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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Tg(Pbsn-cre)4Prb
transgene insertion 4, Pradip Roy-Burman
MGI:2385927
Summary 72 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
cn1
Eaf1tm1.1Zhow/Eaf1tm1.1Zhow
Tg(Pbsn-cre)4Prb/0
B6(Cg)-Eaf1tm1.1Zhow Tg(Pbsn-cre)4Prb MGI:6694948
cn2
Cop1tm2.1Vmd/Cop1+
Tg(Pbsn-cre)4Prb/0
B6N.CgCop1tm2.1Vmd Ptentm1Hwu Tg(Pbsn-cre)4Prb MGI:5013603
cn3
Ptentm1Hwu/Ptentm1Hwu
Cop1tm2.1Vmd/Cop1tm2.1Vmd
Tg(Pbsn-cre)4Prb/0
B6N.CgCop1tm2.1Vmd Ptentm1Hwu Tg(Pbsn-cre)4Prb MGI:5013604
cn4
Cop1tm2.1Vmd/Cop1tm2.1Vmd
Tg(Pbsn-cre)4Prb/0
B6N.Cg-Cop1tm2.1Vmd Tg(Pbsn-cre)4Prb MGI:5013605
cn5
Cop1tm2.1Vmd/Cop1+
Tg(Pbsn-cre)4Prb/0
B6N.Cg-Cop1tm2.1Vmd Tg(Pbsn-cre)4Prb MGI:5013606
cn6
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1+
Tg(Pbsn-cre)4Prb/0
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:7277820
cn7
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1tm2Brn
Tg(Pbsn-cre)4Prb/0
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:7277819
cn8
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:7277821
cn9
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1tm2Brn
Tg(Pbsn-cre)4Prb/0
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:7277828
cn10
Hspa5tm1Alee/Hspa5tm1.1Alee
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/?
involves: 129 * 129S4/SvJae * C57BL/6 * DBA/2 MGI:4943512
cn11
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129 * 129S4/SvJae * C57BL/6 * DBA/2 MGI:3805865
cn12
Hspa5tm1Alee/Hspa5tm1Alee
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/?
involves: 129 * 129S4/SvJae * C57BL/6 * DBA/2 MGI:4943513
cn13
Hspa5tm1Alee/Hspa5+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/?
involves: 129 * 129S4/SvJae * C57BL/6 * DBA/2 MGI:4943514
cn14
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
involves: 129 * C57BL/6 * DBA/2 MGI:5524278
cn15
Pik3cbtm1Jjz/Pik3cbtm1Jjz
Tg(Pbsn-cre)4Prb/0
involves: 129 * C57BL/6 * DBA/2 MGI:3805861
cn16
Pik3catm1Jjz/Pik3catm1Jjz
Tg(Pbsn-cre)4Prb/0
involves: 129 * C57BL/6 * DBA/2 MGI:3805864
cn17
Ptentm1Rdp/Ptentm1Rdp
Smad4tm1Rdp/Smad4tm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129 * C57BL/6 * DBA/2 MGI:5431947
cn18
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key/Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key
Tg(Pbsn-cre)4Prb/0
involves: 129 * C57BL/6 * DBA/2 MGI:5524279
cn19
Hspa5tm1Alee/Hspa5tm1Alee
Tg(Pbsn-cre)4Prb/0
involves: 129 * C57BL/6 * DBA/2 MGI:4943515
cn20
Igs2tm1(CAG-Met)Zsu/Igs2+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129 * C57BL/6 * DBA/2 * FVB/N MGI:6507866
cn21
Ptentm1Rdp/Ptentm1Rdp
Terttm1Rdp/Tert+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5431944
cn22
Ptentm1Rdp/Ptentm1Rdp
Terttm1Rdp/Terttm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5431943
cn23
Ptentm1Rdp/Ptentm1Rdp
Terttm3Rdp/Terttm3Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5431978
cn24
Ptentm1Rdp/Ptentm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5431945
cn25
Eaf1tm1.1Zhow/Eaf1tm1.1Zhow
Eaf2tm1Zhow/Eaf2tm1Zhow
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J * DBA/2 MGI:6694954
cn26
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Brn/Trp53+
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:4819194
cn27
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:4819193
cn28
Brca2tm1Brn/Brca2tm1Brn
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 MGI:4819192
cn29
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+
Ptentm1Mro/Pten+
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * FVB/N MGI:5427498
cn30
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * FVB/N MGI:5427497
cn31
Col1a1tm1(tetO-YAP1*)Fcam/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2 MGI:5705651
cn32
Artm1Verh/Y
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129S4/SvJae * 129X1/SvJ * C57BL/6 * DBA/2 MGI:5009703
cn33
Krastm1Bbd/Kras+
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3836577
cn34
Gt(ROSA)26Sortm1(CAG-PTPN1,-EGFP)Mtr/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:6378625
cn35
Eif4etm1.1Lfur/Eif4etm1.1Lfur
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:4830313
cn36
Ctnnb1tm1Mmt/Ctnnb1+
Krastm1Bbd/Kras+
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 MGI:3836578
cn37
Ctnnb1tm1Mmt/Ctnnb1+
Igs2tm1(CAG-Met)Zsu/Igs2+
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 * FVB/N MGI:6507888
cn38
Igs2tm1(CAG-Met)Zsu/Igs2+
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 * FVB/N MGI:6507865
cn39
Gt(ROSA)26Sortm1(SPOP*F133V)Mrbn/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Pten+
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * C57BL/6 * DBA/2 MGI:6275174
cn40
Ptentm2.1Ppp/Ptentm2.1Ppp
Trp53tm1Thl/Trp53tm1Thl
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * C57BL/6 * DBA/2 MGI:3603330
cn41
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * C57BL/6 * DBA/2 MGI:2679901
cn42
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key/Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * C57BL/6 * DBA/2 MGI:5524280
cn43
Gt(ROSA)26Sortm1(SPOP*F133V)Mrbn/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
involves: 129S1/Sv * C57BL/6 * DBA/2 MGI:6275175
cn44
Eif2ak3tm1.2Drc/Eif2ak3tm1.2Drc
Ptentm1Hwu/Ptentm1Hwu
Tg(CAG-MYC,-GFP*)#Rugg/0
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6J * DBA/2 MGI:6198768
cn45
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA/2 MGI:4420974
cn46
Ptentm1Hwu/Ptentm1Hwu
Tg(CAG-fat-1)1Jxk/0
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA/2 MGI:4847617
cn47
Ptentm1Hwu/Pten+
Tg(ARR2/Pbsn-FGF8)3Prb/0
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA/2 MGI:4843916
cn48
Ptentm1Hwu/Pten+
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA/2 MGI:4420975
cn49
Ptentm1Hwu/Ptentm1Hwu
Tg(CAG-MYC,-GFP*)#Rugg/0
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * DBA/2 MGI:6198766
cn50
Apctm1Tno/Apctm1Tno
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * DBA/2 MGI:5566610
cn51
Ptentm1Hwu/Pten+
Tmprss2tm2.1(ETV1)Sho/Tmprss2tm2.1(ETV1)Sho
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5578649
cn52
Ergtm1.1Sho/Ergtm1.1Sho
Ptentm1Hwu/Ptentm1Hwu
Tmprss2tm3Sho/Tmprss2tm3Sho
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5578652
cn53
Rxratm1Krc/Rxra+
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:2449982
cn54
Krastm4Tyj/Kras+
Ptentm1Hwu/Pten+
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5705328
cn55
Krastm4Tyj/Kras+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5705321
cn56
Rxratm1Krc/Rxratm1Krc
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:2449983
cn57
Gt(ROSA)26Sortm2(H1/tetO-RNAi:Pdpk1)Mrl/Gt(ROSA)26Sor+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5008589
cn58
Gt(ROSA)26Sortm1(H1/tetO-RNAi:Pdpk1)Mrl/Gt(ROSA)26Sor+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:5008586
cn59
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:4358249
cn60
Ptentm1Hwu/Ptentm1Hwu
Ptpn1tm1Bpk/Ptpn1tm1Bpk
Tg(Pbsn-cre)4Prb/0
involves: 129S4/SvJae * C57BL/6 * DBA/2 MGI:6378626
cn61
Zfhx3tm1.1Jtd/Zfhx3tm1.1Jtd
Tg(Pbsn-cre)4Prb/0
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL MGI:5446522
cn62
Artm1Chc/Y
Tg(Pbsn-cre)4Prb/0
involves: 129S/SvEv * C57BL/6 * DBA/2 MGI:3773634
cn63
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/?
Tg(Pbsn-cre)4Prb/?
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:3716207
cn64
Ctnnb1tm1Mmt/Ctnnb1+
Tg(Pbsn-cre)4Prb/0
involves: 129X1/SvJ * C57BL/6 * DBA/2 MGI:3836579
cn65
Tg(CAG-MYC,-GFP*)#Rugg/0
Tg(Pbsn-cre)4Prb/0
involves: C57BL/6 * C57BL/6J * DBA/2 MGI:6198765
cn66
Klf5tm1.1Jtd/Klf5+
Tg(Pbsn-cre)4Prb/0
involves: C57BL/6 * DBA/2 MGI:5551716
cn67
Klf5tm1.1Jtd/Klf5tm1.1Jtd
Tg(Pbsn-cre)4Prb/0
involves: C57BL/6 * DBA/2 MGI:5551715
cn68
Tg(CAG-cat,-ALOX15)1868Klv/0
Tg(Pbsn-cre)4Prb/0
involves: C57BL/6 * DBA/2 MGI:6114993
cn69
Tg(CAG-cat,-ALOX15)1868Klv/Tg(CAG-cat,-ALOX15)1868Klv
Tg(Pbsn-cre)4Prb/?
involves: C57BL/6 * DBA/2 MGI:6114995
cn70
Ptentm1Mro/Pten+
Tg(Pbsn-cre)4Prb/0
involves: C57BL/6 * DBA/2 MGI:5427499
cn71
Gt(ROSA)26Sortm1(SPOP*F133V)Mrbn/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
involves: C57BL/6 * DBA/2 MGI:6275172
cn72
Trp53tm1Thl/Trp53tm1Thl
Tg(Pbsn-cre)4Prb/0
involves: C57BL/6 * DBA/2 MGI:3603329


Genotype
MGI:6694948
cn1
Allelic
Composition
Eaf1tm1.1Zhow/Eaf1tm1.1Zhow
Tg(Pbsn-cre)4Prb/0
Genetic
Background
B6(Cg)-Eaf1tm1.1Zhow Tg(Pbsn-cre)4Prb
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Eaf1tm1.1Zhow mutation (0 available); any Eaf1 mutation (17 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mouse prostatic intraepithelial neoplasia (mPIN) lesions
• increased epithelial cell proliferation in ventral prostate
• stroma inflammation
• increased CD3+ T cell and CD19+ B cell infiltration of ventral prostate

immune system
• stroma inflammation
• increased CD3+ T cell and CD19+ B cell infiltration of ventral prostate

neoplasm
• mouse prostatic intraepithelial neoplasia (mPIN) lesions

reproductive system
• mouse prostatic intraepithelial neoplasia (mPIN) lesions
• increased epithelial cell proliferation in ventral prostate
• stroma inflammation
• increased CD3+ T cell and CD19+ B cell infiltration of ventral prostate




Genotype
MGI:5013603
cn2
Allelic
Composition
Cop1tm2.1Vmd/Cop1+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
B6N.CgCop1tm2.1Vmd Ptentm1Hwu Tg(Pbsn-cre)4Prb
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cop1tm2.1Vmd mutation (0 available); any Cop1 mutation (44 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• invasive in 1 of 6 mice at 30 weeks of age
• high grade in 5 of 6 mice at 30 weeks of age

endocrine/exocrine glands
• invasive in 1 of 6 mice at 30 weeks of age
• high grade in 5 of 6 mice at 30 weeks of age

reproductive system
• invasive in 1 of 6 mice at 30 weeks of age
• high grade in 5 of 6 mice at 30 weeks of age




