Tyj/Kras+
Scribtm1.1Phum/Scrib+
Tg(Pbsn-cre)20Fwan/0
Genetic
Background
involves: 129S4/SvJae * FVB/NCrl
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Scribtm1.1Phum mutation (0 available); any Scrib mutation (54 available)
Tg(Pbsn-cre)20Fwan mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• well-differentiated adenocarcinomas in 13% of mice
• increased cell proliferation and apoptosis compared to in Tg(Pbsn-cre)20Fwan mice

neoplasm
• well-differentiated adenocarcinomas in 13% of mice

digestive/alimentary system
• focal intestinal metaplasia

endocrine/exocrine glands
• well-differentiated adenocarcinomas in 13% of mice
• increased cell proliferation and apoptosis compared to in Tg(Pbsn-cre)20Fwan mice




Genotype
MGI:5317171
cn230
Allelic
Composition
Krastm4Tyj/Kras+
Sftpctm1(cre/ERT2)Blh/Sftpc+
Trp53tm5Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Sftpctm1(cre/ERT2)Blh mutation (1 available); any Sftpc mutation (24 available)
Trp53tm5Tyj mutation (1 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die 14 weeks or less after tamoxifen administration

neoplasm
• at 6-8 weeks of age, animals administered 1dose or 4 doses of tamoxifen develop widespread adenomas in the alveoli by 14 weeks of age, but the bronchoalveolar duct junction remains tumor-free
• at 6-8 weeks of age, animals administered 1dose or 4 doses of tamoxifen develop widespread adenocarcinomas in the alveoli by 14 weeks of age

respiratory system
• at 6-8 weeks of age, animals administered 1dose or 4 doses of tamoxifen develop widespread adenomas in the alveoli by 14 weeks of age, but the bronchoalveolar duct junction remains tumor-free
• at 2 weeks after tamoxifen treatement, brochioalveolar duct junctions (BADJ) appear normal, but small adenomas occur in the alveoli; these progress to adenocarcinoma but the BADJ remain histologically normal




Genotype
MGI:5317170
cn231
Allelic
Composition
Krastm4Tyj/Kras+
Scgb1a1tm1(cre/ERT)Blh/Scgb1a1+
Trp53tm5Tyj/Trp53+
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Scgb1a1tm1(cre/ERT)Blh mutation (1 available); any Scgb1a1 mutation (29 available)
Trp53tm5Tyj mutation (1 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• animal succumb due to tumor burden at 20-24 weeks

neoplasm
• at 6-8 weeks of age, animals administered 4 doses of tamoxifen develop adenomas in the alveoli by 15 weeks; these progress to adenocarcinomas
• papillary adenomas are seen in alveoli at 15 and 21 weeks after tamoxifen treatment
• develop in alveoli and near the bronchioalveolar duct junction by 15 weeks of age with tamoxifen administration at 6-8 weeks
• larger bronchioles and non terminal bronchi appear normal
• advanced papillary adenocarcinomas are observed at 21 weeks after tamoxifen treatment

respiratory system
• at 6-8 weeks of age, animals administered 4 doses of tamoxifen develop adenomas in the alveoli by 15 weeks; these progress to adenocarcinomas
• papillary adenomas are seen in alveoli at 15 and 21 weeks after tamoxifen treatment
• hyperplasia is observed at 3 weeks after tamoxifen induction, and persists at 15 and 21 weeks




Genotype
MGI:5430385
cn232
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Ugdhtm1.1Xzh/Ugdhtm1.1Xzh
H2az2Tg(Wnt1-cre)11Rth/H2az2+
Genetic
Background
involves: 129S4/SvJaeSor * 129S6/SvEvTac * C57BL/6 * CBA/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
H2az2Tg(Wnt1-cre)11Rth mutation (2 available); any H2az2 mutation (26 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Ugdhtm1.1Xzh mutation (1 available); any Ugdh mutation (34 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• disruption of lacrimal gland budding

vision/eye
• disruption of lacrimal gland budding




Genotype
MGI:3695426
cn233
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2a+
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (48 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average tumor-free survival is 12.6 weeks

neoplasm
• 4 of 12 mice develop intraductal papillary mucinous neoplasms
• tumor fibrosis is increased compared to mice wild-type for Smad4
• 8 of 12 mice develop gastric cancer
• 4 of 12 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4

digestive/alimentary system
• 8 of 12 mice develop gastric cancer

endocrine/exocrine glands
• 4 of 12 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4




