Phenotypes associated with this allele

• Allele Symbol: Apc^Min
• Allele Name: multiple intestinal neoplasia
• Allele ID: MGI:1856318
• Summary: 156 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Apc^Min/Apc^Min	involves: AKR/J * C57BL/6J	MGI:5448316
hm2	Apc^Min/Apc^Min	involves: C57BL/6J	MGI:5438590
hm3	Apc^Min/Apc^Min	involves: C57BL/6J * CAST/EiJ	MGI:5447942
hm4	Apc^Min/Apc^Min	involves: C57BL/6 * POMOD	MGI:5448414
ht5	Apc^Min/Apc^+	(AKR/J x C57BL/6J-Apc^Min)F1	MGI:5449072
ht6	Apc^Min/Apc^+	B6(AKR)-Apc^Min	MGI:5446893
ht7	Apc^Min/Apc^+	B6.Cg-Brca2^tm1Mbn Apc^Min	MGI:3814370
ht8	Apc^Min/Apc^+	C57BL/6J-Apc^Min	MGI:2665504
ht9	Apc^Min/Apc^+	C57BL/6J-Apc^Min/J	MGI:6712682
ht10	Apc^Min/Apc^+	involves: 129 * C57BL/6	MGI:4429570
ht11	Apc^Min/Apc^+	involves: 129P2/OlaHsd * C57BL/6	MGI:3834882
ht12	Apc^Min/Apc^+	involves: AKR/J * C57BL/6J	MGI:2175903
ht13	Apc^Min/Apc^+	involves: C57BL/6 * C57BL/6J	MGI:3812012
ht14	Apc^Min/Apc^+	involves: C57BL/6J	MGI:3513858
ht15	Apc^Min/Apc^+	(MA/MyJ x C57BL/6J-Apc^Min)F1	MGI:5763440
ht16	Apc^Min/Apc^tm1.1Klne	B6.Cg-Apc^Min/Apc^tm1.1Klne	MGI:5431900
ht17	Apc^Min/Apc^tm1Tno	involves: 129 * 129S4/SvJae * C57BL/6	MGI:4429565
cn18	Apc^Min/Apc^+ Hsd11b2^tm1.1Mzz/Hsd11b2^tm1.1Mzz Tg(Vil1-cre)997Gum/0	involves: 129 * C57BL/6 * C57BL/6J	MGI:5547498
cn19	Apc^Min/Apc^+ Dnmt3b^tm1Jae/Dnmt3b^tm1Jae Tg(Fabp1-cre)1Jig/0	involves: 129 * C57BL/6 * C57BL/6J * FVB/N	MGI:3625330
cn20	Apc^Min/Apc^+ Tcf7l2^tm1(EGFP/cre)Mrc/Tcf7l2^tm2.1Mrc	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J * C57BL/6NCrl	MGI:4946926
cn21	Apc^Min/Apc^+ Mapkapk2^tm1.1Gkl/Mapkapk2^tm1.1Gkl Tg(Tie1-cre)9Ref/0	involves: 129S1/Sv * 129X1/SvJ * BALB/cJ * C57BL/6J	MGI:6357721
cn22	Apc^Min/Apc^+ Trp53^tm2.1Tyj/Trp53^tm2.1Tyj Tg(Vil1-cre/ERT2)23Syr/0	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * DBA/2	MGI:6448989
cn23	Apc^Min/Apc^+ Pten^tm1Hwu/Pten^tm1Hwu Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL	MGI:4941759
cn24	Apc^Min/Apc^+ Col1a1^tm1(CAG-Sirt1)Dsin/Col1a1^+ Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL	MGI:4430578
cn25	Apc^Min/Apc^+ Rab11a^tm1.1Ngao/Rab11a^tm1.1Ngao Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6J * SJL/J	MGI:7642164
cn26	Apc^Min/Apc^+ Dclk1^tm1.1(cre/ERT2)Seno/Dclk1^+ Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor^tm1(HBEGF)Awai	involves: 129S4/SvJaeSor * C57BL/6	MGI:5475206
cn27	Apc^Min/Apc^+ Erbb3^tm1.1Dwt/Erbb3^tm2.1Dwt Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL	MGI:4360363
cn28	Apc^Min/Apc^+ Gt(ROSA)26Sor^tm2(Rnf187)Jhai/Gt(ROSA)26Sor^+ Tg(Vil1-cre)20Syr/0	involves: 129S6/SvEvTac * C57BL/6 * DBA/2	MGI:5013408
cn29	Apc^Min/Apc^+ Gpa33^tm1(GNAS)Wtsi/Gpa33^+ Hprt1^tm1(CMV-cre)Brd/?	involves: 129S7/SvEvBrd * C57BL/6J	MGI:4889209
cn30	Apc^Min/Apc^+ Mapkapk2^tm1.1Gkl/Mapkapk2^tm1.1Gkl Twist2^tm1.1(cre)Dor/Twist2^+	involves: 129X1/SvJ * BALB/cJ * C57BL/6J	MGI:6357723
cn31	Apc^Min/Apc^+ Lmna^tm4Stw/Lmna^tm4Stw Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J	MGI:5774439
cn32	Apc^Min/Apc^+ Elp3^tm1.1Tac/Elp3^tm1.1Tac Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * C57BL/6NTac * SJL	MGI:5898003
cn33	Apc^Min/Apc^+ Igf2bp1^tm1Vssp/Igf2bp1^tm1Vssp Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:5523866
cx34	Apc^Min/Apc^+ Brca2^tm1Mbn/Brca2^+	B6.Cg-Brca2^tm1Mbn Apc^Min	MGI:3814367
cx35	Apc^Min/Apc^+ Gt(ROSA)26Sor/Gt(ROSA)26Sor^+	B6.Cg-Gt(ROSA)26Sor Apc^Min	MGI:5014351
cx36	Apc^Min/Apc^+ Mir10a^tm1.1Ahl/Mir10a^tm1.1Ahl	B6.Cg-Mir10a^tm1.1Ahl Apc^min	MGI:5567980
cx37	Apc^Min/Apc^+ Mthfs^Gt(RRK291)Byg/Mthfs^+	B6.Cg-Mthfs^Gt(RRK291)Byg Apc^Min	MGI:5430745
cx38	Apc^Min/Apc^+ Nos2^tm1Lau/Nos2^+	B6.Cg-Nos2^tm1Lau Apc^Min	MGI:3767792
cx39	Apc^Min/Apc^+ Nos2^tm1Lau/Nos2^tm1Lau	B6.Cg-Nos2^tm1Lau Apc^Min	MGI:3767791
cx40	Apc^Min/Apc^+ Pla2g4a^tm1Jvb/Pla2g4a^tm1Jvb	B6.Cg-Pla2g4a^tm1Jvb Apc^Min	MGI:4358774
cx41	Apc^Min/Apc^+ Rab25^tm1Jrgo/Rab25^+	B6.Cg-Rab25^tm1Jrgo Apc^Min	MGI:4440864
cx42	Apc^Min/Apc^+ Rab25^tm1Jrgo/Rab25^tm1Jrgo	B6.Cg-Rab25^tm1Jrgo Apc^Min	MGI:4440863
cx43	Apc^Min/Apc^+ Shmt1^Gt(AD0236)Wtsi/Shmt1^Gt(AD0236)Wtsi	B6.Cg-Shmt1^Gt(AD0236)Wtsi Apc^Min	MGI:5426849
cx44	Apc^Min/Apc^+ Tgfbr1^tm1Bopa/Tgfbr1^+	B6.Cg-Tgfbr1^tm1Bopa Apc^Min	MGI:3831112
cx45	Apc^Min/Apc^+ Arhgef4^tm1Taki/Arhgef4^+	B6J.Cg-Arhgef4^tm1Taki Apc^Min	MGI:5881920
cx46	Apc^Min/Apc^+ Arhgef4^tm1Taki/Arhgef4^tm1Taki	B6J.Cg-Arhgef4^tm1Taki Apc^Min	MGI:5881919
cx47	Apc^Min/Apc^+ Arhgef4^tm1Taki/Arhgef4^tm1Taki Spata13^tm1Taki/Spata13^tm1Taki	B6J.Cg-Arhgef4^tm1Taki Spata13^tm1Taki Apc^Min	MGI:5881925
cx48	Apc^Min/Apc^+ Spata13^tm1Taki/Spata13^+	B6J.Cg-Spata13^tm1Taki Apc^Min	MGI:5881917
cx49	Apc^Min/Apc^+ Spata13^tm1Taki/Spata13^tm1Taki	B6J.Cg-Spata13^tm1Taki Apc^Min	MGI:5881916
cx50	Apc^Min/Apc^+ Zfp280c^em1Xss/Zfp280c^+	C57BL/6J-Apc^Min Zfp280c^em1Xss	MGI:7662833
cx51	Apc^Min/Apc^+ Zfp280c^em1Xss/Zfp280c^em1Xss	C57BL/6J-Apc^Min Zfp280c^em1Xss	MGI:7662831
cx52	Apc^Min/Apc^+ Zfp280c^em1Xss/Y	C57BL/6J-Apc^Min Zfp280c^em1Xss	MGI:7662832
cx53	Apc^Min/Apc^+ Fxyd5^em1Namje/Fxyd5^em1Namje	C57BL/6J-Fxyd5^em1Namje Apc^min	MGI:7310033