Genotype
MGI:5013604
cn3
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Cop1tm2.1Vmd/Cop1tm2.1Vmd
Tg(Pbsn-cre)4Prb/0
Genetic
Background
B6N.CgCop1tm2.1Vmd Ptentm1Hwu Tg(Pbsn-cre)4Prb
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cop1tm2.1Vmd mutation (0 available); any Cop1 mutation (44 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
• invasive in 11 of 13 mice at 30 weeks of age
• high grade in 2 of 13 mice at 30 weeks of age

reproductive system
• invasive in 11 of 13 mice at 30 weeks of age
• high grade in 2 of 13 mice at 30 weeks of age

endocrine/exocrine glands
• invasive in 11 of 13 mice at 30 weeks of age
• high grade in 2 of 13 mice at 30 weeks of age




Genotype
MGI:5013605
cn4
Allelic
Composition
Cop1tm2.1Vmd/Cop1tm2.1Vmd
Tg(Pbsn-cre)4Prb/0
Genetic
Background
B6N.Cg-Cop1tm2.1Vmd Tg(Pbsn-cre)4Prb
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cop1tm2.1Vmd mutation (0 available); any Cop1 mutation (44 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• in 3 of 4 mice at 40 weeks of age
• in all mice at 52 weeks of age
• low grade in 2 of 6 mice at 52 weeks of age
• cells in the ventral and lateral prostate exhibit increased proliferation compared to in wild-type mice

neoplasm
• low grade in 2 of 6 mice at 52 weeks of age

endocrine/exocrine glands
• in 3 of 4 mice at 40 weeks of age
• in all mice at 52 weeks of age
• low grade in 2 of 6 mice at 52 weeks of age
• cells in the ventral and lateral prostate exhibit increased proliferation compared to in wild-type mice




Genotype
MGI:5013606
cn5
Allelic
Composition
Cop1tm2.1Vmd/Cop1+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
B6N.Cg-Cop1tm2.1Vmd Tg(Pbsn-cre)4Prb
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Cop1tm2.1Vmd mutation (0 available); any Cop1 mutation (44 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• in 1 of 7 mice at 52 weeks of age

endocrine/exocrine glands
• in 1 of 7 mice at 52 weeks of age




Genotype
MGI:7277820
cn6
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (111 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of 19 weeks

neoplasm
• mice develop large, invasive tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 12 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time

endocrine/exocrine glands
• mice develop large, invasive tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 12 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time

reproductive system
• mice develop large, invasive tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 12 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
prostate neuroendocrine neoplasm DOID:2992 J:307910




Genotype
MGI:7277819
cn7
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1tm2Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (111 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of 12.5 weeks
• castrated mice have a median survival time of 24 weeks

neoplasm
• mice develop large, invasive prostate tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 8 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time
• mice do not respond to surgical castration and continue to grow tumors rapidly
• post-castration tumors harbor foci enriched with divergent differentiated histology compared to adenocarcinoma and increased metastatic potential
• onset of metastasis occurs as early as 8 weeks and by 12 weeks, 100% of mice develop distant metastatic lesions; metastases to the lung, liver, lymph nodes, and kidney primarily consist of large and small cell neuroendocrine histologies that are AR-negative

endocrine/exocrine glands
• mice develop large, invasive prostate tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 8 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time
• mice do not respond to surgical castration and continue to grow tumors rapidly
• post-castration tumors harbor foci enriched with divergent differentiated histology compared to adenocarcinoma and increased metastatic potential

reproductive system
• mice develop large, invasive prostate tumors with androgen receptor (AR)-negative and poorly differentiated foci as early as 8 weeks
• these regions show little resemblance to conventional adenocarcinoma but are negative for neuroendocrine markers, potentially as a transition between conventional adenocarcinoma and neuroendocrine prostate cancer (NEPC) states
• some foci are positive for neuroendocrine markers INSM1, EZH2, and NKX2-1 and some foci display condensed nuclei and scant cytoplasm, characteristic of NEPC morphology
• tumors also include other foci of divergent differentiation like intestinal and squamous, as well as conventional, AR+ adenocarcinoma, but the percentage of conventional adenocarcinoma decreases over time while the percentage of poorly differentiated histology increases over time
• mice do not respond to surgical castration and continue to grow tumors rapidly
• post-castration tumors harbor foci enriched with divergent differentiated histology compared to adenocarcinoma and increased metastatic potential

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
prostate neuroendocrine neoplasm DOID:2992 J:307910




Genotype
MGI:7277821
cn8
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-MYCN,-luc)Jhsc mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Ptentm2.1Ppp mutation (0 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
• median survival time of 26 weeks
• castrated mice have a median survival time of 44 weeks

neoplasm
• mice develop prostate tumors that have primarily high-grade prostatic intraepithelial neoplasia at earlier time points
• tumors regress post-castration but resume growth 24 weeks post-castration

endocrine/exocrine glands
• mice develop prostate tumors that have primarily high-grade prostatic intraepithelial neoplasia at earlier time points
• tumors regress post-castration but resume growth 24 weeks post-castration

reproductive system
• mice develop prostate tumors that have primarily high-grade prostatic intraepithelial neoplasia at earlier time points
• tumors regress post-castration but resume growth 24 weeks post-castration




Genotype
MGI:7277828
cn9
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Rb1tm2Brn/Rb1tm2Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * 129S1/Sv * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Rb1tm2Brn mutation (3 available); any Rb1 mutation (111 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of 38 weeks
• castrated mice have a median survival time of 43.5 weeks

neoplasm
• prostates from 8-week-old mice are composed of androgen receptor-positive, high-grade prostatic intraepithelial neoplasia lesions
• tumors regress post-castration but resume growth 24 weeks post-castration

endocrine/exocrine glands
• prostates from 8-week-old mice are composed of androgen receptor-positive, high-grade prostatic intraepithelial neoplasia lesions
• tumors regress post-castration but resume growth 24 weeks post-castration

reproductive system
• prostates from 8-week-old mice are composed of androgen receptor-positive, high-grade prostatic intraepithelial neoplasia lesions
• tumors regress post-castration but resume growth 24 weeks post-castration




Genotype
MGI:4943512
cn10
Allelic
Composition
Hspa5tm1Alee/Hspa5tm1.1Alee
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/?
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hspa5tm1.1Alee mutation (1 available); any Hspa5 mutation (39 available)
Hspa5tm1Alee mutation (0 available); any Hspa5 mutation (39 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
N
• mice do not develop detectable cancerous or precancerous lesions in the prostate




Genotype
MGI:3805865
cn11
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
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
• mutants develop tumors between 12 to 20 weeks, with 100% penetrance at 20 weeks
• all mice develop invasive adenocarcinoma in all prostate lobes
• malignant cells invade through the basement membrane into the adjacent stroma, inducing both an inflammatory and a desmoplastic response, resulting in growth of fibrous and connective tissue around the tumor
• mice develop prostate intraepithelial neoplasias

reproductive system
• mutants develop tumors between 12 to 20 weeks, with 100% penetrance at 20 weeks
• all mice develop invasive adenocarcinoma in all prostate lobes
• malignant cells invade through the basement membrane into the adjacent stroma, inducing both an inflammatory and a desmoplastic response, resulting in growth of fibrous and connective tissue around the tumor
• mice develop prostate intraepithelial neoplasias

endocrine/exocrine glands
• mutants develop tumors between 12 to 20 weeks, with 100% penetrance at 20 weeks
• all mice develop invasive adenocarcinoma in all prostate lobes
• malignant cells invade through the basement membrane into the adjacent stroma, inducing both an inflammatory and a desmoplastic response, resulting in growth of fibrous and connective tissue around the tumor
• mice develop prostate intraepithelial neoplasias




Genotype
MGI:4943513
cn12
Allelic
Composition
Hspa5tm1Alee/Hspa5tm1Alee
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/?
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hspa5tm1Alee mutation (0 available); any Hspa5 mutation (39 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
N
• mice do not develop detectable cancerous or precancerous lesions in the prostate




Genotype
MGI:4943514
cn13
Allelic
Composition
Hspa5tm1Alee/Hspa5+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/?
Genetic
Background
involves: 129 * 129S4/SvJae * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hspa5tm1Alee mutation (0 available); any Hspa5 mutation (39 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
• mutants exhibit visible solid tumor mass with invasive adenocarcinoma in the anterior prostate, while the dorsolateral prostate and ventral prostate lobes keep their ductual structure, albeit with enlarged ducts
• dorsolateral prostate and ventral prostate exhibit diffusive prostate intraepithelial neoplasia (PIN) with intact basement membrane

endocrine/exocrine glands
• mutants exhibit visible solid tumor mass with invasive adenocarcinoma in the anterior prostate, while the dorsolateral prostate and ventral prostate lobes keep their ductual structure, albeit with enlarged ducts
• dorsolateral prostate and ventral prostate exhibit diffusive prostate intraepithelial neoplasia (PIN) with intact basement membrane

reproductive system
• mutants exhibit visible solid tumor mass with invasive adenocarcinoma in the anterior prostate, while the dorsolateral prostate and ventral prostate lobes keep their ductual structure, albeit with enlarged ducts
• dorsolateral prostate and ventral prostate exhibit diffusive prostate intraepithelial neoplasia (PIN) with intact basement membrane




Genotype
MGI:5524278
cn14
Allelic
Composition
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key mutation (2 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• focal ventral lobe hyperplasia after 1 year of age in 50% of mice

endocrine/exocrine glands
• focal ventral lobe hyperplasia after 1 year of age in 50% of mice




Genotype
MGI:3805861
cn15
Allelic
Composition
Pik3cbtm1Jjz/Pik3cbtm1Jjz
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pik3cbtm1Jjz mutation (1 available); any Pik3cb mutation (152 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• unlike in Pten null mice, tumorigenesis in the prostate is not detected




Genotype
MGI:3805864
cn16
Allelic
Composition
Pik3catm1Jjz/Pik3catm1Jjz
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Pik3catm1Jjz mutation (1 available); any Pik3ca mutation (66 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• following cre-mediated recombination, mouse embryonic fibroblasts (MEFs) undergo reduced levels of immortalization upon exposure to HRas-G12V or EGFR-Del from feeder cells

neoplasm
• mice develop prostate intraepithelial neoplasias

reproductive system
• mice develop prostate intraepithelial neoplasias

endocrine/exocrine glands
• mice develop prostate intraepithelial neoplasias




Genotype
MGI:5431947
cn17
Allelic
Composition
Ptentm1Rdp/Ptentm1Rdp
Smad4tm1Rdp/Smad4tm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Rdp mutation (0 available); any Pten mutation (88 available)
Smad4tm1Rdp mutation (0 available); any Smad4 mutation (48 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• survival time is shorter than in mutant mice wild-type for Smad4
• median survival time of 17.05 weeks

neoplasm
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• tumors are more aggressive than in mutant mice wild-type for Smad4
• bone metastases are seen in some (3 of 24) mice unlike in mutant mice wild-type for Smad4

endocrine/exocrine glands
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• tumors are more aggressive than in mutant mice wild-type for Smad4

reproductive system
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• tumors are more aggressive than in mutant mice wild-type for Smad4




Genotype
MGI:5524279
cn18
Allelic
Composition
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key/Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key mutation (2 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• focal ventral lobe hyperplasia after 1 year of age in 50% of mice

endocrine/exocrine glands
• focal ventral lobe hyperplasia after 1 year of age in 50% of mice




Genotype
MGI:4943515
cn19
Allelic
Composition
Hspa5tm1Alee/Hspa5tm1Alee
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Hspa5tm1Alee mutation (0 available); any Hspa5 mutation (39 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
N
• mice are phenotypically normal and fertile and prostate morphology is normal