Genotype
MGI:3695422
cn234
Allelic
Composition
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (48 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 5 of 8 mice develop gastric cancer with squamous or adenosquamous histology

mortality/aging
• mice die between 8 and 24 weeks of age
• average tumor-free survival is 13.1 weeks

endocrine/exocrine glands
• seen in all mice

growth/size/body
• seen in all mice

neoplasm
• 5 of 8 mice develop intraductal papillary mucinous neoplasms
• 5 of 8 mice develop gastric cancer with squamous or adenosquamous histology




Genotype
MGI:3695429
cn235
Allelic
Composition
Cdkn2atm4Rdp/Cdkn2atm4Rdp
Krastm4Tyj/Kras+
Smad4tm1Rdp/Smad4tm1Rdp
Tg(Pdx1-cre)89.1Dam/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * CBA * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm4Rdp mutation (0 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (48 available)
Tg(Pdx1-cre)89.1Dam mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• average tumor-free survival is 7.4 weeks

neoplasm
• 3 of 10 mice develop intraductal papillary mucinous neoplasms
• tumor fibrosis is increased compared to mice wild-type for Smad4
• 5 of 10 mice develop gastric cancer
• 9 of 10 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4

digestive/alimentary system
• 5 of 10 mice develop gastric cancer

endocrine/exocrine glands
• 9 of 10 mice develop pancreatic ductal adenocarcinoma
• the proportion of undifferentiated carcinomas is decreased compared to mice wild-type for Smad4




Genotype
MGI:4940100
cn236
Allelic
Composition
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Cam mutation (0 available); any Brca2 mutation (132 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 12 of 40 mutants develop pancreatic ductal adenocarcinomas

mortality/aging
• reduction in pancreatic ductal adenocarcinoma-free survival

endocrine/exocrine glands
• 12 of 40 mutants develop pancreatic ductal adenocarcinomas




Genotype
MGI:4940099
cn237
Allelic
Composition
Brca2tm1Cam/Brca2+
Krastm4Tyj/Kras+
Trp53tm3Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * C57BL/6 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Cam mutation (0 available); any Brca2 mutation (132 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm3Tyj mutation (3 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 26 of 30 mutants develop pancreatic ductal adenocarcinomas

mortality/aging
• average survival time is 143 days, with a range of 91-191 days

endocrine/exocrine glands
• 26 of 30 mutants develop pancreatic ductal adenocarcinomas




Genotype
MGI:6113916
cn238
Allelic
Composition
Epha2tm1Jrui/Epha2tm1Jrui
Krastm4Tyj/Kras+
Trp53tm2.1Tyj/Trp53+
Tg(Pdx1-cre)6Tuv/0
Genetic
Background
involves: 129S/SvEv * 129S4/SvJae * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Epha2tm1Jrui mutation (2 available); any Epha2 mutation (96 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(Pdx1-cre)6Tuv mutation (3 available)
Trp53tm2.1Tyj mutation (2 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• phenotypes are relative to the control KPC (KrasG12D/+, p53R172H/+, Pdx1-Cre) PDAC (pancreatic adenocarcinoma) model mice
• size of PDAC primary tumors same as control
• significantly reduced number of detectable PDAC metastases to liver, lung and other tissues
• reduced migration of PDAC cells in vitro

mortality/aging
• survival reduced compared to control




Genotype
MGI:5704424
cn239
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182tm1.1Dgk
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Mir182tm1.1Dgk mutation (1 available); any Mir182 mutation (8 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 13% of mice develop lung metastases within 6 months following amputation of limb injected with cre-expressing adenovirus
• in the absence of the Mir18tm1.1Dgk allele, 43% of mice develop lung metastases
• number of metastatic nodules and metastatic burden in the lung are decreased compared to mice without the Mir18tm1.1Dgk allele