cx54	Apc^Min/Apc^+ Pla2g2a^Mom1-r/Pla2g2a^+	either: (AKR/J x C57BL/6J-Apc^Min)F1 or (MA/MyJ x C57BL/6J-Apc^Min)F1 or (CAST/EiJ x C57BL/6J-Apc^Min)F1	MGI:5529263
cx55	Apc^Min/Apc^tm1Tno Ctnnb1^tm4.1Wbm/Ctnnb1^+	involves: 129 * 129P2/OlaHsd * 129S4/SvJae * C57BL/6	MGI:4429574
cx56	Apc^Min/Apc^Min Ctnnb1^tm4.1Wbm/Ctnnb1^+	involves: 129 * 129P2/OlaHsd * C57BL/6	MGI:4429575
cx57	Apc^Min/Apc^+ Hltf^tm1.1Hdin/Hltf^tm1.1Hdin	involves: 129 * C57BL/6 * FVB/N	MGI:6108175
cx58	Apc^Min/Apc^+ Hpgds^tm1Urad/Hpgds^+	involves: 129 * C57BL/6J	MGI:3700063
cx59	Apc^Min/Apc^+ Hpgds^tm1Urad/Hpgds^tm1Urad	involves: 129 * C57BL/6J	MGI:3700064
cx60	Apc^Min/Apc^+ Msh2^tm1Mak/Msh2^tm1Mak Nos2^tm1Mrl/Nos2^tm1Mrl	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J	MGI:5636670
cx61	Apc^Min/Apc^+ Msh2^tm1Mak/Msh2^+ Nos2^tm1Mrl/Nos2^tm1Mrl	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J	MGI:5636667
cx62	Apc^Min/Apc^+ Blm^tm1Grdn/Blm^+	involves: 129P2/OlaHsd * 129S/SvEv * Black Swiss * C57BL/6J	MGI:3582674
cx63	Apc^Min/Apc^+ Msh2^tm1Htr/Msh2^tm1Htr	involves: 129P2/OlaHsd * BALB/c * C57BL/6J	MGI:4429611
cx64	Apc^Min/Apc^+ Ccdc80^tm1.1Ftk/Ccdc80^tm1.1Ftk	involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 * C57BL/6J * C57BL/6N	MGI:5693797
cx65	Apc^Min/Apc^+ Foxl1^tm1Khk/Foxl1^tm1Khk	involves: 129P2/OlaHsd * C57BL/6	MGI:3834880
cx66	Apc^Min/Apc^+ Zbtb33^tm1.1Bird/Y	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:3613447
cx67	Apc^Min/Apc^+ Mbd2^tm1Bh/Mbd2^+	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:3579839
cx68	Apc^Min/Apc^+ Mbd2^tm1Bh/Mbd2^tm1Bh	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:3579838
cx69	Apc^Min/Apc^+ Phgdh^tm1.1Shfu/Phgdh^+	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:5426846
cx70	Apc^Min/Apc^+ Cd44^tm1Mak/Cd44^tm1Mak	involves: 129P2/OlaHsd * C57BL/6J	MGI:4946621
cx71	Apc^Min/Apc^+ Mom5^129P2/OlaHsd/?	involves: 129P2/OlaHsd * C57BL/6J	MGI:4359622
cx72	Apc^Min/Apc^+ Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366246
cx73	Apc^Min/Apc^+ Ptgs1^tm1Unc/Ptgs1^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366247
cx74	Apc^Min/Apc^+ Ptgs1^tm1Unc/Ptgs1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366248
cx75	Apc^Min/Apc^+ Mbd4^tm1Bird/Mbd4^tm1Bird	involves: 129P2/OlaHsd * C57BL/6J	MGI:3719427
cx76	Apc^Min/Apc^+ Tcf7^tm1Cle/Tcf7^tm1Cle	involves: 129P2/OlaHsd * C57BL/6J	MGI:5319648
cx77	Apc^Min/Apc^+ Ptgds^tm1Ohy/Ptgds^tm1Ohy	involves: 129P2/OlaHsd * C57BL/6J	MGI:3700062
cx78	Apc^Min/Apc^+ Hp^tm1Skl/Hp^tm1Skl	involves: 129P2/OlaHsd * C57BL/6J	MGI:3610196
cx79	Apc^Min/Apc^+ Msh2^tm1Mak/Msh2^tm1Mak	involves: 129P2/OlaHsd * C57BL/6J	MGI:5636659
cx80	Apc^Min/Apc^+ Trp53^tm1Mlh/Trp53^tm1Mlh	involves: 129P2/OlaHsd * C57BL/6 * SWR	MGI:5448541
cx81	Apc^Min/Apc^+ Dnd1^Ter/Dnd1^+	involves: 129P3/J * C57BL/6J	MGI:5696099
cx82	Apc^Min/Apc^Min Rr27^tm1Rohl/Rr27^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:3722288
cx83	Apc^Min/Apc^+ Tcf7l2^tm1.1(EGFP/cre)Mrc/Tcf7l2^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:4946925
cx84	Apc^Min/Apc^+ Tgfbr1^tm1Bopa/Tgfbr1^+	involves: 129S1/SvImJ * C57BL/6J	MGI:3831111
cx85	Apc^Min/Apc^+ Il6^tm1Kopf/Il6^tm1Kopf	involves: 129S2/SvPas * C57BL/6	MGI:4365606
cx86	Apc^Min/Apc^+ Esr1^tm1.1Mma/Esr1^tm1.1Mma	involves: 129S2/SvPas * C57BL/6J	MGI:5298870
cx87	Apc^Min/Apc^+ Pms2^tm1Lisk/Pms2^tm1Lisk	involves: 129S2/SvPas * C57BL/6J	MGI:4820588
cx88	Apc^Min/Apc^+ Hdac2^Gt(W035F03)Joe/Hdac2^Gt(W035F03)Joe	involves: 129S2/SvPas * C57BL/6J	MGI:4357790
cx89	Apc^Min/Apc^+ Esr1^tm1.1Mma/Esr1^+	involves: 129S2/SvPas * C57BL/6J	MGI:5298871
cx90	Apc^Min/Apc^+ Esr2^tm1Mma/Esr2^+	involves: 129S2/SvPas * C57BL/6J	MGI:5298868
cx91	Apc^Min/Apc^+ Esr2^tm1Mma/Esr2^tm1Mma	involves: 129S2/SvPas * C57BL/6J	MGI:5298869
cx92	Apc^Min/Apc^+ Col1a1^tm11(tetO-Nup88)Jvd/Col1a1^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:6377634
cx93	Apc^Min/Apc^+ Col1a1^tm1(CAG-Sirt1)Dsin/Col1a1^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:4430577
cx94	Apc^Min/Apc^+ Ptprh^tm1.1Mato/Ptprh^tm1.1Mato	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:3839104
cx95	Apc^Min/Apc^+ Col1a1^tm9(tetO-Dnmt3b_i1)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5313419
cx96	Apc^Min/Apc^+ Col1a1^tm10(tetO-Dnmt3b_i3)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5313420
cx97	Apc^Min/Apc^+ Col1a1^tm11(tetO-Dnmt3b_i6)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5313421
cx98	Apc^Min/Apc^+ Col1a1^tm12(tetO-Dnmt3a_i1)Jae/Col1a1^+ Gt(ROSA)26Sor^tm1(rtTA*M2)Jae/Gt(ROSA)26Sor^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:5313423
cx99	Apc^Min/Apc^+ Dnmt1^tm1Jae/Dnmt1^+	involves: 129S4/SvJae * C57BL/6J	MGI:3848451
cx100	Apc^Min/Apc^+ Dnmt1^tm1Pwl/Dnmt1^+	involves: 129S4/SvJae * C57BL/6J	MGI:3848450
cx101	Apc^Min/Apc^+ Dnmt1^tm1Jae/Dnmt1^tm1Pwl	involves: 129S4/SvJae * C57BL/6J	MGI:3848453
cx102	Apc^Min/Apc^+ Map9^tm1.2Bcgen/Map9^+	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6 * C57BL/6J	MGI:6502661