Genotype
MGI:6507866
cn20
Allelic
Composition
Igs2tm1(CAG-Met)Zsu/Igs2+
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129 * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igs2tm1(CAG-Met)Zsu mutation (0 available); any Igs2 mutation (72 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
endocrine/exocrine glands
• mice develop prostatic sarcomatoid carcinoma
• mice show a more aggressive prostatic tumor phenotype than single conditional Ptentm1Hwu mice
• mice develop prostatic adenocarcinomas and invasive carcinomas
• 5 of 5 mice develop multifocal high grade intraepithelial neoplasia (PIN) before 4 months of age

neoplasm
• mice develop prostatic sarcomatoid carcinoma
• mice show a more aggressive prostatic tumor phenotype than single conditional Ptentm1Hwu mice
• mice develop prostatic adenocarcinomas and invasive carcinomas
• 5 of 5 mice develop multifocal high grade intraepithelial neoplasia (PIN) before 4 months of age
• prostate cancer metastasis after 10 months of age with 62.5% of mice showing metastatic lesions
• metastasis to lungs and periprostatic lymph nodes is seen
• mice show an overall more invasive tumor phenotype than single conditional Ptentm1Hwu mice
• 1 of 5 mice show invasive pancreatic carcinoma at 4-10 months and 6 of 8 mice develop invasive carcinoma after 10 months of age; 5 of 8 mice have invasive carcinoma with epithelial-mesenchymal transition and 5 of 8 mice have invasive carcinoma with metastasis
• mice exhibit a transition from prostatic adenocarcinoma and invasive carcinoma lesions to pathology resembling prostatic sarcamoid carcinomas
• sarcamoid carcinomas show spindle-like tumor cells, tumor cells with a multitude of mitotic figures, and haphazard acini and lobules of pleomorphic cells, indicating that these lesions possess mesenchymal morphology and proliferative and invasive features

reproductive system
• mice develop prostatic sarcomatoid carcinoma
• mice show a more aggressive prostatic tumor phenotype than single conditional Ptentm1Hwu mice
• mice develop prostatic adenocarcinomas and invasive carcinomas
• 5 of 5 mice develop multifocal high grade intraepithelial neoplasia (PIN) before 4 months of age




Genotype
MGI:5431944
cn21
Allelic
Composition
Ptentm1Rdp/Ptentm1Rdp
Terttm1Rdp/Tert+
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Rdp mutation (0 available); any Pten mutation (88 available)
Terttm1Rdp mutation (0 available); any Tert mutation (55 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

neoplasm
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age

reproductive system
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age

endocrine/exocrine glands
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age




Genotype
MGI:5431943
cn22
Allelic
Composition
Ptentm1Rdp/Ptentm1Rdp
Terttm1Rdp/Terttm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Rdp mutation (0 available); any Pten mutation (88 available)
Terttm1Rdp mutation (0 available); any Tert mutation (55 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• at generations 3 and 4 (G3/4), all mice develop smaller, poorly progressive tumors compared to G0 mice
• high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age
• most tumors fail to progress beyond HPIN by 24 weeks of age unlike in G0 mice
• smaller, poorly progressive tumors compared to tumors in G0 mice
• markedly increased apoptosis and decreased proliferation in tumor cells compared tumor cells from G0 mice

endocrine/exocrine glands
• at generations 3 and 4 (G3/4), all mice develop smaller, poorly progressive tumors compared to G0 mice
• high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age
• most tumors fail to progress beyond HPIN by 24 weeks of age unlike in G0 mice

cellular
• reduced at G3/4

reproductive system
• at generations 3 and 4 (G3/4), all mice develop smaller, poorly progressive tumors compared to G0 mice
• high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age
• most tumors fail to progress beyond HPIN by 24 weeks of age unlike in G0 mice




Genotype
MGI:5431978
cn23
Allelic
Composition
Ptentm1Rdp/Ptentm1Rdp
Terttm3Rdp/Terttm3Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Rdp mutation (0 available); any Pten mutation (88 available)
Terttm3Rdp mutation (0 available); any Tert mutation (55 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• develop bulky lethal tumors by age 24 weeks of age

endocrine/exocrine glands
• at generations 3 and 4 (G3/4), all develop invasive prostate adenocarcinomas by 24 weeks of age
• at G3/4, high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age

neoplasm
• at generations 3 and 4 (G3/4), all develop invasive prostate adenocarcinomas by 24 weeks of age
• at G3/4, high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age
• in some (5 of 20) G3/4 mice lumbar spine metastases are seen unlike in G0 mice

reproductive system
• at generations 3 and 4 (G3/4), all develop invasive prostate adenocarcinomas by 24 weeks of age
• at G3/4, high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age

cellular
• increase in the number of chromosomal aberrations in tumor cells from G3/4 mice compared to G0 mice
• increased length in prostate tumor cells compared to G3/4 mice homozygous for Terttm1Rdp, Ptentm1Rdp and Trp53tm1Brn and hemizygous for Tg(Pbsn-cre)4Prb




Genotype
MGI:5431945
cn24
Allelic
Composition
Ptentm1Rdp/Ptentm1Rdp
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Rdp mutation (0 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival time of 26.3 weeks

neoplasm
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age

reproductive system
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age

endocrine/exocrine glands
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• high-grade prostate intraepithelial neoplasia (HPIN) in all mice by 9 weeks of age




Genotype
MGI:6694954
cn25
Allelic
Composition
Eaf1tm1.1Zhow/Eaf1tm1.1Zhow
Eaf2tm1Zhow/Eaf2tm1Zhow
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * 129S6/SvEvTac * C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Eaf1tm1.1Zhow mutation (0 available); any Eaf1 mutation (17 available)
Eaf2tm1Zhow mutation (0 available); any Eaf2 mutation (19 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mouse prostatic intraepithelial neoplasia (mPIN) lesions
• increased epithelial cell proliferation in ventral prostate
• stroma inflammation
• increased CD3+ T cell and CD19+ B cell infiltration of ventral prostate

immune system
• stroma inflammation
• increased CD3+ T cell and CD19+ B cell infiltration of ventral prostate

neoplasm
• mouse prostatic intraepithelial neoplasia (mPIN) lesions

reproductive system
• mouse prostatic intraepithelial neoplasia (mPIN) lesions
• increased epithelial cell proliferation in ventral prostate
• stroma inflammation
• increased CD3+ T cell and CD19+ B cell infiltration of ventral prostate




Genotype
MGI:4819194
cn26
Allelic
Composition
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Brn/Trp53+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (5 available); any Brca2 mutation (132 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

High-grade prostate intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Tg(Pbsn-cre)4Prb/0 Trp53tm1Brn/Trp53tm1Brn and prostate hyperplasia and intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Trp53tm1Brn/Trp53+ Tg(Pbsn-cre)4Prb/0 mice

neoplasm
• focal low grade PIN are seen at 10 - 14 months of age
• by 15 - 20 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• levels of cell proliferation are 9 fold higher in PIN lesions

reproductive system
• focal hyperplasia is seen beginning at 10 -14 months of age
• focal low grade PIN are seen at 10 - 14 months of age
• by 15 - 20 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• levels of cell proliferation are 9 fold higher in PIN lesions
• areas of hyperplasia are positive for markers of DNA damage
• 4 fold increase in apoptotic cells in PIN foci

endocrine/exocrine glands
• focal hyperplasia is seen beginning at 10 -14 months of age
• focal low grade PIN are seen at 10 - 14 months of age
• by 15 - 20 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• levels of cell proliferation are 9 fold higher in PIN lesions
• areas of hyperplasia are positive for markers of DNA damage
• 4 fold increase in apoptotic cells in PIN foci




Genotype
MGI:4819193
cn27
Allelic
Composition
Brca2tm1Brn/Brca2tm1Brn
Trp53tm1Brn/Trp53tm1Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (5 available); any Brca2 mutation (132 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Brn mutation (18 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

High-grade prostate intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Tg(Pbsn-cre)4Prb/0 Trp53tm1Brn/Trp53tm1Brn and prostate hyperplasia and intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Trp53tm1Brn/Trp53+ Tg(Pbsn-cre)4Prb/0 mice

neoplasm
• by 10 - 14 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• frequently multiple ducts of each lobe have high grade PIN, which are present in proximal and distal regions of the prostate and consist of many atypical cells filling the lumen
• high grade PIN lesions are predominantly seen in the anterior and dorsal prostate
• levels of cell proliferation are 30 fold higher in PIN lesions
• high grade PIN lesions frequently contain large groups of basal cells some of which are rounder in shape and positioned near the lumen
• high grade lesions continue to proliferate post castration

reproductive system
• focal hyperplasia is seen beginning as early as 6 months of age
• by 10 - 14 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• frequently multiple ducts of each lobe have high grade PIN, which are present in proximal and distal regions of the prostate and consist of many atypical cells filling the lumen
• high grade PIN lesions are predominantly seen in the anterior and dorsal prostate
• levels of cell proliferation are 30 fold higher in PIN lesions
• high grade PIN lesions frequently contain large groups of basal cells some of which are rounder in shape and positioned near the lumen
• high grade lesions continue to proliferate post castration
• areas of hyperplasia are positive for markers of DNA damage
• 20 fold increase in apoptotic cells in areas of high grade PIN

endocrine/exocrine glands
• focal hyperplasia is seen beginning as early as 6 months of age
• by 10 - 14 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• frequently multiple ducts of each lobe have high grade PIN, which are present in proximal and distal regions of the prostate and consist of many atypical cells filling the lumen
• high grade PIN lesions are predominantly seen in the anterior and dorsal prostate
• levels of cell proliferation are 30 fold higher in PIN lesions
• high grade PIN lesions frequently contain large groups of basal cells some of which are rounder in shape and positioned near the lumen
• high grade lesions continue to proliferate post castration
• areas of hyperplasia are positive for markers of DNA damage
• 20 fold increase in apoptotic cells in areas of high grade PIN




Genotype
MGI:4819192
cn28
Allelic
Composition
Brca2tm1Brn/Brca2tm1Brn
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Brca2tm1Brn mutation (5 available); any Brca2 mutation (132 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Prostate hyperplasia and low-grade prostate intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Tg(Pbsn-cre)4Prb/0 mice

neoplasm
• focal low grade PIN are seen in the lumen at 15 - 20 months of age
• low grade PIN lesions form characteristic tufting and cribiform patterns
• hyperplasia and low grade PIN are seen all 4 lobes

reproductive system
• focal hyperplasia containing atypical cells is seen beginning at 10 -14 months of age
• hyperplasia and low grade PIN are seen all 4 lobes
• focal low grade PIN are seen in the lumen at 15 - 20 months of age
• low grade PIN lesions form characteristic tufting and cribiform patterns
• hyperplasia and low grade PIN are seen all 4 lobes
• areas of hyperplasia are positive for markers of DNA damage
• 3 fold increase in apoptotic cells in areas of hyperplasia and low grade PIN

endocrine/exocrine glands
• focal hyperplasia containing atypical cells is seen beginning at 10 -14 months of age
• hyperplasia and low grade PIN are seen all 4 lobes
• focal low grade PIN are seen in the lumen at 15 - 20 months of age
• low grade PIN lesions form characteristic tufting and cribiform patterns
• hyperplasia and low grade PIN are seen all 4 lobes
• areas of hyperplasia are positive for markers of DNA damage
• 3 fold increase in apoptotic cells in areas of hyperplasia and low grade PIN




Genotype
MGI:5427498
cn29
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+
Ptentm1Mro/Pten+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Ptentm1Mro mutation (1 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Prostate cancer progression in Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+, Tg(Pbsn-cre)4Prb/0 Ptentm1Mro/Pten+, and Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+ Ptentm1Mro/Pten+ mice

neoplasm
• 55% penetrance at 1 year
• multifocal, predominantly localized in the dorsolateral lobe that are locally invasive and highly vascularized

renal/urinary system

endocrine/exocrine glands
• 55% penetrance at 1 year
• multifocal, predominantly localized in the dorsolateral lobe that are locally invasive and highly vascularized

reproductive system
• 55% penetrance at 1 year
• multifocal, predominantly localized in the dorsolateral lobe that are locally invasive and highly vascularized




Genotype
MGI:5427497
cn30
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Prostate cancer progression in Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+, Tg(Pbsn-cre)4Prb/0 Ptentm1Mro/Pten+, and Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+ Ptentm1Mro/Pten+ mice

reproductive system
• at 6 months, mice exhibit atypical hyperplastic foci in the prostate lobes unlike control mice

neoplasm
N
• mice do not develop adenocarcinomas

endocrine/exocrine glands
• at 6 months, mice exhibit atypical hyperplastic foci in the prostate lobes unlike control mice