Genotype
MGI:4948963
cn240
Allelic
Composition
Krastm4Tyj/Kras+
Mapk8tm1Wag/Mapk8+
Mapk9tm1Mka/Mapk9tm1Mka
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Mapk8tm1Wag mutation (1 available); any Mapk8 mutation (74 available)
Mapk9tm1Mka mutation (1 available); any Mapk9 mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice

respiratory system
• following adenovirus cre infection, mice exhibit increased lung tumor burden compared with control mice




Genotype
MGI:5704425
cn241
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Mir182)Dgk/Gt(ROSA)26Sortm1(CAG-Mir182)Dgk
Krastm4Tyj/Krastm4Tyj
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Mir182)Dgk mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 75% of mice develop lung metastases by 120 days following amputation of limb injected with cre-expressing adenovirus
• in the absence of the Gt(ROSA)26Sortm1(CAG-Mir182)Dgk allele, 43% of mice develop lung metastases
• number of number of metastatic nodules in the lung is increased compared to mice without the Gt(ROSA)26Sortm1(CAG-Mir182)Dgk allel




Genotype
MGI:5704427
cn242
Allelic
Composition
Krastm4Tyj/Krastm4Tyj
Mir182tm1.1Dgk/Mir182+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Mir182tm1.1Dgk mutation (1 available); any Mir182 mutation (8 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 20% of mice develop lung metastases by 120 days following amputation of limb injected with cre-expressing adenovirus
• in the absence of the Mir18tm1.1Dgk allele, 43% of mice develop lung metastases
• number of metastatic nodules and metastatic burden in the lung are decreased compared to mice without the Mir18tm1.1Dgk allele




Genotype
MGI:5547938
cn243
Allelic
Composition
Krastm4Tyj/Kras+
Pax7tm2.1(cre/ERT2)Fan/Pax7+
Trp53tm1Brn/Trp53tm1Brn
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * 129X1/SvJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pax7tm2.1(cre/ERT2)Fan mutation (1 available); any Pax7 mutation (38 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• when mice older than 6 weeks are given systemic tamoxifen treatment by intraperitoneal delivery, mice develop multiple tumors (avg. 3.9 per mouse) with 100% penetrance within 1-2 months; median tumor-free survival is 44 days
• tumors develop at various locations, including clinically relevant sites including the orbit
• tamoxifen treated mice develop tumors displaying a histological spectrum ranging from undifferentiated pleomorphic sarcoma (UPS) to rhabdomyosarcoma (RMS)
• tumors mimic embryonic RMS, pleomorphic RMS, or myogenic or nonmyogenic UPS
• sarcomas can appear in the body wall (37%), the extremities (31%), head and neck (23%), with some being subcutaneous (9%)




Genotype
MGI:3714152
cn244
Allelic
Composition
Pggt1btm1Mbrg/Pggt1btm1Mbrg
Krastm4Tyj/Kras+
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Pggt1btm1Mbrg mutation (0 available); any Pggt1b mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• cre-activation leads to a rounded cell shape
• however, farnesylation of RHOA and CDC42 restores normal cell shape
• cre-activation leads to decreased cell proliferation
• however, farnesylation of RHOA and CDC42 restores proliferation induced by Krastm4Tyj




Genotype
MGI:3714154
cn245
Allelic
Composition
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1b+
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Lyz2tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (40 available)
Pggt1btm1Mbrg mutation (0 available); any Pggt1b mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice are normal until day 17 when they begin to die or must be euthanized median survival is to day 20

neoplasm
• tumors range from atypical adenomatous hyperplasia, adenoma and adenocarcinoma at day 11 to diffuse adenocarsinoma that obliterate alveolar space by day 20
• beginning at day 11 and obliterating alveolar space by day 20

respiratory system
• lung weight increases 10-fold between day 18 and 22
• tumors range from atypical adenomatous hyperplasia, adenoma and adenocarcinoma at day 11 to diffuse adenocarsinoma that obliterate alveolar space by day 20
• beginning at day 11 and obliterating alveolar space by day 20
• after day 17