cx103	Apc^Min/Apc^+ Map9^tm1.2Bcgen/Map9^tm1.2Bcgen	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6 * C57BL/6J	MGI:6502660
cx104	Apc^Min/Apc^+ Zfp82^tm1.2Cya/Zfp82^tm1.2Cya	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6NTac	MGI:6849775
cx105	Apc^Min/Apc^+ Zfp82^tm1.2Cya/Zfp82^+	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6NTac	MGI:6849776
cx106	Apc^Min/Apc^Min Asph^tm1Jed/Asph^tm1Jed	involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6J * C57BL/6NTac	MGI:2653701
cx107	Apc^Min/Apc^+ Dp(17Nfkbil1-Or2h1)1Cogr/0	involves: 129S6/SvEvTac * C57BL/6J	MGI:5451046
cx108	Apc^Min/Apc^+ Ereg^tm1Dwt/Ereg^tm1Dwt	involves: 129S6/SvEvTac * C57BL/6J	MGI:3512138
cx109	Apc^Min/Apc^+ Il22ra2^tm2Vlcg/Il22ra2^tm2Vlcg	involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac	MGI:5446699
cx110	Apc^Min/Apc^+ Myc^tm1Jlc/Myc^+	involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J	MGI:3812011
cx111	Apc^Min/Apc^+ Recql4^tm1Glu/Recql4^tm1Glu	involves: 129S7/SvEvBrd * C57BL/6J	MGI:3575580
cx112	Apc^Min/Apc^+ Ppard^tm1Jps/Ppard^tm1Jps	involves: 129/Sv * AKR/J * C57BL/6 * C57BL/6J	MGI:3510235
cx113	Apc^Min/Apc^+ Il22^tm1Flv/Il22^tm1Flv	involves: 129/Sv * C57BL/6 * C57BL/6J	MGI:5446700
cx114	Apc^Min/Apc^+ Mmom2^129X1/SvJ/Mmom2^C57BL/6J	involves: 129X1/SvJ * C57BL/6J	MGI:3803126
cx115	Apc^Min/Apc^Min Sat1^tm1Alh/Y	involves: 129X1/SvJ * C57BL/6J	MGI:3709984
cx116	Apc^Min/Apc^+ Egfr^Wa5/Egfr^+	involves: BALB/cAnN * C3H/HeN * C57BL/6J	MGI:3623317
cx117	Apc^Min/Apc^+ Pla2g2a^Mom1-r/? Prkdc^dxnph/Prkdc^dxnph	involves: BALB/cByJ * C57BL/6	MGI:4461429
cx118	Apc^Min/Apc^+ Mapkapk2^tm1.2Gkl/Mapkapk2^tm1.2Gkl	involves: BALB/cJ * C57BL/6J	MGI:6357720
cx119	Apc^Min/Apc^+ Del(15Rr357-Rr303293)2Jta/Del(15Rr357-Rr303293)2Jta	involves: C57BL/6	MGI:7434699
cx120	Apc^Min/Apc^+ Dclk1^tm1.1(cre/ERT2)Seno/Dclk1^tm1.1(cre/ERT2)Seno	involves: C57BL/6	MGI:5475210
cx121	Apc^Min/Apc^+ Tg(Rorc-EGFP)1Ebe/?	involves: C57BL/6	MGI:3829423
cx122	Apc^Min/Apc^+ Rr21^tm1Jta/Rr21^+	involves: C57BL/6	MGI:5463417
cx123	Apc^Min/Apc^+ Bcl2l14^tm1.1Boui/Bcl2l14^tm1.1Boui	involves: C57BL/6 * C57BL/6J	MGI:6470552
cx124	Apc^Min/Apc^+ Slc5a8^tm1.1Boet/Slc5a8^tm1.1Boet	involves: C57BL/6 * C57BL/6J	MGI:3811523
cx125	Apc^Min/Apc^+ Mmp7^tm1Lmm/Mmp7^tm1Lmm	involves: C57BL/6 * C57BL/6J	MGI:2183289
cx126	Apc^Min/Apc^+ Tnfaip8l1^em1Huwa/Tnfaip8l1^em1Huwa	involves: C57BL/6 * C57BL/6J	MGI:7568795
cx127	Apc^Min/Apc^+ Rr21^tm1.1Jta/Rr21^tm1.1Jta	involves: C57BL/6 * FVB/N	MGI:5463415
cx128	Apc^Min/Apc^+ Dcc^tm1Wbg/Dcc^+	involves: C57BL/6J	MGI:2446655
cx129	Apc^Min/Apc^+ Glp2r^tm1Ddr/Glp2r^+	involves: C57BL/6J	MGI:3827117
cx130	Apc^Min/Apc^+ Glp2r^tm1Ddr/Glp2r^tm1Ddr	involves: C57BL/6J	MGI:3827123
cx131	Apc^Min/Apc^+ Mom5^C57BL/6J/Mom5^C57BL/6J	involves: C57BL/6J	MGI:4359621
cx132	Apc^Min/Apc^Min Ppard^tm1.1Rev/Ppard^tm1.1Rev	involves: C57BL/6J	MGI:3715726
cx133	Apc^Min/Apc^+ Tcf7l2^tm2.2Mrc/Tcf7l2^+	involves: C57BL/6J	MGI:4946927
cx134	Apc^Min/Apc^+ Cd44^tm2Stpa/Cd44^tm2Stpa	involves: C57BL/6J	MGI:5544112
cx135	Apc^Min/Apc^+ Cd44^tm1Stpa/Cd44^tm2Stpa	involves: C57BL/6J	MGI:5544114
cx136	Apc^Min/Apc^+ Cd44^tm1Mak/Cd44^tm1Mak	involves: C57BL/6J	MGI:5544115
cx137	Apc^Min/Apc^+ Tnik^tm1Teya/Tnik^tm1Teya	involves: C57BL/6J	MGI:6113599
cx138	Apc^Min/Apc^+ Spata18^tm1.2Hifa/Spata18^tm1.2Hifa	involves: C57BL/6J	MGI:6121392
cx139	Apc^Min/Apc^+ Spata18^tm1.2Hifa/Spata18^+	involves: C57BL/6J	MGI:6121393
cx140	Apc^Min/Apc^+ Ccnd1^tm1Dsn/Ccnd1^tm1Dsn	involves: C57BL/6J	MGI:3045027
cx141	Apc^Min/Apc^+ Thbs1^tm1Hyn/Thbs1^tm1Hyn	involves: C57BL/6J	MGI:3032868
cx142	Gata6os^em1Zfa/Gata6os^em1Zfa Apc^Min/Apc^+	involves: C57BL/6J	MGI:6367566
cx143	Apc^Min/Apc^+ Cd44^tm1Stpa/Cd44^tm1Stpa	involves: C57BL/6J * C57BL/6JIco	MGI:5544111
cx144	Apc^Min/Apc^+ Mir708^tm1Wtsi/Mir708^tm1Wtsi	involves: C57BL/6J * C57BL/6N	MGI:6864129
cx145	Apc^Min/Apc^+ Tmem9^tm1d(EUCOMM)Wtsi/Tmem9^+	involves: C57BL/6J * C57BL/6N	MGI:6806148
cx146	Apc^Min/Apc^+ Tmem9^tm1d(EUCOMM)Wtsi/Tmem9^tm1d(EUCOMM)Wtsi	involves: C57BL/6J * C57BL/6N	MGI:6806147
cx147	Apc^Min/Apc^+ Atp5f1a^Mom2/Atp5f1a^+	involves: C57BL/6J * DBA/2J	MGI:3653360
cx148	Apc^Min/Apc^+ Atp5f1a^Mom2/Atp5f1a^Mom2	involves: C57BL/6J * DBA/2J	MGI:3653359
cx149	Apc^Min/Apc^+ Tg(CAG-PGDS)S-55Hjl/0	involves: C57BL/6J * FVB/N	MGI:3700065
cx150	Apc^Min/Apc^+ Tg(Vil1-PPARGC1A)#Amos/0	involves: C57BL/6J * FVB/N	MGI:4950747
cx151	Apc^Min/Apc^+ Mmom1^C57BL/6J/Mmom1^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803123
cx152	Apc^Min/Apc^+ Mmom1^C57BL/6J/Mmom1^FVB/NTac Mmom3^C57BL/6J/Mmom3^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803124
cx153	Apc^Min/Apc^+ Mmom2^C57BL/6J/Mmom2^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803125
cx154	Apc^Min/Apc^+ Mmom2^C57BL/6J/Mmom2^FVB/NTac Mmom3^C57BL/6J/Mmom3^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803127
cx155	Apc^Min/Apc^+ Mmom2^C57BL/6J/Mmom2^FVB/NTac Mmom4^C57BL/6J/Mmom4^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803128
cx156	Apc^Min/Apc^+ Mmom4^C57BL/6J/Mmom4^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803129