Genotype
MGI:5705651
cn31
Allelic
Composition
Col1a1tm1(tetO-YAP1*)Fcam/Col1a1+
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
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:
Col1a1tm1(tetO-YAP1*)Fcam mutation (0 available); any Col1a1 mutation (163 available)
Gt(ROSA)26Sortm1(rtTA,EGFP)Nagy mutation (5 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• 4 of 11 mice administered doxycycline at 3 months of age develop prostate tumors with age
• tumors include adenocarcinomas, sarcomatoid carcinomas (epithelial-mesenchymal transition-like epithelial tumor), and stromal-type tumors

endocrine/exocrine glands
• 4 of 11 mice administered doxycycline at 3 months of age develop prostate tumors with age
• tumors include adenocarcinomas, sarcomatoid carcinomas (epithelial-mesenchymal transition-like epithelial tumor), and stromal-type tumors

reproductive system
• 4 of 11 mice administered doxycycline at 3 months of age develop prostate tumors with age
• tumors include adenocarcinomas, sarcomatoid carcinomas (epithelial-mesenchymal transition-like epithelial tumor), and stromal-type tumors




Genotype
MGI:5009703
cn32
Allelic
Composition
Artm1Verh/Y
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
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:
Artm1Verh mutation (1 available); any Ar mutation (23 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
• mutants develop adenocarcinoma in the dorsolateral lobes of the prostate
• cancer progression is similar to single conditional Pten mice
• proliferation and apoptotic indexes are increased in the cancers, most notably in the proximal regions of the dorsal-lateral lobe
• mutant tumors contain low or no p63+ cells, similar to human prostate cancer
• castrated mutants develop cancer outgrowths in the dorsolateral lobes, indicating that mutants develop castrate-resistant prostate cancer
• castrated mice treated with rapamycin show a reduction in prostate volume and reduced prostate proliferation

reproductive system
• mutants develop adenocarcinoma in the dorsolateral lobes of the prostate
• cancer progression is similar to single conditional Pten mice
• proliferation and apoptotic indexes are increased in the cancers, most notably in the proximal regions of the dorsal-lateral lobe
• mutant tumors contain low or no p63+ cells, similar to human prostate cancer
• castrated mutants develop cancer outgrowths in the dorsolateral lobes, indicating that mutants develop castrate-resistant prostate cancer
• castrated mice treated with rapamycin show a reduction in prostate volume and reduced prostate proliferation

endocrine/exocrine glands
• mutants develop adenocarcinoma in the dorsolateral lobes of the prostate
• cancer progression is similar to single conditional Pten mice
• proliferation and apoptotic indexes are increased in the cancers, most notably in the proximal regions of the dorsal-lateral lobe
• mutant tumors contain low or no p63+ cells, similar to human prostate cancer
• castrated mutants develop cancer outgrowths in the dorsolateral lobes, indicating that mutants develop castrate-resistant prostate cancer
• castrated mice treated with rapamycin show a reduction in prostate volume and reduced prostate proliferation




Genotype
MGI:3836577
cn33
Allelic
Composition
Krastm1Bbd/Kras+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Krastm1Bbd mutation (2 available); any Kras mutation (84 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• at 200 days, 100% of mice exhibit atypical hyperplasia unlike wild-type mice
• at 500 days, 93% of mice exhibit atypical hyperplasia unlike wild-type mice
• at 200 days, 67% of mice develop prostate intraepithelial neoplasia that display foci of small solid and cribiform intraluminal proliferation of atypical cells and nuclear atypia unlike wild-type mice
• at 500 days, 60% of mice exhibit prostate intraepithelial neoplasia unlike in wild-type mice

neoplasm
• at 200 days, 67% of mice develop prostate intraepithelial neoplasia that display foci of small solid and cribiform intraluminal proliferation of atypical cells and nuclear atypia unlike wild-type mice
• at 500 days, 60% of mice exhibit prostate intraepithelial neoplasia unlike in wild-type mice

endocrine/exocrine glands
• at 200 days, 100% of mice exhibit atypical hyperplasia unlike wild-type mice
• at 500 days, 93% of mice exhibit atypical hyperplasia unlike wild-type mice
• at 200 days, 67% of mice develop prostate intraepithelial neoplasia that display foci of small solid and cribiform intraluminal proliferation of atypical cells and nuclear atypia unlike wild-type mice
• at 500 days, 60% of mice exhibit prostate intraepithelial neoplasia unlike in wild-type mice




Genotype
MGI:6378625
cn34
Allelic
Composition
Gt(ROSA)26Sortm1(CAG-PTPN1,-EGFP)Mtr/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(CAG-PTPN1,-EGFP)Mtr mutation (0 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice show a moderate incidence of epithelial hyperplasia in the anterior prostate
• one mouse shows a prostatic intraepithelial neoplasia (mPIN) in the dorsolateral prostate

neoplasm
• one mouse shows a prostatic intraepithelial neoplasia (mPIN) in the dorsolateral prostate

reproductive system
• mice show a moderate incidence of epithelial hyperplasia in the anterior prostate
• one mouse shows a prostatic intraepithelial neoplasia (mPIN) in the dorsolateral prostate




Genotype
MGI:4830313
cn35
Allelic
Composition
Eif4etm1.1Lfur/Eif4etm1.1Lfur
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Eif4etm1.1Lfur mutation (0 available); any Eif4e mutation (42 available)
Ptentm2.1Ppp mutation (0 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
• at 7 months, mice exhibit fewer incidence of high grade prostate intraepithelial neoplasia due to delayed onset and decreased cell proliferation compared with Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice
• mice do not exhibit infiltrating adenocarcinoma in the prostate unlike Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice




Genotype
MGI:3836578
cn36
Allelic
Composition
Ctnnb1tm1Mmt/Ctnnb1+
Krastm1Bbd/Kras+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (49 available)
Krastm1Bbd mutation (2 available); any Kras mutation (84 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die prior to day 300

reproductive system
• mice exhibit keratinized squamous metaplasia in the bulbourethral gland unlike wild-type mice
• all mice develop diffuse, locally invasive carcinomas in the prostate that develop from solid or sheet-like proliferation with occasional rosette structures, nuclear atypia, apoptotic bodies, and mitosis unlike in wild-type mice

neoplasm
• all mice develop diffuse, locally invasive carcinomas in the prostate that develop from solid or sheet-like proliferation with occasional rosette structures, nuclear atypia, apoptotic bodies, and mitosis unlike in wild-type mice

renal/urinary system
• mice exhibit keratinized squamous metaplasia in the urethral gland unlike wild-type mice

endocrine/exocrine glands
• mice exhibit keratinized squamous metaplasia in the bulbourethral gland unlike wild-type mice
• all mice develop diffuse, locally invasive carcinomas in the prostate that develop from solid or sheet-like proliferation with occasional rosette structures, nuclear atypia, apoptotic bodies, and mitosis unlike in wild-type mice
• mice exhibit keratinized squamous metaplasia in the urethral gland unlike wild-type mice




Genotype
MGI:6507888
cn37
Allelic
Composition
Ctnnb1tm1Mmt/Ctnnb1+
Igs2tm1(CAG-Met)Zsu/Igs2+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (49 available)
Igs2tm1(CAG-Met)Zsu mutation (0 available); any Igs2 mutation (72 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice develop aggressive adenocarcinomas that occur with much higher frequency than in single Ctnnb1tm1Mmt conditional mutants, developing prostatic invasive adenocarcinomas as early as 7 months of age
• 4 of 4 mice show intracystic adenocarcinoma at 6-9 months of age, with 1 of 4 mice showing invasive adenocarcinoma
• 13 of 13 mice show intracystic adenocarcinoma at 9 months or older, with 5 of 13 showing invasive adenocarcinoma
• mice develop PIN lesions starting at 4-6 weeks of age, with 5 of 5 mice showing high grade PIN before 6 months of age
• mice develop more severe PIN lesions and faster disease progression than single Ctnnb1tm1Mmt conditional mutants
• lesions in the anterior, dorsal, and lateral prostate lobes are more severe than in the ventral prostate
• typical cribriform and papilliferous structures completely fill the lumen of prostatic glands

neoplasm
• mice develop aggressive adenocarcinomas that occur with much higher frequency than in single Ctnnb1tm1Mmt conditional mutants, developing prostatic invasive adenocarcinomas as early as 7 months of age
• 4 of 4 mice show intracystic adenocarcinoma at 6-9 months of age, with 1 of 4 mice showing invasive adenocarcinoma
• 13 of 13 mice show intracystic adenocarcinoma at 9 months or older, with 5 of 13 showing invasive adenocarcinoma
• mice develop PIN lesions starting at 4-6 weeks of age, with 5 of 5 mice showing high grade PIN before 6 months of age
• mice develop more severe PIN lesions and faster disease progression than single Ctnnb1tm1Mmt conditional mutants
• lesions in the anterior, dorsal, and lateral prostate lobes are more severe than in the ventral prostate
• typical cribriform and papilliferous structures completely fill the lumen of prostatic glands

reproductive system
• mice develop aggressive adenocarcinomas that occur with much higher frequency than in single Ctnnb1tm1Mmt conditional mutants, developing prostatic invasive adenocarcinomas as early as 7 months of age
• 4 of 4 mice show intracystic adenocarcinoma at 6-9 months of age, with 1 of 4 mice showing invasive adenocarcinoma
• 13 of 13 mice show intracystic adenocarcinoma at 9 months or older, with 5 of 13 showing invasive adenocarcinoma
• mice develop PIN lesions starting at 4-6 weeks of age, with 5 of 5 mice showing high grade PIN before 6 months of age
• mice develop more severe PIN lesions and faster disease progression than single Ctnnb1tm1Mmt conditional mutants
• lesions in the anterior, dorsal, and lateral prostate lobes are more severe than in the ventral prostate
• typical cribriform and papilliferous structures completely fill the lumen of prostatic glands




Genotype
MGI:6507865
cn38
Allelic
Composition
Igs2tm1(CAG-Met)Zsu/Igs2+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6 * DBA/2 * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Igs2tm1(CAG-Met)Zsu mutation (0 available); any Igs2 mutation (72 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• mice do not show any obvious pathological changes in prostate tissues from birth to 20 months of age
• mice administered recombinant human hepatocyte growth factor at 6 months of age show lesions of typical low-grade prostatic intraepithelial neoplasia not seen in hepatocyte growth factor-administered wild-type mice
• however, hepatocyte growth factor-administered mice do not develop prostate carcinomas

reproductive system
• mice administered recombinant human hepatocyte growth factor at 6 months of age show lesions of typical low-grade prostatic intraepithelial neoplasia not seen in hepatocyte growth factor-administered wild-type mice
• however, hepatocyte growth factor-administered mice do not develop prostate carcinomas

neoplasm
• mice administered recombinant human hepatocyte growth factor at 6 months of age show lesions of typical low-grade prostatic intraepithelial neoplasia not seen in hepatocyte growth factor-administered wild-type mice
• however, hepatocyte growth factor-administered mice do not develop prostate carcinomas




Genotype
MGI:6275174
cn39
Allelic
Composition
Gt(ROSA)26Sortm1(SPOP*F133V)Mrbn/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Pten+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(SPOP*F133V)Mrbn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• 1 of 5 mice older than 12 months exhibit areas of invasive prostate carcinoma
• mice exhibit a high penetrance of focal areas of high-grade prostatic intraepithelial neoplasia by 6 months of age, characterized by nuclear atypia

neoplasm
• 1 of 5 mice older than 12 months exhibit areas of invasive prostate carcinoma
• mice exhibit a high penetrance of focal areas of high-grade prostatic intraepithelial neoplasia by 6 months of age, characterized by nuclear atypia

reproductive system
• 1 of 5 mice older than 12 months exhibit areas of invasive prostate carcinoma
• mice exhibit a high penetrance of focal areas of high-grade prostatic intraepithelial neoplasia by 6 months of age, characterized by nuclear atypia