immune system
• percentage of neutrophil is higher in peripheral blood than in controls
• percentage of lymphocytes is lower than in controls
• pools of immature myeloid are present in the spleen

hematopoietic system
• pools of immature myeloid are present in the spleen
• myeloid proliferation is increased
• percentage of neutrophil is higher in peripheral blood than in controls
• percentage of lymphocytes is lower than in controls
• pools of immature myeloid are present in the spleen

liver/biliary system
• myeloid infiltration of the liver occurs

growth/size/body
• after day 17
• lung weight increases 10-fold between day 18 and 22




Genotype
MGI:3714153
cn246
Allelic
Composition
Krastm4Tyj/Kras+
Pggt1btm1Mbrg/Pggt1btm1Mbrg
Lyz2tm1(cre)Ifo/Lyz2+
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Lyz2tm1(cre)Ifo mutation (14 available); any Lyz2 mutation (40 available)
Pggt1btm1Mbrg mutation (0 available); any Pggt1b mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive longer than Pggt1btm1Mbrg Lyzstm1(cre)Ifo Krastm4Tyj heterozygotes with some surviving until day 98 when they were euthanized

neoplasm
• few, very mild adenomatous hyperplasia are present at day 11 and increase in occurence by day 62
• however, many segments of the lung are normal at day 62
• at day 98, progressed and scattered adenomas are present

respiratory system
• lung weight is less than in Pggt1btm1Mbrg Lyzstm1(cre)Ifo Krastm4Tyj heterozygotes but higher than in normal mice
• few, very mild adenomatous hyperplasia are present at day 11 and increase in occurence by day 62
• however, many segments of the lung are normal at day 62
• at day 98, progressed and scattered adenomas are present

growth/size/body
• after day 40, mice grow slower than controls
• however, up to day 40 mice grow normally
• lung weight is less than in Pggt1btm1Mbrg Lyzstm1(cre)Ifo Krastm4Tyj heterozygotes but higher than in normal mice




Genotype
MGI:3722605
cn247
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm1Brn
Tg(KRT5-cre/PGR)1Der/?
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(KRT5-cre/PGR)1Der mutation (0 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following treatment with RU486 and TPA, mice develop less tumors than in Krastm4Tyj Trp53tm1Brn/Trp53tm3Glo Tg(KRT5-cre/PGR)1Der mice
• after RU486 and TPA treatment, carcinomas that develop following treatment with RU486 and TPA are squamous cell carcinomas with abundant keratin pearls and an absence of spindle cells

homeostasis/metabolism
• following treatment with RU486 and TPA, mice develop less tumors than in Krastm4Tyj Trp53tm1Brn/Trp53tm3Glo Tg(KRT5-cre/PGR)1Der mice




Genotype
MGI:3722603
cn248
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53+
Tg(KRT5-cre/PGR)1Der/?
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(KRT5-cre/PGR)1Der mutation (0 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• after RU486 and TPA treatment, 30% of mice develop skin carcinomas compared to 5% of Krastm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes




Genotype
MGI:3722604
cn249
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm1Brn/Trp53tm3Glo
Tg(KRT5-cre/PGR)1Der/?
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * FVB * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(KRT5-cre/PGR)1Der mutation (0 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
Trp53tm3Glo mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• following treatment with RU486 and TPA, mice develop more tumors than in Krastm4Tyj Trp53tm1Brn/ Trp53tm1Brn Tg(KRT5-cre/PGR)1Der mice
• following treatment with RU486 and TPA, conversion to malignant carcinoma is accelerated relative to in Krastm4Tyj Trp53tm1Brn/ Trp53tm1Brn Tg(KRT5-cre/PGR)1Der mice
• after RU486 and TPA treatment, 60% of tumors that develop are spindle cell carcinomas

homeostasis/metabolism
• following treatment with RU486 and TPA, mice develop more tumors than in Krastm4Tyj Trp53tm1Brn/ Trp53tm1Brn Tg(KRT5-cre/PGR)1Der mice