Genotype
MGI:5448316

hm1

• Allelic Composition: Apc^Min/Apc^Min
• Genetic Background: involves: AKR/J * C57BL/6J

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

embryo

abnormal embryo development ( J:27993 )

abnormal embryo size ( J:27993 )

• at E6.5 there is a range of abnormal development, underdeveloped embryonic tissue and associated maternal cells, with no obvious primitive ectoderm or proamniotic cavity to disorganized embryonic and extraembryonic tissue

abnormal egg cylinder morphology ( J:27993 )

• empty space is seen in the distal region where primitive ectoderm is expected

growth/size/body

abnormal embryo size ( J:27993 )

• at E6.5 there is a range of abnormal development, underdeveloped embryonic tissue and associated maternal cells, with no obvious primitive ectoderm or proamniotic cavity to disorganized embryonic and extraembryonic tissue

Genotype
MGI:5438590

hm2

• Allelic Composition: Apc^Min/Apc^Min
• Genetic Background: involves: C57BL/6J

cellular

abnormal cell physiology ( J:187862 )

• cultured adenomatous tissue form highly clonogenic spheroids

Genotype
MGI:5447942

hm3

• Allelic Composition: Apc^Min/Apc^Min
• Genetic Background: involves: C57BL/6J * CAST/EiJ

mortality/aging

embryonic lethality, complete penetrance ( J:27993 )

• inferred from no recovery of mice homozygous for embryos typed as homozygous for the identifying, linked B6 D18Mitl4 marker among a significant number of E10.5 and E13.5 progeny

• at E10.5 histological analysis shows trophoblast giant cells and a small cluster of embryonic cells, source unknown

• at E13.5 decidual swellings were necrotic with remnants of trophoblast giant cells

Genotype
MGI:5448414

hm4

• Allelic Composition: Apc^Min/Apc^Min
• Genetic Background: involves: C57BL/6 * POMOD

embryo

abnormal embryo development ( J:27993 )

• at E7.5 embryos are disorganized,showing significant reduction in embryo growth and reduction of primitive ectoderm

• failure of primitive ectoderm development shortly after implantation

decreased embryo size ( J:27993 )

• embryos are small and embedded in maternal tissue

growth/size/body

decreased embryo size ( J:27993 )

• embryos are small and embedded in maternal tissue

mortality/aging

embryonic lethality between implantation and placentation ( J:27993 )

embryonic lethality, complete penetrance ( J:27993 )

Genotype
MGI:5449072

ht5

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: (AKR/J x C57BL/6J-Apc^Min)F1

mortality/aging

extended life span ( J:1879 )

• Background Sensitivity: relative to heterozygous mice on an inbred C57BL/6J background

neoplasm

decreased intestinal adenoma incidence ( J:1879 )

• Background Sensitivity: decrease in the average number of tumors per mouse (6 vs 29) relative to heterozygous mice on an inbred C57BL/6J background

• however, all heterozygous mice developed tumors

increased intestinal adenocarcinoma incidence ( J:21369 )

• a range of 1 to 12 with an average of 3 adenomas were found per mouse

increased incidence of tumors by chemical induction ( J:15101 )

digestive/alimentary system

decreased intestinal adenoma incidence ( J:1879 )

• Background Sensitivity: decrease in the average number of tumors per mouse (6 vs 29) relative to heterozygous mice on an inbred C57BL/6J background

• however, all heterozygous mice developed tumors

increased intestinal adenocarcinoma incidence ( J:21369 )

• a range of 1 to 12 with an average of 3 adenomas were found per mouse

cellular

aneuploidy ( J:21369 )

• quantitative polymerase chain reaction analysis of all intestinal adenomas sampled showed loss of Chr 18 carrying the wild-type Apc⁺ allele

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:15101 )

Genotype
MGI:5446893

ht6

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: B6(AKR)-Apc^Min

mortality/aging

premature death ( J:10209 )

• mutant mice do not a have a normal life-span, most rarely survive longer than 120 days of age

• Background Sensitivity: average life-span has not decreased after N6 of backcrossing, suggesting genetic background influences effects of the mutation

neoplasm

increased intestinal adenocarcinoma incidence ( J:10209 )

• in N4-N8 backcross mice tumors are presesnt throughout the small and large intestines

• localization of tumors in the small and large intestines varies among mice

increased intestinal adenoma incidence ( J:10209 )

increased mammary gland tumor incidence ( J:15101 )

• on this background colony maintenance data show that mammary tumors occasionally develop in heterozygous females but not in wild-type female siblings

reproductive system

abnormal pregnancy ( J:10209 )

• females are rarely able to maintain a pregnancy due to compromised health

hematopoietic system

anemia ( J:10209 )

• anemia is diagnosed by 60 days of age

• follows development of multiple adenomas which bleed into the intestinal lumen

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:15101 )

• on this background colony maintenance data show that mammary tumors occasionally develop in heterozygous females but not in wild-type female siblings

mammary gland hyperplasia ( J:15101 )

• females of this genotype have an increased susceptibility to developing mammary neoplasia

integument

increased mammary gland tumor incidence ( J:15101 )

• on this background colony maintenance data show that mammary tumors occasionally develop in heterozygous females but not in wild-type female siblings

mammary gland hyperplasia ( J:15101 )

• females of this genotype have an increased susceptibility to developing mammary neoplasia

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:10209 )

• in N4-N8 backcross mice tumors are presesnt throughout the small and large intestines

• localization of tumors in the small and large intestines varies among mice

increased intestinal adenoma incidence ( J:10209 )

Genotype
MGI:3814370

ht7

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: B6.Cg-Brca2^tm1Mbn Apc^Min

growth/size/body

decreased body weight ( J:67445 )

• body weight of mice at time of sacrifice differs significantly from Brca2-heterozygous and wild-type animals; mice show lower weight gain from start to end of experiment compared to other experimental genotypes

reproductive system

reproductive system phenotype ( J:67445 )

N • only observed in 1/9 ENU-treated males, similar to wild-type males (1/9)

absent corpus luteum ( J:67445 )

♀ • absent in 26% of ENU-treated females

abnormal ovarian follicle morphology ( J:67445 )

♀ • remaining follicles are degenerating in ENU-treated females

abnormal ovarian folliculogenesis ( J:67445 )

♀ • arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice

absent mature ovarian follicles ( J:67445 )

♀

ovary atrophy ( J:67445 )

♀ • complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females

uterus atrophy ( J:67445 )

♀ • observed in ENU-treated females displaying ovarian failure (atrophy); endometrium and myometrium appear immature

abnormal vagina epithelium morphology ( J:67445 )

♀ • reduced in thickness and lined with vacuolated cells indicative of anestrus in ENU-treated females

neoplasm

increased mammary gland tumor incidence ( J:67445 )

• by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 6.7 +/- 2.8

• males develop tumors at a very low incidence and with a tumor multiplicity of 0.4 +/- 0.5, whereas no wild-type or Brca2-heterozygous males developed mammary tumors

• tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types

• tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris

• invasion or metastases into the mammary lymph nodes was not observed during time course of study

increased incidence of induced tumors ( J:67445 )

• multiple intestinal tumors are observed in ENU-treated mice, similar to Apc-heterozygous mice

endocrine/exocrine glands

adrenal gland hyperplasia ( J:67445 )

♀ • females exhibit some adrenal hyperplasia, while none is observed in males

abnormal mammary gland development ( J:67445 )

♂ • in ENU treated mice, male mammary ducts are elongated and in most males have extended to the lymph node of the fourth mammary gland, whereas wild-type and Brca2-heterozygous males are born with a small mammary gland rudiment, which grows no further, and no nipple

♂ • no differences are observed in branching of female mammary glands among genotypes or wild-type females

absent nipple ( J:67445 )

♀

increased mammary gland tumor incidence ( J:67445 )

• by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 6.7 +/- 2.8

• males develop tumors at a very low incidence and with a tumor multiplicity of 0.4 +/- 0.5, whereas no wild-type or Brca2-heterozygous males developed mammary tumors

• tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types

• tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris

• invasion or metastases into the mammary lymph nodes was not observed during time course of study

absent corpus luteum ( J:67445 )

♀ • absent in 26% of ENU-treated females

abnormal ovarian follicle morphology ( J:67445 )

♀ • remaining follicles are degenerating in ENU-treated females

abnormal ovarian folliculogenesis ( J:67445 )

♀ • arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice

absent mature ovarian follicles ( J:67445 )

♀

ovary atrophy ( J:67445 )

♀ • complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females

integument

abnormal mammary gland development ( J:67445 )

♂ • in ENU treated mice, male mammary ducts are elongated and in most males have extended to the lymph node of the fourth mammary gland, whereas wild-type and Brca2-heterozygous males are born with a small mammary gland rudiment, which grows no further, and no nipple

♂ • no differences are observed in branching of female mammary glands among genotypes or wild-type females

absent nipple ( J:67445 )

♀

increased mammary gland tumor incidence ( J:67445 )

• by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 6.7 +/- 2.8

• males develop tumors at a very low incidence and with a tumor multiplicity of 0.4 +/- 0.5, whereas no wild-type or Brca2-heterozygous males developed mammary tumors

• tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types

• tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris

• invasion or metastases into the mammary lymph nodes was not observed during time course of study

Genotype
MGI:2665504

ht8

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: C57BL/6J-Apc^Min

Rab25^tm1Jrgo/Rab25^tm1Jrgo Apc^Min/Apc⁺ mice exhibit increased intestinal adenoma formation compared to Apc^Min/Apc⁺ mice

mortality/aging

premature death ( J:1879 )

• average lifespan is 118 +/- 26 days

• Background Sensitivity: life span is reduced compared to mice on an (MA/MyJ x C57BL/6J-Apc)F1 or (AKR/J x C57BL/6J-Apc)F1 background

neoplasm

increased intestinal adenoma incidence ( J:1879 , J:85142 , J:158733 , J:241611 )