Genotype
MGI:3603330
cn40
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Trp53tm1Thl/Trp53tm1Thl
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mutants died by 7 months of age

neoplasm
• invasive prostatic cancer is seen in all mutants by 10 weeks of age
• average tumor weight is increased 32-fold compared to mutants wild-type for Trp53 and these tumors encompass the entire genitourinary tract and pelvis
• no increase is seen in the number of senescent cells compared to wild-type prostates unlike in mutants wild-type for Trp53
• by 11 weeks of age invasive adenocarcinoma develops

renal/urinary system
• bladder obstruction

reproductive system
• invasive prostatic cancer is seen in all mutants by 10 weeks of age
• average tumor weight is increased 32-fold compared to mutants wild-type for Trp53 and these tumors encompass the entire genitourinary tract and pelvis
• no increase is seen in the number of senescent cells compared to wild-type prostates unlike in mutants wild-type for Trp53

endocrine/exocrine glands
• invasive prostatic cancer is seen in all mutants by 10 weeks of age
• average tumor weight is increased 32-fold compared to mutants wild-type for Trp53 and these tumors encompass the entire genitourinary tract and pelvis
• no increase is seen in the number of senescent cells compared to wild-type prostates unlike in mutants wild-type for Trp53




Genotype
MGI:2679901
cn41
Allelic
Composition
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• large, irregular cells, occasionally forming cryptic glandular structures
• prostate epithelial dysplasia
• focal areas of epithelial hyperplasia (J:86212)
• increased proliferation of epithelial cells (J:86212)
• mutant prostates contain a 20-fold increase in senescent epithelial cells compared to wild-type prostates (J:100683)
• massive enlargement of all prostatic lobes evident at 2 to 3 months of age, complete penetrance
• tumors were undifferentiated and often affected multiple lobes, suggesting multifocal origns (J:86212)
• complete penetrance of invasive and diffuse prostate cancer with disruption of basement membrane and signs of organ infiltration (J:86212)
• invasive prostatic cancer develops after a 4-6 month latency; however none of the mutants had died of prostatic cancer by 10 months of age (J:100683)
• tumors retain clearly defined urogenital organ boundaries (J:100683)
• high-grade prostatic intraepithelial neoplasia are seen in all 3 prostatic lobes in 9-week old mutants (J:100683)
(J:163589)
• that does not progress to grossly invasive disease (J:200002)
• mice develop diffuse, highly proliferative high-grade prostatic intraepithelial neoplasia without invasive cancer but with cystic enlargement of the anterior prostate (J:239660)

neoplasm
• tumors were undifferentiated and often affected multiple lobes, suggesting multifocal origns (J:86212)
• complete penetrance of invasive and diffuse prostate cancer with disruption of basement membrane and signs of organ infiltration (J:86212)
• invasive prostatic cancer develops after a 4-6 month latency; however none of the mutants had died of prostatic cancer by 10 months of age (J:100683)
• tumors retain clearly defined urogenital organ boundaries (J:100683)
• high-grade prostatic intraepithelial neoplasia are seen in all 3 prostatic lobes in 9-week old mutants (J:100683)
(J:163589)
• that does not progress to grossly invasive disease (J:200002)
• mice develop diffuse, highly proliferative high-grade prostatic intraepithelial neoplasia without invasive cancer but with cystic enlargement of the anterior prostate (J:239660)

endocrine/exocrine glands
• large, irregular cells, occasionally forming cryptic glandular structures
• prostate epithelial dysplasia
• focal areas of epithelial hyperplasia (J:86212)
• increased proliferation of epithelial cells (J:86212)
• mutant prostates contain a 20-fold increase in senescent epithelial cells compared to wild-type prostates (J:100683)
• massive enlargement of all prostatic lobes evident at 2 to 3 months of age, complete penetrance
• tumors were undifferentiated and often affected multiple lobes, suggesting multifocal origns (J:86212)
• complete penetrance of invasive and diffuse prostate cancer with disruption of basement membrane and signs of organ infiltration (J:86212)
• invasive prostatic cancer develops after a 4-6 month latency; however none of the mutants had died of prostatic cancer by 10 months of age (J:100683)
• tumors retain clearly defined urogenital organ boundaries (J:100683)
• high-grade prostatic intraepithelial neoplasia are seen in all 3 prostatic lobes in 9-week old mutants (J:100683)
(J:163589)
• that does not progress to grossly invasive disease (J:200002)
• mice develop diffuse, highly proliferative high-grade prostatic intraepithelial neoplasia without invasive cancer but with cystic enlargement of the anterior prostate (J:239660)




Genotype
MGI:5524280
cn42
Allelic
Composition
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key/Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(TMPRSS2/ERG)Key mutation (2 available); any Gt(ROSA)26Sor mutation (993 available)
Ptentm2.1Ppp mutation (0 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
• shortened survival compared with Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice

reproductive system
• enlarged and hardened by 6 months
• invasive with small irregular glandular structures composed of malignant cells with large, pleiomorphic nuclei and pale cytoplasm by 8 weeks
• with a proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice
• proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice

neoplasm
• invasive with small irregular glandular structures composed of malignant cells with large, pleiomorphic nuclei and pale cytoplasm by 8 weeks
• with a proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice

renal/urinary system

growth/size/body
• increased abdominal girth

endocrine/exocrine glands
• enlarged and hardened by 6 months
• invasive with small irregular glandular structures composed of malignant cells with large, pleiomorphic nuclei and pale cytoplasm by 8 weeks
• with a proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice
• proliferative index only slightly higher than in Ptentm2.1Ppp/Ptentm2.1Ppp Tg(Pbsn-cre)4Prb mice




Genotype
MGI:6275175
cn43
Allelic
Composition
Gt(ROSA)26Sortm1(SPOP*F133V)Mrbn/Gt(ROSA)26Sor+
Ptentm2.1Ppp/Ptentm2.1Ppp
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S1/Sv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(SPOP*F133V)Mrbn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Ptentm2.1Ppp mutation (0 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice exhibit severely enlarged prostates with areas of solid tumor by 12 months of age
• 80% of mice display invasive, poorly differentiated carcinomas; tumors are highly proliferative with transitional sarcomatoid differentiation and maintain expression of androgen receptor

neoplasm
• mice exhibit severely enlarged prostates with areas of solid tumor by 12 months of age
• 80% of mice display invasive, poorly differentiated carcinomas; tumors are highly proliferative with transitional sarcomatoid differentiation and maintain expression of androgen receptor

reproductive system
• mice exhibit severely enlarged prostates with areas of solid tumor by 12 months of age
• 80% of mice display invasive, poorly differentiated carcinomas; tumors are highly proliferative with transitional sarcomatoid differentiation and maintain expression of androgen receptor




Genotype
MGI:6198768
cn44
Allelic
Composition
Eif2ak3tm1.2Drc/Eif2ak3tm1.2Drc
Ptentm1Hwu/Ptentm1Hwu
Tg(CAG-MYC,-GFP*)#Rugg/0
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Eif2ak3tm1.2Drc mutation (1 available); any Eif2ak3 mutation (53 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(CAG-MYC,-GFP*)#Rugg mutation (0 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice show reduced prostate growth, with a decrease prostate cancer progression and cell proliferation compared to Ptentm1Hwu/Ptentm1Hwu Tg(Pbsn-cre)4Prb/0 Tg(CAG-MYC,-GFP)#Rugg/0 mice

neoplasm
• mice show reduced prostate growth, with a decrease prostate cancer progression and cell proliferation compared to Ptentm1Hwu/Ptentm1Hwu Tg(Pbsn-cre)4Prb/0 Tg(CAG-MYC,-GFP)#Rugg/0 mice

reproductive system
• mice show reduced prostate growth, with a decrease prostate cancer progression and cell proliferation compared to Ptentm1Hwu/Ptentm1Hwu Tg(Pbsn-cre)4Prb/0 Tg(CAG-MYC,-GFP)#Rugg/0 mice




Genotype
MGI:4420974
cn45
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
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
• 3 of 14 mice die by age 12 to 29 weeks
• however, all castrated mice survive from 7 to 10 months
• 12 month survival rate of mutants is 60% on the high-omega-3 diet, 10% on the low-omega-3 diet and 0% on the high-omega-6 diet
• mutants on a high-omega-6 diet do not survive beyond 10 months of age and die due to bladder obstruction by the prostate tumor compressing the urethra

reproductive system
• prostate lobes are enlarged and exhibit increased vascularity and cellularity
• at 4 weeks, epithelium cells in the lateral prostate are larger than in Ptentm1Hwu homozygotes
• without cellular atypia by 4 weeks of age
• mice exhibit progressive enlargement of the prostate gland compared to in Ptentm1Hwu homozygotes
• however, castration reduces prostate size
• prostate weight is higher than in controls starting at 8 weeks of age
• prostate weight gain from 5 to 24 weeks is significantly less in mice fed a high-omega-3 diet than in mice fed a high-omega-6 diet
• at 4 weeks, mice develop multifocal hyperplasia compared to in Ptentm1Hwu homozygotes
• hyperplasia is initially observed in the dorsolateral and ventral lobe with subsequent involvement of the anterior lobes
• males develop prostate cancer
• mice develop invasive adenocarcinoma by 9 weeks of age in all lobes (J:93902)
• prostate cancers are metastatic (J:93902)
• castrated mice still develop invasive adenocarcinoma (J:93902)
• 80% of mutants fed a high-omega-6 diet develop invasive carcinoma while 50% of mutants fed a high-omega-3 diet develop invasive carcinoma (J:124208)
• by 6 weeks of age, all mice develop prostate intraepithelial neoplasia (J:93902)
• latency to prostate intraepithelial neoplasia is 1.5 months (J:93902)
• males develop PIN lesions after 16 months of age (J:106650)
• prostate cancer cells exhibit increased proliferation compared to in Ptentm1Hwu homozygotes (J:93902)
• cancer cells induce a desmoplastic response (J:93902)
• castrated mice exhibit increased proliferation compared with similarly treated Ptentm1Hwu homozygotes (J:93902)
• higher numbers of apoptotic cells are seen in mutant prostates from mice on the high-omega-3 diet than on the high-omega-6 diet (J:124208)
• cancer cells induce inflammation

neoplasm
• males develop prostate cancer
• prostate cancers are metastatic (J:93902)
• castrated mice still develop invasive adenocarcinoma (J:93902)
• mice develop invasive adenocarcinoma by 9 weeks of age in all lobes (J:93902)
• 80% of mutants fed a high-omega-6 diet develop invasive carcinoma while 50% of mutants fed a high-omega-3 diet develop invasive carcinoma (J:124208)
• by 6 weeks of age, all mice develop prostate intraepithelial neoplasia (J:93902)
• latency to prostate intraepithelial neoplasia is 1.5 months (J:93902)
• males develop PIN lesions after 16 months of age (J:106650)
• omega-3 polyunsaturated fatty acids (PUFAs) slow the progression of prostate tumors in 5- to 8-week old mutants; once carcinoma develops, omega-3 PUFAs induce apoptosis and decrease the growth of the tumor

immune system
• cancer cells induce inflammation
• mutants surviving 6 months or longer exhibit pyelonephritis

endocrine/exocrine glands
• prostate lobes are enlarged and exhibit increased vascularity and cellularity
• at 4 weeks, epithelium cells in the lateral prostate are larger than in Ptentm1Hwu homozygotes
• without cellular atypia by 4 weeks of age
• mice exhibit progressive enlargement of the prostate gland compared to in Ptentm1Hwu homozygotes
• however, castration reduces prostate size
• prostate weight is higher than in controls starting at 8 weeks of age
• prostate weight gain from 5 to 24 weeks is significantly less in mice fed a high-omega-3 diet than in mice fed a high-omega-6 diet
• at 4 weeks, mice develop multifocal hyperplasia compared to in Ptentm1Hwu homozygotes
• hyperplasia is initially observed in the dorsolateral and ventral lobe with subsequent involvement of the anterior lobes
• males develop prostate cancer
• mice develop invasive adenocarcinoma by 9 weeks of age in all lobes (J:93902)
• prostate cancers are metastatic (J:93902)
• castrated mice still develop invasive adenocarcinoma (J:93902)
• 80% of mutants fed a high-omega-6 diet develop invasive carcinoma while 50% of mutants fed a high-omega-3 diet develop invasive carcinoma (J:124208)
• by 6 weeks of age, all mice develop prostate intraepithelial neoplasia (J:93902)
• latency to prostate intraepithelial neoplasia is 1.5 months (J:93902)
• males develop PIN lesions after 16 months of age (J:106650)
• prostate cancer cells exhibit increased proliferation compared to in Ptentm1Hwu homozygotes (J:93902)
• cancer cells induce a desmoplastic response (J:93902)
• castrated mice exhibit increased proliferation compared with similarly treated Ptentm1Hwu homozygotes (J:93902)
• higher numbers of apoptotic cells are seen in mutant prostates from mice on the high-omega-3 diet than on the high-omega-6 diet (J:124208)
• cancer cells induce inflammation

renal/urinary system
• mutants surviving 6 months or longer exhibit retention of urine in the anterior prostate lobes
• mutants surviving 6 months or longer exhibit pyelonephritis