Genotype
MGI:5659895
cn250
Allelic
Composition
Cdkn2atm1Rdp/Cdkn2atm1Rdp
Krastm4Tyj/Kras+
Genetic
Background
involves: 129/Sv * 129S4/SvJae * C57BL/6 * FVB/N * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cdkn2atm1Rdp mutation (6 available); any Cdkn2a mutation (67 available)
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice inoculated with an adenovirus expressing cre recombinase (ad-cre) by inhalation have a median survival of 22 weeks after ad-cre inoculation

neoplasm
• mice inoculated with ad-cre by inhalation develop lung adenocarcinomas with high multiplicity, however metastasis is not observed

respiratory system
• mice inoculated with ad-cre by inhalation develop lung adenocarcinomas with high multiplicity, however metastasis is not observed




Genotype
MGI:3716394
cn251
Allelic
Composition
Krastm4Tyj/Kras+
Tg(SFTPC-rtTA)5Jaw/0
Tg(tetO-cre)1Jaw/0
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(SFTPC-rtTA)5Jaw mutation (4 available)
Tg(tetO-cre)1Jaw mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• death in the early postnatal period

respiratory system
• with doxycycline treatment beginning at E6.5, a dramatic lung branching defect is observed
• at E16.5, lungs show even more severe defects than in Kras:Meox2-cre embryos, with large epithelial-lined pouches in place of finely branched network of airways seen in wild-type
• branching defect persists through late gestation leading to early postnatal lethality
• branching defect originates in epithelium rather than mesenchyme
• markers of ciliated and Clara cells in the bronchi are significantly reduced at E18.5 compared to controls, indicating block in differentiation of lung epithelium




Genotype
MGI:3722600
cn252
Allelic
Composition
Krastm4Tyj/Kras+
Tg(KRT5-cre/PGR)1Der/?
Genetic
Background
involves: 129/Sv * C57BL/6 * FVB * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(KRT5-cre/PGR)1Der mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 7 to 10 weeks after treatment with RU486 to activate the cre transgene, mice develop epidermal papillomas

integument
• 7 to 10 weeks after treatment with RU486 to activate the cre transgene, mice develop epidermal papillomas




Genotype
MGI:3722602
cn253
Allelic
Composition
Krastm4Tyj/Kras+
Trp53tm3Glo/Trp53+
Tg(KRT5-cre/PGR)1Der/?
Genetic
Background
involves: 129/Sv * C57BL/6 * FVB * ICR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm4Tyj mutation (9 available); any Kras mutation (84 available)
Tg(KRT5-cre/PGR)1Der mutation (0 available)
Trp53tm3Glo mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• after RU486 and TPA treatment, mice develop three-fold more tumors than Krastm4Tyj Trp53tm1Brn heterozygotes and Krastm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes
• after RU486 and TPA treatment, 60% of mice develop metastasis in the lungs and/or lymph nodes compared to no wild-type mice
• after RU486 and TPA treatment, 42% of tumors exhibit aneuplody compared to 23% of Krastm4Tyj Trp53tm1Brn heterozygotes and 20% of Krastm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes
• after RU486 and TPA treatment, tumors exhibit centrosome amplification in 3% to 5% of tumors cells
• after RU486 and TPA treatment, carcinoma development is accelerated compared to in Krastm4Tyj Trp53tm1Brn heterozygotes and Krastm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes
• after RU486 and TPA treatment, 90% of mice develop skin carcinomas compared to 30% of Krastm4Tyj Trp53tm1Brn heterozygotes and 5% of Krastm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes

cellular
• after RU486 and TPA treatment, tumors exhibit centrosome amplification in 3% to 5% of tumors cells

homeostasis/metabolism
• after RU486 and TPA treatment, mice develop three-fold more tumors than Krastm4Tyj Trp53tm1Brn heterozygotes and Krastm4Tyj Tg(KRT5-cre/PGR)1Der heterozygotes





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
12/10/2024
MGI 6.24
The Jackson Laboratory