• develop adenomatous polyps with moderate dysplasia, mild nuclear atypia and frequent mitotic figures throughout the duodenal-to-colonic axis (J:1879)

• serotonergic cells were found in 18 of 18 adenomas (J:1879)

• most mutants exhibit a few small or medium-sized adenomas at 5 weeks of age, with numbers increasing significantly between 5 and 8 weeks and then staying at the same level thereafter (J:85142)

• mean diameter of adenomas and adenoma burden increases significantly between weeks 5 and 8 and between weeks 8 and 15 (J:85142)

• at 8 and 15 weeks of age, females have proportionally more small adenomas and fewer medium-sized adenomas than males (J:85142)

• mice fed a beef or inulin diet develop a similar number of adenomas as mice fed the rodent chow diet (J:85142)

• tubular adenomas in the intestine (J:158733)

• mice treated with a novel TNIK inhibitor NCB-0846 show reduced multiplicity and size of tumors that develop in the small intestine (J:241611)

increased colon adenoma incidence ( J:158733 , J:160399 )

• tubular adenomas in the colon (J:158733)

digestive/alimentary system

increased intestinal adenoma incidence ( J:1879 , J:85142 , J:158733 , J:241611 )

• develop adenomatous polyps with moderate dysplasia, mild nuclear atypia and frequent mitotic figures throughout the duodenal-to-colonic axis (J:1879)

• serotonergic cells were found in 18 of 18 adenomas (J:1879)

• most mutants exhibit a few small or medium-sized adenomas at 5 weeks of age, with numbers increasing significantly between 5 and 8 weeks and then staying at the same level thereafter (J:85142)

• mean diameter of adenomas and adenoma burden increases significantly between weeks 5 and 8 and between weeks 8 and 15 (J:85142)

• at 8 and 15 weeks of age, females have proportionally more small adenomas and fewer medium-sized adenomas than males (J:85142)

• mice fed a beef or inulin diet develop a similar number of adenomas as mice fed the rodent chow diet (J:85142)

• tubular adenomas in the intestine (J:158733)

• mice treated with a novel TNIK inhibitor NCB-0846 show reduced multiplicity and size of tumors that develop in the small intestine (J:241611)

increased colon adenoma incidence ( J:158733 , J:160399 )

• tubular adenomas in the colon (J:158733)

homeostasis/metabolism

increased circulating free fatty acids level ( J:86036 )

♀ • females exhibit increased free fatty acid levels at 15 weeks of age

increased circulating triglyceride level ( J:86036 )

♀ • females show increased triglyceride levels at 15 weeks of age

increased prostaglandin level ( J:85142 )

• increase in luminal prostaglandin E2 at 15 weeks of age

liver/biliary system

hepatic steatosis ( J:86036 )

• centrilobular-restricted steatosis is seen in the livers of mutants at 15 weeks of age

growth/size/body

postnatal growth retardation ( J:85142 )

♂ • regular chow-fed males stop gaining weight, lose more weight, and are smaller at 15 weeks than beef-fed males

hematopoietic system

decreased macrophage cell number ( J:85142 )

• fewer Mac-1+ (macrophages) cells in ileal mucosa at 5 weeks of age, however numbers are normal at later time points and in all dietary treatments

• however, luminal IgA, IL-12, and TNF-alpha concentrations are normal

immune system

decreased macrophage cell number ( J:85142 )

• fewer Mac-1+ (macrophages) cells in ileal mucosa at 5 weeks of age, however numbers are normal at later time points and in all dietary treatments

• however, luminal IgA, IL-12, and TNF-alpha concentrations are normal

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:85142
familial adenomatous polyposis		DOID:0050424	OMIM:PS175100	J:86036

Genotype
MGI:6712682

ht9

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: C57BL/6J-Apc^Min/J

mortality/aging

premature death ( J:331404 )

• mice show a median survival time of 24.6 weeks

neoplasm

increased intestinal adenoma incidence ( J:331404 )

• mice exhibit frequent carcinoma-like high-grade adenomas in the small intestine and colon

increased colon adenoma incidence ( J:331404 )

immune system

abnormal interleukin secretion ( J:305794 )

• naive T cells polarized toward the TH22 cell lineage show an increase in IL-22 secretion

digestive/alimentary system

increased intestinal adenoma incidence ( J:331404 )

• mice exhibit frequent carcinoma-like high-grade adenomas in the small intestine and colon

increased colon adenoma incidence ( J:331404 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:331404

Genotype
MGI:4429570

ht10

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: involves: 129 * C57BL/6

digestive/alimentary system

intestine polyps ( J:156864 )

• macroscopic lesions primarily within the proximal portion of the small intestine in mutant (n=22)

hematopoietic system

decreased NK cell number ( J:156864 )

• decreased DX5+, CD3- NK-cells in the spleen at 17 weeks old

decreased T cell number ( J:156864 )

• reduction in splenic CD3+ T cells at 17 weeks old

decreased splenocyte number ( J:156864 )

• a strong reduction of mature single positive CD4+ and CD8+ cells in the spleen at 17 weeks old

• a less pronounced reduction in immature double positive CD4+,CD8+ cells in the spleen at 17 weeks old

• reduction in splenic CD3+ T cells at 17 weeks old

• decreased DX5+, CD3- NK-cells in the spleen at 17 weeks old

immune system

decreased NK cell number ( J:156864 )

• decreased DX5+, CD3- NK-cells in the spleen at 17 weeks old

decreased T cell number ( J:156864 )

• reduction in splenic CD3+ T cells at 17 weeks old

decreased splenocyte number ( J:156864 )

• a strong reduction of mature single positive CD4+ and CD8+ cells in the spleen at 17 weeks old

• a less pronounced reduction in immature double positive CD4+,CD8+ cells in the spleen at 17 weeks old

• reduction in splenic CD3+ T cells at 17 weeks old

• decreased DX5+, CD3- NK-cells in the spleen at 17 weeks old

Genotype
MGI:3834882

ht11

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

neoplasm

neoplasm ( J:95893 )

N • no gastric adenomas are observed at 30 days of age

N • at 30 days, no colonic adenomas are found and normal colonic architecture and cellular morphology is observed

increased intestinal adenoma incidence ( J:95893 )

• adenomas are present at 70 days of age

• loss of heterozygosity at 70 days of age is similar to heterozygous mice that are also homozygous for Foxl1^tm1Khk

digestive/alimentary system

increased intestinal adenoma incidence ( J:95893 )

• adenomas are present at 70 days of age

• loss of heterozygosity at 70 days of age is similar to heterozygous mice that are also homozygous for Foxl1^tm1Khk

Genotype
MGI:2175903

ht12

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: involves: AKR/J * C57BL/6J

neoplasm

increased intestinal adenocarcinoma incidence ( J:10209 )

• locally invasive tumors seen in older animals but no metastasis

• sometimes small areas of carcinomas in anemic animals only

• if mice are not anemic by 150 days of age, then tumors are not seen at 300 days of age

increased intestinal adenoma incidence ( J:10209 )

• visible tumors of the large and small intestine

• either polyploid, papillary or sessile adenomas

digestive/alimentary system

melena ( J:10209 )

• bloody feces

increased intestinal adenocarcinoma incidence ( J:10209 )

• locally invasive tumors seen in older animals but no metastasis

• sometimes small areas of carcinomas in anemic animals only

• if mice are not anemic by 150 days of age, then tumors are not seen at 300 days of age

increased intestinal adenoma incidence ( J:10209 )

• visible tumors of the large and small intestine

• either polyploid, papillary or sessile adenomas

hematopoietic system

anemia ( J:10209 )

• progressive adult onset anemia beconming severe and chronic

• diagnosed in mutant mice by 60 days of age

• with few exceptions, likely the cause of lethality by 120 days of age

decreased hematocrit ( J:10209 )

• moribund animals with hematocrits around 10-20%

homeostasis/metabolism

hyperlipidemia ( J:10209 )

mortality/aging

premature death ( J:10209 )

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
familial adenomatous polyposis		DOID:0050424	OMIM:PS175100	J:830

Genotype
MGI:3812012

ht13

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: involves: C57BL/6 * C57BL/6J

mortality/aging

premature death ( J:134087 )

• mice die at 169 days

digestive/alimentary system

intestine polyps ( J:134087 )

• mice develop more and bigger polyps than in Apc^Min Myc^tm1Jlc heterozygotes

Genotype
MGI:3513858

ht14

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: involves: C57BL/6J

mortality/aging

premature death ( J:75393 , J:94108 )

• mice become moribound and die from anemia and intestinal obstruction by 160-180 days of age (J:75393)

• heterozygotes begin to die at 7 months of age (J:94108)

integument

increased mammary adenocarcinoma incidence ( J:94108 )

• 12% of heterozygotes developed mammary adenocanthomas

neoplasm

decreased intestinal adenoma incidence ( J:268691 )