Genotype
MGI:4847617
cn46
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Tg(CAG-fat-1)1Jxk/0
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(CAG-fat-1)1Jxk mutation (1 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice fed a high-omega-6 diet exhibit significantly lower prostate weights than mice without Tg(CAG-fat-1)1Jxk

homeostasis/metabolism
• mice fed a high-omega-6 diet exhibit a much lower omega-6/omega-3 ratio in the blood and prostate than mice without the Tg(CAG-fat-1)1Jxk transgene, indicating that fat-1 is able to convert most of the omega-6 polyunsaturated fatty acids to omega-3

reproductive system
• mice fed a high-omega-6 diet exhibit significantly lower prostate weights than mice without Tg(CAG-fat-1)1Jxk




Genotype
MGI:4843916
cn47
Allelic
Composition
Ptentm1Hwu/Pten+
Tg(ARR2/Pbsn-FGF8)3Prb/0
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(ARR2/Pbsn-FGF8)3Prb mutation (1 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• enlarged prostate gland due to epithelial hyperplasia
• prostatic adenocarcinomas are seen from 9 months onward
• adenocarcinomas are seen in all lobes, although more often in the dorsolateral and ventral lobes than anterior lobes
• 6 of 17 mutants at 9-16.2 months of age and 9 of 10 mutants at 18.2-19.1 months exhibit adenocarcinomas
• adenocarcinomas show loss of heterozygosity of Pten
• 2 of 31 mutants develop a rare form of mucinous adenocarcinoma
• males by 6.5 months of age exhibit hyperplasia and focal-low grade PIN lesions in the prostate
• males older than 7.5 months of age exhibit high-grade PINs

reproductive system
• enlarged prostate gland due to epithelial hyperplasia
• prostatic adenocarcinomas are seen from 9 months onward
• adenocarcinomas are seen in all lobes, although more often in the dorsolateral and ventral lobes than anterior lobes
• 6 of 17 mutants at 9-16.2 months of age and 9 of 10 mutants at 18.2-19.1 months exhibit adenocarcinomas
• adenocarcinomas show loss of heterozygosity of Pten
• 2 of 31 mutants develop a rare form of mucinous adenocarcinoma
• males by 6.5 months of age exhibit hyperplasia and focal-low grade PIN lesions in the prostate
• males older than 7.5 months of age exhibit high-grade PINs

neoplasm
• prostatic adenocarcinomas are seen from 9 months onward
• adenocarcinomas are seen in all lobes, although more often in the dorsolateral and ventral lobes than anterior lobes
• 6 of 17 mutants at 9-16.2 months of age and 9 of 10 mutants at 18.2-19.1 months exhibit adenocarcinomas
• adenocarcinomas show loss of heterozygosity of Pten
• 2 of 31 mutants develop a rare form of mucinous adenocarcinoma
• males by 6.5 months of age exhibit hyperplasia and focal-low grade PIN lesions in the prostate
• males older than 7.5 months of age exhibit high-grade PINs
• metastasis of adenocarcionma into lymph nodes is observed, with 50-60% penetrance




Genotype
MGI:4420975
cn48
Allelic
Composition
Ptentm1Hwu/Pten+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
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
• latency to prostate intraepithelial neoplasia is 8 to 10 months

endocrine/exocrine glands
• latency to prostate intraepithelial neoplasia is 8 to 10 months

reproductive system
• latency to prostate intraepithelial neoplasia is 8 to 10 months




Genotype
MGI:6198766
cn49
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Tg(CAG-MYC,-GFP*)#Rugg/0
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(CAG-MYC,-GFP*)#Rugg mutation (0 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice show decreased overall survival, with a mean life span of 75 weeks

endocrine/exocrine glands
• mice develop prostatic adenocarcinoma by 10 weeks of age
• mice with developed tumors treated with a small-molecule inhibitor of P-eIF2alpha activity, ISRIB, show tumor regression within 3 weeks of treatment, with no signs of toxicity
• mice show enlargement of prostate growth by 6 weeks of age and accelerated development of high-grade prostatic intraepithelial neoplasia compared to single conditional Ptentm1Hwu mutants

neoplasm
• mice develop prostatic adenocarcinoma by 10 weeks of age
• mice with developed tumors treated with a small-molecule inhibitor of P-eIF2alpha activity, ISRIB, show tumor regression within 3 weeks of treatment, with no signs of toxicity
• mice show enlargement of prostate growth by 6 weeks of age and accelerated development of high-grade prostatic intraepithelial neoplasia compared to single conditional Ptentm1Hwu mutants

reproductive system
• mice develop prostatic adenocarcinoma by 10 weeks of age
• mice with developed tumors treated with a small-molecule inhibitor of P-eIF2alpha activity, ISRIB, show tumor regression within 3 weeks of treatment, with no signs of toxicity
• mice show enlargement of prostate growth by 6 weeks of age and accelerated development of high-grade prostatic intraepithelial neoplasia compared to single conditional Ptentm1Hwu mutants




Genotype
MGI:5566610
cn50
Allelic
Composition
Apctm1Tno/Apctm1Tno
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Tno mutation (6 available); any Apc mutation (158 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice die by 15 months of age

neoplasm
• a few mice develop unidentified tumors in the scrotal region, not obviously associated with the testes; these tumors are cystic and epithelial in origin
• all prostate lobes exhibit neoplasia with hyperplasia, multiple foci of squamous metaplasia and keratinization, and a prominent stromal reaction, including edema, inflammatory reaction and stromal hyperplasia by 7 months of age indicating adenocarcinoma
• the anterior prostate shows the most severe phenotype, followed by the dorsal-lateral and then ventral prostate
• small foci of tumor invasion into the stroma is seen but this is not common
• mice castrated at 6 weeks show regions of hyperplasia, and squamous metaplasia at 32 weeks later, but not carcinoma, indicating inhibition of tumor formation
• mice castrated after tumors still exhibit carcinoma 2 months postcastration
• mice develop prostatic epithelial hyperplasia and prostatic intraepithelial neoplasia (PIN) as early as 4.5 to 7 weeks of age

endocrine/exocrine glands
• mice develop prostatic epithelial hyperplasia as early as 4.5 to 7 weeks of age
• all prostate lobes exhibit neoplasia with hyperplasia, multiple foci of squamous metaplasia and keratinization, and a prominent stromal reaction, including edema, inflammatory reaction and stromal hyperplasia by 7 months of age indicating adenocarcinoma
• the anterior prostate shows the most severe phenotype, followed by the dorsal-lateral and then ventral prostate
• small foci of tumor invasion into the stroma is seen but this is not common
• mice castrated at 6 weeks show regions of hyperplasia, and squamous metaplasia at 32 weeks later, but not carcinoma, indicating inhibition of tumor formation
• mice castrated after tumors still exhibit carcinoma 2 months postcastration
• mice develop prostatic epithelial hyperplasia and prostatic intraepithelial neoplasia (PIN) as early as 4.5 to 7 weeks of age

reproductive system
• mice develop prostatic epithelial hyperplasia as early as 4.5 to 7 weeks of age
• all prostate lobes exhibit neoplasia with hyperplasia, multiple foci of squamous metaplasia and keratinization, and a prominent stromal reaction, including edema, inflammatory reaction and stromal hyperplasia by 7 months of age indicating adenocarcinoma
• the anterior prostate shows the most severe phenotype, followed by the dorsal-lateral and then ventral prostate
• small foci of tumor invasion into the stroma is seen but this is not common
• mice castrated at 6 weeks show regions of hyperplasia, and squamous metaplasia at 32 weeks later, but not carcinoma, indicating inhibition of tumor formation
• mice castrated after tumors still exhibit carcinoma 2 months postcastration
• mice develop prostatic epithelial hyperplasia and prostatic intraepithelial neoplasia (PIN) as early as 4.5 to 7 weeks of age




Genotype
MGI:5578649
cn51
Allelic
Composition
Ptentm1Hwu/Pten+
Tmprss2tm2.1(ETV1)Sho/Tmprss2tm2.1(ETV1)Sho
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:
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Tmprss2tm2.1(ETV1)Sho mutation (0 available); any Tmprss2 mutation (55 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mice die before 1 year of age

reproductive system
• invasive with metastasis into the prostate stroma and urogenital area

neoplasm
• invasive with metastasis into the prostate stroma and urogenital area

endocrine/exocrine glands
• invasive with metastasis into the prostate stroma and urogenital area

growth/size/body




Genotype
MGI:5578652
cn52
Allelic
Composition
Ergtm1.1Sho/Ergtm1.1Sho
Ptentm1Hwu/Ptentm1Hwu
Tmprss2tm3Sho/Tmprss2tm3Sho
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:
Ergtm1.1Sho mutation (0 available); any Erg mutation (27 available)
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
Tmprss2tm3Sho mutation (0 available); any Tmprss2 mutation (55 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• regions of invasive prostate adenocarcinoma in mice over 1 year of age

mortality/aging
N
• mice survive at least 1 year

neoplasm
• regions of invasive prostate adenocarcinoma in mice over 1 year of age

reproductive system
• regions of invasive prostate adenocarcinoma in mice over 1 year of age




Genotype
MGI:2449982
cn53
Allelic
Composition
Rxratm1Krc/Rxra+
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:
Rxratm1Krc mutation (1 available); any Rxra mutation (30 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• branching morphogenesis of the prostate ductal system is increased 54% and 52% in the lateral prostate and anterior prostate, respectively
• prostate hyperplasia after 11 months of age
• low grade prostatic intraepithelial neoplasia after 14 months of age
• after 18 months of age, some animals progress to high grade prostatic intraepithelial neoplasia

endocrine/exocrine glands
• branching morphogenesis of the prostate ductal system is increased 54% and 52% in the lateral prostate and anterior prostate, respectively
• prostate hyperplasia after 11 months of age
• low grade prostatic intraepithelial neoplasia after 14 months of age
• after 18 months of age, some animals progress to high grade prostatic intraepithelial neoplasia

neoplasm
• low grade prostatic intraepithelial neoplasia after 14 months of age
• after 18 months of age, some animals progress to high grade prostatic intraepithelial neoplasia




Genotype
MGI:5705328
cn54
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:5705321
cn55
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:2449983
cn56
Allelic
Composition
Rxratm1Krc/Rxratm1Krc
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:
Rxratm1Krc mutation (1 available); any Rxra mutation (30 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
• branching morphogenesis of the prostate ductal system is increased 54% and 52% in the lateral prostate and anterior prostate, respectively
• 71% incidence of prostatic intraepithelial neoplasia after 4 months of age
• lesions progress to low grade prostatic intraepithelial neoplasia after 5 months of age
• after 10 months of age, some animals progress to high grade prostatic intraepithelial neoplasia
• change in protein profile of secretory proteins
• increase in prostatic cell proliferation rate

endocrine/exocrine glands
• branching morphogenesis of the prostate ductal system is increased 54% and 52% in the lateral prostate and anterior prostate, respectively
• 71% incidence of prostatic intraepithelial neoplasia after 4 months of age
• lesions progress to low grade prostatic intraepithelial neoplasia after 5 months of age
• after 10 months of age, some animals progress to high grade prostatic intraepithelial neoplasia
• change in protein profile of secretory proteins
• increase in prostatic cell proliferation rate

neoplasm
• 71% incidence of prostatic intraepithelial neoplasia after 4 months of age
• lesions progress to low grade prostatic intraepithelial neoplasia after 5 months of age
• after 10 months of age, some animals progress to high grade prostatic intraepithelial neoplasia