• mice treated with vacuolar adenosine triphosphatase (v-ATPase) inhibitor bafilomycin A1 (BAF) or concanamycin A (CMA) show a decrease in intestinal adenoma number relative to vehicle-treated control mice

increased intestinal adenoma incidence ( J:75393 , J:94108 , J:299895 )

• mice develop intestinal adenomas and colorectal adenomas by 160-180 days of age (J:75393)

• small and large adenomas are seen throughout the intestine with more lesions found in the ileum compared to Apc^tm1Cip heterozygotes (J:94108)

• 50% of mice develop intestinal adenomas at 3 months of age, with 3 of 10 mice showing multiple tumors (J:299895)

increased mammary adenocarcinoma incidence ( J:94108 )

• 12% of heterozygotes developed mammary adenocanthomas

abnormal tumor pathology ( J:268691 )

• mice treated with vacuolar adenosine triphosphatase (v-ATPase) inhibitors, bafilomycin A1 (BAF) or concanamycin A (CMA), show a decrease in beta-catenin protein level, beta-catenin target expression, and tumor cell proliferation (% of Ki67+ cells) relative to vehicle-treated control mice

• however, intestinal epithelial cell differentiation is not affected by v-ATPase inhibitors

decreased tumor growth/size ( J:268691 )

• mice treated with v-ATPase inhibitor BAF or CMA show a decrease in tumor cell proliferation (% of Ki67+ cells) relative to vehicle-treated control mice

• intestinal tumor organoids treated with v-ATPase inhibitors exhibit reduced tumor growth, unlike wild-type crypt organoids which show normal growth and expansion

digestive/alimentary system

abnormal enterocyte proliferation ( J:118600 )

• reduced proliferation of cells in the colon in ovariectomized

• however, 17beta-estradiol replacement increases colonocyte proliferation 2-fold

abnormal intestinal mucosa morphology ( J:118600 )

• ovariectomized mice exhibit abnormal submucosal with thickening of the muscularis mucosae and enrichment of stromal components compared with control mice

abnormal intestinal goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevelant pregoblet cells in ovariectomized mcie treated with 17beta-estradiol

• the goblet cell ratio in ovariectomized mice is increased compared to in intact mice

abnormal large intestine crypts of Lieberkuhn morphology ( J:118600 )

• ovariectomized mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice

rectal prolapse ( J:94108 )

• rectal prolapse is seen in 28% of surviving mutants at 7 months of age

decreased intestinal adenoma incidence ( J:268691 )

• mice treated with vacuolar adenosine triphosphatase (v-ATPase) inhibitor bafilomycin A1 (BAF) or concanamycin A (CMA) show a decrease in intestinal adenoma number relative to vehicle-treated control mice

increased intestinal adenoma incidence ( J:75393 , J:94108 , J:299895 )

• mice develop intestinal adenomas and colorectal adenomas by 160-180 days of age (J:75393)

• small and large adenomas are seen throughout the intestine with more lesions found in the ileum compared to Apc^tm1Cip heterozygotes (J:94108)

• 50% of mice develop intestinal adenomas at 3 months of age, with 3 of 10 mice showing multiple tumors (J:299895)

intestine polyps ( J:191217 )

intestinal obstruction ( J:75393 )

• due to tumors

cellular

abnormal intestinal goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevelant pregoblet cells in ovariectomized mcie treated with 17beta-estradiol

• the goblet cell ratio in ovariectomized mice is increased compared to in intact mice

abnormal enterocyte proliferation ( J:118600 )

• reduced proliferation of cells in the colon in ovariectomized

• however, 17beta-estradiol replacement increases colonocyte proliferation 2-fold

endocrine/exocrine glands

abnormal large intestine crypts of Lieberkuhn morphology ( J:118600 )

• ovariectomized mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice

increased mammary adenocarcinoma incidence ( J:94108 )

• 12% of heterozygotes developed mammary adenocanthomas

hematopoietic system

anemia ( J:75393 )

Genotype
MGI:5763440

ht15

• Allelic Composition: Apc^Min/Apc⁺
• Genetic Background: (MA/MyJ x C57BL/6J-Apc^Min)F1

mortality/aging

extended life span ( J:1879 )

• Background Sensitivity: relative to heterozygous mice on an inbred C57BL/6J background

neoplasm

decreased intestinal adenoma incidence ( J:1879 )

• Background Sensitivity: decrease in the average number of tumors per mouse (6 vs 29) relative to heterozygous mice on an inbred C57BL/6J background

• however, all heterozygous mice developed tumors

digestive/alimentary system

decreased intestinal adenoma incidence ( J:1879 )

• Background Sensitivity: decrease in the average number of tumors per mouse (6 vs 29) relative to heterozygous mice on an inbred C57BL/6J background

• however, all heterozygous mice developed tumors

Genotype
MGI:5431900

ht16

• Allelic Composition: Apc^Min/Apc^tm1.1Klne
• Genetic Background: B6.Cg-Apc^Min/Apc^tm1.1Klne

digestive/alimentary system

abnormal enterocyte proliferation ( J:186132 )

• increased compared with Apc^Min heterozygotes

intestine polyps ( J:186132 )

• mice develop more polyps in the jejunum, ileum, duodenum and stomach compared with Apc^Min heterozygotes

• mice exhibit larger polyps in the jejunum and ileum compared with Apc^Min heterozygotes

• however, the number of polyps in the colon is the same as in Apc^Min heterozygotes

cellular

abnormal enterocyte proliferation ( J:186132 )

• increased compared with Apc^Min heterozygotes

Genotype
MGI:4429565

ht17

• Allelic Composition: Apc^Min/Apc^tm1Tno
• Genetic Background: involves: 129 * 129S4/SvJae * C57BL/6

Anterior head defects during embryonic development in Apc^Min/Apc^tm1Tno embryos and rescue of head defects by Ctnnb1^tm4.1Wbm/Ctnnb1⁺

mortality/aging

perinatal lethality, complete penetrance ( J:156864 )

• no mutant mice found at term

lethality throughout fetal growth and development, incomplete penetrance ( J:156864 )

• live embryos could still be detected at embryonic day 17.5 (E17.5), but at less than the expected Mendelian ratio

nervous system

abnormal brain development ( J:156864 )

• lack all structures anterior to the hindbrain at E12

• first become visible in E8.5-E9.5

absent midbrain ( J:156864 )

absent forebrain ( J:156864 )

craniofacial

absent mandible ( J:156864 )

• a prominent cap of neural tissue at the most anterior part of the embryo at E12

• absent mandible at E12

acrania ( J:156864 )

• a prominent cap of neural tissue at the most anterior part of the embryo at E12

• absent cranial structures at E12

skeleton

absent mandible ( J:156864 )

• a prominent cap of neural tissue at the most anterior part of the embryo at E12

• absent mandible at E12

acrania ( J:156864 )

• a prominent cap of neural tissue at the most anterior part of the embryo at E12

• absent cranial structures at E12

Genotype
MGI:5547498

cn18

• Allelic Composition: Apc^Min/Apc⁺; Hsd11b2^tm1.1Mzz/Hsd11b2^tm1.1Mzz; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129 * C57BL/6 * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:205456 )

• fewer total intestinal adenoma at 20 weeks with prevented initiation of polyp formation compared with Apc^Min heterozygotes

decreased tumor growth/size ( J:205456 )

• reduced proliferation and increased apoptosis compared with tumors from Apc^Min heterozygotes

homeostasis/metabolism

abnormal corticosterone level ( J:205456 )

• 10-fold higher corticosterone (active glucocorticoid) levels in the intestine compared with Apc^Min heterozygotes

• 11-keto-corticosterone (inactive glucocorticoid) levels is lower in the intestine compared with Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:205456 )

• fewer total intestinal adenoma at 20 weeks with prevented initiation of polyp formation compared with Apc^Min heterozygotes

Genotype
MGI:3625330

cn19

• Allelic Composition: Apc^Min/Apc⁺; Dnmt3b^tm1Jae/Dnmt3b^tm1Jae; Tg(Fabp1-cre)1Jig/0
• Genetic Background: involves: 129 * C57BL/6 * C57BL/6J * FVB/N

neoplasm

decreased tumor incidence ( J:107386 )

• significant decrease in the formation of macroscopic colonic adenomas in Apc^Min/+ mice

• no impact on microadenoma formation

• no noticeable effect on later stages of tumor growth

Genotype
MGI:4946926

cn20

• Allelic Composition: Apc^Min/Apc⁺; Tcf7l2^{tm1(EGFP/cre)Mrc}/Tcf7l2^tm2.1Mrc
• Genetic Background: involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J * C57BL/6NCrl

neoplasm

neoplasm ( J:170088 )

N • mice do not exhibit develop intestinal adenomas

Genotype
MGI:6357721

cn21

• Allelic Composition: Apc^Min/Apc⁺; Mapkapk2^tm1.1Gkl/Mapkapk2^tm1.1Gkl; Tg(Tie1-cre)9Ref/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * BALB/cJ * C57BL/6J

neoplasm

decreased tumor growth/size ( J:262876 )