Genotype
MGI:5008589
cn57
Allelic
Composition
Gt(ROSA)26Sortm2(H1/tetO-RNAi:Pdpk1)Mrl/Gt(ROSA)26Sor+
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:
Gt(ROSA)26Sortm2(H1/tetO-RNAi:Pdpk1)Mrl mutation (0 available); any Gt(ROSA)26Sor mutation (993 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
reproductive system
• in doxycycline-treated mice
• in doxycycline-treated mice
• in doxycycline-treated mice
• doxycycline-treated mice exhibit microinvasive tumors in the prostate gland unlike in Pdpk1tm1Dral homozygotes

neoplasm
• doxycycline-treated mice exhibit microinvasive tumors in the prostate gland unlike in Pdpk1tm1Dral homozygotes

endocrine/exocrine glands
• in doxycycline-treated mice
• in doxycycline-treated mice
• in doxycycline-treated mice
• doxycycline-treated mice exhibit microinvasive tumors in the prostate gland unlike in Pdpk1tm1Dral homozygotes




Genotype
MGI:5008586
cn58
Allelic
Composition
Gt(ROSA)26Sortm1(H1/tetO-RNAi:Pdpk1)Mrl/Gt(ROSA)26Sor+
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:
Gt(ROSA)26Sortm1(H1/tetO-RNAi:Pdpk1)Mrl mutation (0 available); any Gt(ROSA)26Sor mutation (993 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
reproductive system
• in doxycycline-treated mice
• in doxycycline-treated mice
• in doxycycline-treated mice
• doxycycline-treated mice exhibit microinvasive tumors in the prostate gland unlike in Pdk1tm1Dral homozygotes
• doxycycline-treated mice exhibit increased proliferation in the prostate gland compared to in Pdk1tm1Dral homozygotes

neoplasm
• doxycycline-treated mice exhibit microinvasive tumors in the prostate gland unlike in Pdk1tm1Dral homozygotes

endocrine/exocrine glands
• in doxycycline-treated mice
• in doxycycline-treated mice
• in doxycycline-treated mice
• doxycycline-treated mice exhibit microinvasive tumors in the prostate gland unlike in Pdk1tm1Dral homozygotes
• doxycycline-treated mice exhibit increased proliferation in the prostate gland compared to in Pdk1tm1Dral homozygotes




Genotype
MGI:4358249
cn59
Allelic
Composition
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:
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
N
• mice survive at least 1 year

reproductive system
• mice exhibit microinvasive tumors in the prostate gland unlike in Pdpk1tm1Dral homozygotes (J:170965)
• mutants develop castrate-resistant prostate cancer (J:172730)
• mice develop intracystic prostatic carcinomas between 4 and 10 months of age (J:268934)
• mice predominately develop adenocarcinoma localized to the dorsolateral lobes of the prostate (J:184935)
• localized lesions that slowly progress to prostate adenocarcinomas (J:212219)
• 4 of 8 mice develop prostatic adenocarcinoma and 3 of 8 mice exhibit invasive carcinomas after 10 months (J:268934)
• in lesions, basal cells are not disorganized in contrast to Tg(Pbsn-ERG*)1Vv mice at 7 weeks (J:131932)
• localized lesions that slowly progress to prostate adenocarcinomas (J:212219)
• 4 of 4 mice develop low grade pancreatic intraepithelial neoplasia (PIN) and 2 of 4 mice show multifocal high grade PIN before 4 months of age (J:268934)
• 6 of 6 mice exhibit multifocal high grade PIN at 4-10 months of age (J:268934)

neoplasm
• mice exhibit microinvasive tumors in the prostate gland unlike in Pdpk1tm1Dral homozygotes (J:170965)
• mutants develop castrate-resistant prostate cancer (J:172730)
• mice develop intracystic prostatic carcinomas between 4 and 10 months of age (J:268934)
• mice predominately develop adenocarcinoma localized to the dorsolateral lobes of the prostate (J:184935)
• localized lesions that slowly progress to prostate adenocarcinomas (J:212219)
• 4 of 8 mice develop prostatic adenocarcinoma and 3 of 8 mice exhibit invasive carcinomas after 10 months (J:268934)
• in lesions, basal cells are not disorganized in contrast to Tg(Pbsn-ERG*)1Vv mice at 7 weeks (J:131932)
• localized lesions that slowly progress to prostate adenocarcinomas (J:212219)
• 4 of 4 mice develop low grade pancreatic intraepithelial neoplasia (PIN) and 2 of 4 mice show multifocal high grade PIN before 4 months of age (J:268934)
• 6 of 6 mice exhibit multifocal high grade PIN at 4-10 months of age (J:268934)
• prostate cancer metastasis after 10 months of age, with 12.5% of mice showing metastatic lesions to lungs and lymph nodes
• 2 of 6 mice develop intracystic prostatic carcinomas between 4 and 10 months of age
• 6 of 8 mice show intracystic prostatic carcinoma after 10 months of age

endocrine/exocrine glands
• mice exhibit microinvasive tumors in the prostate gland unlike in Pdpk1tm1Dral homozygotes (J:170965)
• mutants develop castrate-resistant prostate cancer (J:172730)
• mice develop intracystic prostatic carcinomas between 4 and 10 months of age (J:268934)
• mice predominately develop adenocarcinoma localized to the dorsolateral lobes of the prostate (J:184935)
• localized lesions that slowly progress to prostate adenocarcinomas (J:212219)
• 4 of 8 mice develop prostatic adenocarcinoma and 3 of 8 mice exhibit invasive carcinomas after 10 months (J:268934)
• in lesions, basal cells are not disorganized in contrast to Tg(Pbsn-ERG*)1Vv mice at 7 weeks (J:131932)
• localized lesions that slowly progress to prostate adenocarcinomas (J:212219)
• 4 of 4 mice develop low grade pancreatic intraepithelial neoplasia (PIN) and 2 of 4 mice show multifocal high grade PIN before 4 months of age (J:268934)
• 6 of 6 mice exhibit multifocal high grade PIN at 4-10 months of age (J:268934)




Genotype
MGI:6378626
cn60
Allelic
Composition
Ptentm1Hwu/Ptentm1Hwu
Ptpn1tm1Bpk/Ptpn1tm1Bpk
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:
Ptentm1Hwu mutation (16 available); any Pten mutation (88 available)
Ptpn1tm1Bpk mutation (0 available); any Ptpn1 mutation (36 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• one mouse at 6 weeks of age shows a microinvasive adenocarcinoma
• mice fed a high-fat diet upon weaning show an increase in the penetrance and number of microinvasive foci of microinvasive adenocarcinoma
• mice show a similar number of prostate ductules affected by intraepithelial neoplasia (mPIN) as single Ptentm1Hwu conditional mice

neoplasm
• one mouse at 6 weeks of age shows a microinvasive adenocarcinoma
• mice fed a high-fat diet upon weaning show an increase in the penetrance and number of microinvasive foci of microinvasive adenocarcinoma
• mice show a similar number of prostate ductules affected by intraepithelial neoplasia (mPIN) as single Ptentm1Hwu conditional mice

reproductive system
• one mouse at 6 weeks of age shows a microinvasive adenocarcinoma
• mice fed a high-fat diet upon weaning show an increase in the penetrance and number of microinvasive foci of microinvasive adenocarcinoma
• mice show a similar number of prostate ductules affected by intraepithelial neoplasia (mPIN) as single Ptentm1Hwu conditional mice




Genotype
MGI:5446522
cn61
Allelic
Composition
Zfhx3tm1.1Jtd/Zfhx3tm1.1Jtd
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Pbsn-cre)4Prb mutation (2 available)
Zfhx3tm1.1Jtd mutation (1 available); any Zfhx3 mutation (130 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• in mice with cre-expression in the prostate

neoplasm
• in mice with cre-expression in the prostate

reproductive system
• in mice with cre-expression in the prostate




Genotype
MGI:3773634
cn62
Allelic
Composition
Artm1Chc/Y
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129S/SvEv * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Artm1Chc mutation (0 available); any Ar mutation (23 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
reproductive system
N
• anogenital distances and internal urogenital organs, with exception of prostate gland, show no differences from wild-type
• no difference relative to wild-type in terms of fertility is observed
• at 9 weeks of age, some ventral prostate ducts lose glandular infoldings and have abnormal epithelial cells; enlarged ducts have many sloughed epithelial cells
• by 14 weeks, glandular infoldings have become smaller and shorter, some with constriction at their base, and layers of sloughed epithelial cells are observed in prostate lumen; by 32 weeks, mutant tissue lacks glandular infolding
• by week 24, layers of sloughed epithelium, immune cells and DNA fragments are observed in lumen of ducts in ventral prostate; many TUNEL-positive cells are detected in prostatic lumen at 24 weeks
• at 9 weeks of age, some ducts in the ventral prostate contain short or low cuboidal cells compared to taller or columnar epithelial cells in wild-type males; at 14 weeks, around 50% of ducts within the ventral prostate have altered epithelial architecture, with short poorly differentiated epithelial cells
• at 14-32 weeks, epithelial cells are shrunken
• by week 24, proliferation in the epithelium of all lobes except for anterior prostatic lobe is increased significantly compared to wild-type prostates
• epithelial cells appear to undergo anoikis and detach from the basement membrane
• at week 24, ventral prostates of mutants are substantially larger than in wild-type males
• however, dorsal-lateral prostates and anterior prostates show no changes in size

endocrine/exocrine glands
• at 9 weeks of age, some ventral prostate ducts lose glandular infoldings and have abnormal epithelial cells; enlarged ducts have many sloughed epithelial cells
• by 14 weeks, glandular infoldings have become smaller and shorter, some with constriction at their base, and layers of sloughed epithelial cells are observed in prostate lumen; by 32 weeks, mutant tissue lacks glandular infolding
• by week 24, layers of sloughed epithelium, immune cells and DNA fragments are observed in lumen of ducts in ventral prostate; many TUNEL-positive cells are detected in prostatic lumen at 24 weeks
• at 9 weeks of age, some ducts in the ventral prostate contain short or low cuboidal cells compared to taller or columnar epithelial cells in wild-type males; at 14 weeks, around 50% of ducts within the ventral prostate have altered epithelial architecture, with short poorly differentiated epithelial cells
• at 14-32 weeks, epithelial cells are shrunken
• by week 24, proliferation in the epithelium of all lobes except for anterior prostatic lobe is increased significantly compared to wild-type prostates
• epithelial cells appear to undergo anoikis and detach from the basement membrane
• at week 24, ventral prostates of mutants are substantially larger than in wild-type males
• however, dorsal-lateral prostates and anterior prostates show no changes in size

homeostasis/metabolism
N
• serum testosterone levels at 12 and 24 weeks of age are similar to those in wild-type males




Genotype
MGI:3716207
cn63
Allelic
Composition
Gt(ROSA)26Sortm1(Smo/EYFP)Amc/?
Tg(Pbsn-cre)4Prb/?
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(Smo/EYFP)Amc mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
N
• no increased hyperproliferative lesions or neoplastic transformation of the prostate are observed




Genotype
MGI:3836579
cn64
Allelic
Composition
Ctnnb1tm1Mmt/Ctnnb1+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: 129X1/SvJ * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ctnnb1tm1Mmt mutation (0 available); any Ctnnb1 mutation (49 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• at 428 days

reproductive system
• keratinized squamous metaplasia of the preputial gland develops at 100 days (67% incidence), 200 days and at end-point (100% incidence)
• mice exhibit keratinized squamous metaplasia in the bulbourethral gland with incidence of 67% at 100 days and 100% at 200 days unlike wild-type mice
• at 200 days, mice develop adenocarcinoma foci (J:143034)
• at end-point, 100% of mice develop diffuse and locally invasive adenocarcinoma unlike wild-type mice (J:143034)
• prostatic tumor tissues show changes consistent with prostatic intracystic adenocarcinomas (J:284956)
• 3 of 5 mice show intracystic adenocarcinoma at 6-9 months of age (J:284956)
• 9 of 12 mice show intracystic adenocarcinoma at 9 months or older, with 1 of 12 showing invasive adenocarcinoma (J:284956)
• at 100 days, mice exhibit diffuse prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)
• at 200 days, mice exhibit high-grade prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)
• mice develop PIN lesions starting at 4-6 weeks of age (J:284956)
• 4 of 4 mice develop low grade PIN before 6 months of age and 3 of 4 mice show high grade PIN before 6 months of age (J:284956)
• 5 of 5 mice develop high grade PIN at 6-9 months of age (J:284956)

neoplasm
• at 200 days, mice develop adenocarcinoma foci (J:143034)
• at end-point, 100% of mice develop diffuse and locally invasive adenocarcinoma unlike wild-type mice (J:143034)
• prostatic tumor tissues show changes consistent with prostatic intracystic adenocarcinomas (J:284956)
• 3 of 5 mice show intracystic adenocarcinoma at 6-9 months of age (J:284956)
• 9 of 12 mice show intracystic adenocarcinoma at 9 months or older, with 1 of 12 showing invasive adenocarcinoma (J:284956)
• at 100 days, mice exhibit diffuse prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)
• at 200 days, mice exhibit high-grade prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)
• mice develop PIN lesions starting at 4-6 weeks of age (J:284956)
• 4 of 4 mice develop low grade PIN before 6 months of age and 3 of 4 mice show high grade PIN before 6 months of age (J:284956)
• 5 of 5 mice develop high grade PIN at 6-9 months of age (J:284956)

renal/urinary system
• urethral keratinized squamous metaplasia develops in 17% at day 200 and 28% at end-points unlike in wild-type mice

endocrine/exocrine glands
• keratinized squamous metaplasia of the preputial gland develops at 100 days (67% incidence), 200 days and at end-point (100% incidence)
• mice exhibit keratinized squamous metaplasia in the bulbourethral gland with incidence of 67% at 100 days and 100% at 200 days unlike wild-type mice
• at 200 days, mice develop adenocarcinoma foci (J:143034)
• at end-point, 100% of mice develop diffuse and locally invasive adenocarcinoma unlike wild-type mice (J:143034)
• prostatic tumor tissues show changes consistent with prostatic intracystic adenocarcinomas (J:284956)
• 3 of 5 mice show intracystic adenocarcinoma at 6-9 months of age (J:284956)
• 9 of 12 mice show intracystic adenocarcinoma at 9 months or older, with 1 of 12 showing invasive adenocarcinoma (J:284956)
• at 100 days, mice exhibit diffuse prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)
• at 200 days, mice exhibit high-grade prostate intraepithelial neoplasia-like keratinized squamous metaplasia unlike in wild-type mice (J:143034)
• mice develop PIN lesions starting at 4-6 weeks of age (J:284956)
• 4 of 4 mice develop low grade PIN before 6 months of age and 3 of 4 mice show high grade PIN before 6 months of age (J:284956)
• 5 of 5 mice develop high grade PIN at 6-9 months of age (J:284956)
• urethral keratinized squamous metaplasia develops in 17% at day 200 and 28% at end-points unlike in wild-type mice

integument
• keratinized squamous metaplasia of the preputial gland develops at 100 days (67% incidence), 200 days and at end-point (100% incidence)




Genotype
MGI:6198765
cn65
Allelic
Composition
Tg(CAG-MYC,-GFP*)#Rugg/0
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: C57BL/6 * C57BL/6J * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-MYC,-GFP*)#Rugg mutation (0 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• mice exhibit increased proliferation in the prostate epithelium but do not develop adenocarcinoma by 1 year of age

neoplasm
N
• mice do not develop prostate gland adenocarcinoma by 1 year of age

reproductive system
• mice exhibit increased proliferation in the prostate epithelium but do not develop adenocarcinoma by 1 year of age




Genotype
MGI:5551716
cn66
Allelic
Composition
Klf5tm1.1Jtd/Klf5+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Klf5tm1.1Jtd mutation (0 available); any Klf5 mutation (37 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Abnormal prostate morphology in Klf5tm1.1Jtd/Klf5+ Tg(Pbsn-cre)4Prb/0 and Klf5tm1.1Jtd/Klf5tm1.1Jtd Tg(Pbsn-cre)4Prb/0 males

reproductive system
• increased castration-induced shrinkage of the prostate
• however, administration of androgen restores weight
• more severe than in Klf5tm1.1Jtd/Klf5tm1.1Jtd Tg(Pbsn-cre)4Prb mice
• increased cell proliferation compared to in Klf5tm1.1Jtd/Klf5tm1.1Jtd Tg(Pbsn-cre)4Prb mice and mice with wild-type alleles

neoplasm
N
• at 1 and 2 years, mice do not develop increased incidence of prostatic intraepithelial neoplasia

endocrine/exocrine glands
• increased castration-induced shrinkage of the prostate
• however, administration of androgen restores weight
• more severe than in Klf5tm1.1Jtd/Klf5tm1.1Jtd Tg(Pbsn-cre)4Prb mice
• increased cell proliferation compared to in Klf5tm1.1Jtd/Klf5tm1.1Jtd Tg(Pbsn-cre)4Prb mice and mice with wild-type alleles




Genotype
MGI:5551715
cn67
Allelic
Composition
Klf5tm1.1Jtd/Klf5tm1.1Jtd
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Klf5tm1.1Jtd mutation (0 available); any Klf5 mutation (37 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Abnormal prostate morphology in Klf5tm1.1Jtd/Klf5+ Tg(Pbsn-cre)4Prb/0 and Klf5tm1.1Jtd/Klf5tm1.1Jtd Tg(Pbsn-cre)4Prb/0 males

reproductive system
• increased castration-induced shrinkage of the prostate
• however, administration of androgen restores weight
• increased cell apoptosis compared to in Klf5tm1.1Jtd/Klf5+ Tg(Pbsn-cre)4Prb mice and mice with wild-type alleles

neoplasm
N
• at 1 and 2 years, mice do not develop increased incidence of prostatic intraepithelial neoplasia

endocrine/exocrine glands
• increased castration-induced shrinkage of the prostate
• however, administration of androgen restores weight
• increased cell apoptosis compared to in Klf5tm1.1Jtd/Klf5+ Tg(Pbsn-cre)4Prb mice and mice with wild-type alleles




Genotype
MGI:6114993
cn68
Allelic
Composition
Tg(CAG-cat,-ALOX15)1868Klv/0
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-cat,-ALOX15)1868Klv mutation (0 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• dorsolateral and ventral prostates show age-dependent focal and progressive epithelial hyperplasia with atypia which shows increased proliferation indicating high grade prostatic intraepithelial neoplasia after 5 months of age
• micropapillary projections of mildly atypical epithelium are seen in distal dorsal prostate lumens and nuclei show mild enlargement, including elongation and hyperchromasia
• lateral prostate shows progressively severe nuclear stratification, with nuclear atypia with some enlargement and hyperchromasia with chromatin clumping
• however, no progression to invasive prostate cancer was seen up to 35 weeks

neoplasm
• dorsolateral and ventral prostates show age-dependent focal and progressive epithelial hyperplasia with atypia which shows increased proliferation indicating high grade prostatic intraepithelial neoplasia after 5 months of age
• micropapillary projections of mildly atypical epithelium are seen in distal dorsal prostate lumens and nuclei show mild enlargement, including elongation and hyperchromasia
• lateral prostate shows progressively severe nuclear stratification, with nuclear atypia with some enlargement and hyperchromasia with chromatin clumping
• however, no progression to invasive prostate cancer was seen up to 35 weeks

reproductive system
• dorsolateral and ventral prostates show age-dependent focal and progressive epithelial hyperplasia with atypia which shows increased proliferation indicating high grade prostatic intraepithelial neoplasia after 5 months of age
• micropapillary projections of mildly atypical epithelium are seen in distal dorsal prostate lumens and nuclei show mild enlargement, including elongation and hyperchromasia
• lateral prostate shows progressively severe nuclear stratification, with nuclear atypia with some enlargement and hyperchromasia with chromatin clumping
• however, no progression to invasive prostate cancer was seen up to 35 weeks




Genotype
MGI:6114995
cn69
Allelic
Composition
Tg(CAG-cat,-ALOX15)1868Klv/Tg(CAG-cat,-ALOX15)1868Klv
Tg(Pbsn-cre)4Prb/?
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(CAG-cat,-ALOX15)1868Klv mutation (0 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• dorsolateral and ventral prostates show age-dependent focal and progressive epithelial hyperplasia with atypia which shows increased proliferation indicating high grade prostatic intraepithelial neoplasia after 5 months of age
• micropapillary projections of mildly atypical epithelium are seen in distal dorsal prostate lumens and nuclei show mild enlargement, including elongation and hyperchromasia
• lateral prostate shows progressively severe nuclear stratification, with nuclear atypia with some enlargement and hyperchromasia with chromatin clumping
• however, no progression to invasive prostate cancer was seen up to 35 weeks

neoplasm
• dorsolateral and ventral prostates show age-dependent focal and progressive epithelial hyperplasia with atypia which shows increased proliferation indicating high grade prostatic intraepithelial neoplasia after 5 months of age
• micropapillary projections of mildly atypical epithelium are seen in distal dorsal prostate lumens and nuclei show mild enlargement, including elongation and hyperchromasia
• lateral prostate shows progressively severe nuclear stratification, with nuclear atypia with some enlargement and hyperchromasia with chromatin clumping
• however, no progression to invasive prostate cancer was seen up to 35 weeks

reproductive system
• dorsolateral and ventral prostates show age-dependent focal and progressive epithelial hyperplasia with atypia which shows increased proliferation indicating high grade prostatic intraepithelial neoplasia after 5 months of age
• micropapillary projections of mildly atypical epithelium are seen in distal dorsal prostate lumens and nuclei show mild enlargement, including elongation and hyperchromasia
• lateral prostate shows progressively severe nuclear stratification, with nuclear atypia with some enlargement and hyperchromasia with chromatin clumping
• however, no progression to invasive prostate cancer was seen up to 35 weeks




Genotype
MGI:5427499
cn70
Allelic
Composition
Ptentm1Mro/Pten+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ptentm1Mro mutation (1 available); any Pten mutation (88 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Prostate cancer progression in Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+, Tg(Pbsn-cre)4Prb/0 Ptentm1Mro/Pten+, and Tg(Pbsn-cre)4Prb/0 Gt(ROSA)26Sortm1(CAG-Bmi1,-EGFP)Nki/Gt(ROSA)26Sor+ Ptentm1Mro/Pten+ mice

neoplasm

reproductive system

endocrine/exocrine glands




Genotype
MGI:6275172
cn71
Allelic
Composition
Gt(ROSA)26Sortm1(SPOP*F133V)Mrbn/Gt(ROSA)26Sor+
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Gt(ROSA)26Sortm1(SPOP*F133V)Mrbn mutation (1 available); any Gt(ROSA)26Sor mutation (993 available)
Tg(Pbsn-cre)4Prb mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• rare areas in prostate show outlier levels of androgen receptor expression and rare cells show cytologic atypia with enlarged nuclei in mice older than 12 months
• however, mice show minimal alterations in prostate grandular architecture and histology, no differences in proliferation or androgen receptor expression

reproductive system
• rare areas in prostate show outlier levels of androgen receptor expression and rare cells show cytologic atypia with enlarged nuclei in mice older than 12 months
• however, mice show minimal alterations in prostate grandular architecture and histology, no differences in proliferation or androgen receptor expression




Genotype
MGI:3603329
cn72
Allelic
Composition
Trp53tm1Thl/Trp53tm1Thl
Tg(Pbsn-cre)4Prb/0
Genetic
Background
involves: C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Tg(Pbsn-cre)4Prb mutation (2 available)
Trp53tm1Thl mutation (0 available); any Trp53 mutation (240 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
N
• no prostatic tumors are detected in 9-week old mutants





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last database update
11/12/2024
MGI 6.24
The Jackson Laboratory