• reduced proliferation and increased apoptosis of tumor cells compared to in Apc^min heterozygotes

Genotype
MGI:6448989

cn22

• Allelic Composition: Apc^Min/Apc⁺; Trp53^tm2.1Tyj/Trp53^tm2.1Tyj; Tg(Vil1-cre/ERT2)23Syr/0
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J * DBA/2

neoplasm

increased intestinal adenoma incidence ( J:291671 )

• as in Apc^Min heterozygotes with enhancement of tumorigenesis in the colon but reduced tumor burden in the proximal gastrointestinal tract

increased colon adenoma incidence ( J:291671 )

• enhancement of tumorigenesis in the colon compared with Apc^Min heterozygotes

decreased alimentary system tumor incidence ( J:291671 )

• reduced tumor burden in the proximal gastrointestinal tract compared with Apc^Min heterozygotes

• however, treatment with gallic acid abolishes the tumor suppressive effect of the mutant Trp53

digestive/alimentary system

increased intestinal adenoma incidence ( J:291671 )

• as in Apc^Min heterozygotes with enhancement of tumorigenesis in the colon but reduced tumor burden in the proximal gastrointestinal tract

increased colon adenoma incidence ( J:291671 )

• enhancement of tumorigenesis in the colon compared with Apc^Min heterozygotes

decreased alimentary system tumor incidence ( J:291671 )

• reduced tumor burden in the proximal gastrointestinal tract compared with Apc^Min heterozygotes

• however, treatment with gallic acid abolishes the tumor suppressive effect of the mutant Trp53

Genotype
MGI:4941759

cn23

• Allelic Composition: Apc^Min/Apc⁺; Pten^tm1Hwu/Pten^tm1Hwu; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL

mortality/aging

premature death ( J:150553 )

• all mutants die within 80 days

neoplasm

increased intestinal adenoma incidence ( J:150553 )

• adenomas in the small intestine

digestive/alimentary system

increased intestinal adenoma incidence ( J:150553 )

• adenomas in the small intestine

intestine polyps ( J:150553 )

• mutants develop an average of 20.1 intestinal polyps per mouse, an 11.17-fold increase over the numbers seen in heterozygous Apc mice

Genotype
MGI:4430578

cn24

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm1(CAG-Sirt1)Dsin}/Col1a1⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL

neoplasm

decreased tumor incidence ( J:134301 )

• mice do not develop tumors morbidities, including anemia and cachaxia, unlike Col1a1^{tm1(CAG-Sirt1)Dsin} Apc^Min heterozygotes

• mice develop fewer intestinal tumors than Col1a1^{tm1(CAG-Sirt1)Dsin} Apc^Min heterozygotes

Genotype
MGI:7642164

cn25

• Allelic Composition: Apc^Min/Apc⁺; Rab11a^tm1.1Ngao/Rab11a^tm1.1Ngao; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6J * SJL/J

mortality/aging

decreased tumor-free survival time ( J:278932 )

• mice show higher mortality due to increased tumor burden compared to single Apc^Min mice

neoplasm

increased intestinal adenoma incidence ( J:278932 )

• 2-month-old mice develop twice the number of adenomas that are 5 times larger and occupy larger epithelial fields as compared with tumor fields in single Apc^Min mice

• mice show higher mortality due to increased tumor burden compared to single Apc^Min mice

digestive/alimentary system

increased intestinal adenoma incidence ( J:278932 )

• 2-month-old mice develop twice the number of adenomas that are 5 times larger and occupy larger epithelial fields as compared with tumor fields in single Apc^Min mice

• mice show higher mortality due to increased tumor burden compared to single Apc^Min mice

Genotype
MGI:5475206

cn26

• Allelic Composition: Apc^Min/Apc⁺; Dclk1^{tm1.1(cre/ERT2)Seno}/Dclk1⁺; Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor^{tm1(HBEGF)Awai}
• Genetic Background: involves: 129S4/SvJaeSor * C57BL/6

neoplasm

abnormal tumor morphology ( J:193873 )

• after tamoxifen treatment and a single injection of diphtheria toxin (DT), polyps contain many Dclk1-positive apoptotic tumor cells and are severely injured or collapsed with Dclk1-negative polyps not displaying DT-induced apoptosis

digestive/alimentary system

digestive/alimentary phenotype ( J:193873 )

N • after tamoxifen treatment and multiple diphtheria toxin injections to ablate Dclk1-positive cells, these cells are absent from the normal intestine with no significant damage to organ architecture observed in the intestine or stomach

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:193873 )

N • after tamoxifen treatment and multiple diphtheria toxin injections to ablate Dclk1-positive cells, no significant damage in organ architecture is observed in the pancreas or gallbladder

Genotype
MGI:4360363

cn27

• Allelic Composition: Apc^Min/Apc⁺; Erbb3^tm1.1Dwt/Erbb3^tm2.1Dwt; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL

digestive/alimentary system

digestive/alimentary phenotype ( J:152703 )

N • unlike Apc^Min heterozygotes, mice do not develop colonic polyps

intestine polyps ( J:152703 )

• mice develop fewer intestinal polyps compared to in Apc^Min heterozygotes

neoplasm

decreased tumor incidence ( J:152703 )

• the number and size of microadenomas in the intestine are decreased compared to in Apc^Min heterozygotes due to an increased in Caspase-3 dependent apoptosis

• mice fail to develop colon tumors unlike Apc^Min heterozygotes

Genotype
MGI:5013408

cn28

• Allelic Composition: Apc^Min/Apc⁺; Gt(ROSA)26Sor^{tm2(Rnf187)Jhai}/Gt(ROSA)26Sor⁺; Tg(Vil1-cre)20Syr/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6 * DBA/2

neoplasm

increased gastrointestinal tumor incidence ( J:173145 )

• intestinal tumors are increased in number compared to in Apc^Min/Apc⁺ Tg(Vil-cre)20Syr

increased tumor growth/size ( J:173145 )

• intestinal tumors exhibit increased cell proliferation and size compared to in Apc^Min/Apc⁺ Tg(Vil-cre)20Syr

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:173145 )

• intestinal tumors are increased in number compared to in Apc^Min/Apc⁺ Tg(Vil-cre)20Syr

Genotype
MGI:4889209

cn29

• Allelic Composition: Apc^Min/Apc⁺; Gpa33^{tm1(GNAS)Wtsi}/Gpa33⁺; Hprt1^{tm1(CMV-cre)Brd}/?
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:168378 )

• compared with Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:168378 )

• compared with Apc^Min heterozygotes

Genotype
MGI:6357723

cn30

• Allelic Composition: Apc^Min/Apc⁺; Mapkapk2^tm1.1Gkl/Mapkapk2^tm1.1Gkl; Twist2^{tm1.1(cre)Dor}/Twist2⁺
• Genetic Background: involves: 129X1/SvJ * BALB/cJ * C57BL/6J

neoplasm

decreased tumor growth/size ( J:262876 )

• compared with Apc^min heterozygotes

• reduced proliferation and increased apoptosis of tumor cells compared with Apc^min heterozygotes

decreased tumor incidence ( J:262876 )

• compared with Apc^min heterozygotes

Genotype
MGI:5774439

cn31

• Allelic Composition: Apc^Min/Apc⁺; Lmna^tm4Stw/Lmna^tm4Stw; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J

digestive/alimentary system

duodenum polyps ( J:220874 )

• at 16-32 weeks of age, mice show a 1.5-fold increase in the frequency of larger polyps (2-5 mm) in the duodenum relative to Apc^Min heterozygous controls

jejunum polyps ( J:220874 )

• mice show a 3-fold increase in the frequency of larger polyps (2-5 mm) in the proximal jejunum relative to Apc^Min heterozygous controls

• however, the total number of polyps found in the gastrointestinal tract (duodenum, proximal and distal jejunum, ileum and colon) is not significantly altered relative to ApcMin heterozygous controls

Genotype
MGI:5898003

cn32

• Allelic Composition: Apc^Min/Apc⁺; Elp3^tm1.1Tac/Elp3^tm1.1Tac; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6 * C57BL/6J * C57BL/6NTac * SJL

cellular

abnormal gastrointestinal brush cell morphology ( J:227334 )

• the number of Tuft cells in the intestinal epithelium are slightly decreased

digestive/alimentary system

digestive/alimentary phenotype ( J:227334 )

N • crypt cell proliferation and cell apoptosis at the top of the villi remain unchanged compared to single Apc^Min mutants

abnormal gastrointestinal brush cell morphology ( J:227334 )

• the number of Tuft cells in the intestinal epithelium are slightly decreased

abnormal intestinal epithelium morphology ( J:227334 )

• the number of Dclk1+ cells in both tumors and adjacent regions are decreased in the intestine

• the number of Tuft cells are slightly decreased

• the number of Dckl1+/acetylated alpha-tubulin-negative cells are highly decreased

decreased intestinal adenoma incidence ( J:227334 )

• mice exhibit decreased tumor number in proximal, middle, and distal intestines compared to single Apc^Min mutants and expanded life span

neoplasm

decreased intestinal adenoma incidence ( J:227334 )

• mice exhibit decreased tumor number in proximal, middle, and distal intestines compared to single Apc^Min mutants and expanded life span

increased tumor latency ( J:227334 )

• mice exhibit delayed tumor appearance in intestinal epithelia compared to single Apc^Min mutants

hematopoietic system

hematopoietic system phenotype ( J:227334 )

N • mice do not exhibit decreased hematocrit levels as seen in single Apc^Min mutants

immune system

immune system phenotype ( J:227334 )

N • mice do not exhibit splenomegaly

Genotype
MGI:5523866

cn33

• Allelic Composition: Apc^Min/Apc⁺; Igf2bp1^tm1Vssp/Igf2bp1^tm1Vssp; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: C57BL/6J * SJL

neoplasm

abnormal tumor incidence ( J:202774 )

• mice develop reduced number of intestinal tumors compared with Apc^min heterozygotes at 90 days

Genotype
MGI:3814367

cx34

• Allelic Composition: Apc^Min/Apc⁺; Brca2^tm1Mbn/Brca2⁺
• Genetic Background: B6.Cg-Brca2^tm1Mbn Apc^Min

growth/size/body

growth/size/body region phenotype ( J:67445 )

N • body weight of mice at time of sacrifice does not differ significantly from Apc-heterozygous, Brca2-heterozygous, or wild-type animals

reproductive system

reproductive system phenotype ( J:67445 )

N • only observed in 1/8 ENU-treated males, similar to wild-type males (1/9)

absent corpus luteum ( J:67445 )

♀ • absent in 22% of ENU-treated females

abnormal ovarian follicle morphology ( J:67445 )

♀ • remaining follicles are degenerating in ENU-treated females

abnormal ovarian folliculogenesis ( J:67445 )

♀ • arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice

absent mature ovarian follicles ( J:67445 )

♀

ovary atrophy ( J:67445 )

♀ • complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females

uterus atrophy ( J:67445 )

♀ • observed in ENU-treated females displaying ovarian failure (atrophy); endometrium and myometrium appear immature

abnormal vagina epithelium morphology ( J:67445 )

♀ • reduced in thickness and lined with vacuolated cells indicative of anestrus in ENU-treated females

neoplasm

increased mammary gland tumor incidence ( J:67445 )

• by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 7.2 +/- 2.7, whereas only 7% of wild-type females develop tumors

• males develop tumors at a very low incidence and with a tumor multiplicity of 0.2 +/- 0.3, whereas no wild-type or Brca2-heterozygous males developed mammary tumors

• tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types

• tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris

• invasion or metastases into the mammary lymph nodes was not observed during time course of study

increased incidence of induced tumors ( J:67445 )

• multiple intestinal tumors are observed in ENU-treated mice

increased incidence of tumors by chemical induction ( J:67445 )

endocrine/exocrine glands

abnormal adrenal gland morphology ( J:67445 )

abnormal mammary gland development ( J:67445 )

♂ • in ENU treated mice, male mammary ducts are elongated and in most males have extended to the lymph node of the fourth mammary gland, whereas wild-type and Brca2-heterozygous males are born with a small mammary gland rudiment, which grows no further, and no nipple

♂ • no differences are observed in branching of female mammary glands among genotypes or wild-type females

absent nipple ( J:67445 )

♀

increased mammary gland tumor incidence ( J:67445 )

• by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 7.2 +/- 2.7, whereas only 7% of wild-type females develop tumors

• males develop tumors at a very low incidence and with a tumor multiplicity of 0.2 +/- 0.3, whereas no wild-type or Brca2-heterozygous males developed mammary tumors

• tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types

• tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris

• invasion or metastases into the mammary lymph nodes was not observed during time course of study

absent corpus luteum ( J:67445 )

♀ • absent in 22% of ENU-treated females

abnormal ovarian follicle morphology ( J:67445 )

♀ • remaining follicles are degenerating in ENU-treated females

abnormal ovarian folliculogenesis ( J:67445 )

♀ • arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice

absent mature ovarian follicles ( J:67445 )

♀

ovary atrophy ( J:67445 )

♀ • complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females

homeostasis/metabolism

increased incidence of tumors by chemical induction ( J:67445 )

integument

abnormal mammary gland development ( J:67445 )

♂ • in ENU treated mice, male mammary ducts are elongated and in most males have extended to the lymph node of the fourth mammary gland, whereas wild-type and Brca2-heterozygous males are born with a small mammary gland rudiment, which grows no further, and no nipple

♂ • no differences are observed in branching of female mammary glands among genotypes or wild-type females

absent nipple ( J:67445 )

♀

increased mammary gland tumor incidence ( J:67445 )

• by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 7.2 +/- 2.7, whereas only 7% of wild-type females develop tumors

• males develop tumors at a very low incidence and with a tumor multiplicity of 0.2 +/- 0.3, whereas no wild-type or Brca2-heterozygous males developed mammary tumors

• tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types

• tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris

• invasion or metastases into the mammary lymph nodes was not observed during time course of study

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:67445

Genotype
MGI:5014351

cx35

• Allelic Composition: Apc^Min/Apc⁺; Gt(ROSA)26Sor/Gt(ROSA)26Sor⁺
• Genetic Background: B6.Cg-Gt(ROSA)26Sor Apc^Min

neoplasm

abnormal tumor susceptibility ( J:66060 )

• female mice treated with ENU survive for 86 days as compared to 66-71 days for mice carrying Apc^Min alone

decreased alimentary system tumor incidence ( J:66060 )

• female mice treated with ENU develop significantly fewer intestinal tumors than mice carrying either Apc^Min alone or C57BL/6 controls

decreased mammary gland tumor incidence ( J:66060 )

• female mice treated with ENU develop significantly fewer mammary tumors than mice carrying either Apc^Min alone or C57BL/6 controls

decreased incidence of tumors by chemical induction ( J:66060 )

• female mice treated with ENU develop significantly fewer mammary or intestinal tumors than mice carrying either Apc^Min alone or C57BL/6 controls

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:66060 )

• female mice treated with ENU develop significantly fewer mammary or intestinal tumors than mice carrying either Apc^Min alone or C57BL/6 controls

integument

decreased mammary gland tumor incidence ( J:66060 )

• female mice treated with ENU develop significantly fewer mammary tumors than mice carrying either Apc^Min alone or C57BL/6 controls

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:66060 )

• female mice treated with ENU develop significantly fewer mammary tumors than mice carrying either Apc^Min alone or C57BL/6 controls

digestive/alimentary system

decreased alimentary system tumor incidence ( J:66060 )

• female mice treated with ENU develop significantly fewer intestinal tumors than mice carrying either Apc^Min alone or C57BL/6 controls

Genotype
MGI:5567980

cx36

• Allelic Composition: Apc^Min/Apc⁺; Mir10a^tm1.1Ahl/Mir10a^tm1.1Ahl
• Genetic Background: B6.Cg-Mir10a^tm1.1Ahl Apc^min

Enhanced intestinal tumorigenesis in Apc^Min/Apc⁺ Mir10a^tm1.1Ahl/Mir10a^tm1.1Ahl mice

neoplasm

increased gastrointestinal tumor incidence ( J:205135 )

♀ • twice as many tumors in the small intestine as in Apc^min heterozygotes

♀ • however, tumor multiplicity in male mice is the same as in Apc^min heterozygotes

increased intestinal adenoma incidence ( J:205135 )

• in the small intestine of female and male mice with increased frequency with of high-grade dysplasia and higher incidence of tubule-villous adenomas (more evident in female mice than male mice)

• however, tumor size is the same as in Apc^min heterozygotes

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:205135 )

♀ • twice as many tumors in the small intestine as in Apc^min heterozygotes

♀ • however, tumor multiplicity in male mice is the same as in Apc^min heterozygotes

increased intestinal adenoma incidence ( J:205135 )

• in the small intestine of female and male mice with increased frequency with of high-grade dysplasia and higher incidence of tubule-villous adenomas (more evident in female mice than male mice)

• however, tumor size is the same as in Apc^min heterozygotes

Genotype
MGI:5430745

cx37

• Allelic Composition: Apc^Min/Apc⁺; Mthfs^{Gt(RRK291)Byg}/Mthfs⁺
• Genetic Background: B6.Cg-Mthfs^{Gt(RRK291)Byg} Apc^Min

neoplasm

neoplasm ( J:185874 )

N • small intestine and colon tumor incidence is similar to mice heterozygous for Apc^Min alone

Genotype
MGI:3767792

cx38

• Allelic Composition: Apc^Min/Apc⁺; Nos2^tm1Lau/Nos2⁺
• Genetic Background: B6.Cg-Nos2^tm1Lau Apc^Min

neoplasm

decreased tumor growth/size ( J:73152 )

• polyp size reduced

decreased tumor incidence ( J:73152 )

• 68% of tumor incidence observed in controls

• multiplicity of tumors reduced to about 33% of control level

Genotype
MGI:3767791

cx39

• Allelic Composition: Apc^Min/Apc⁺; Nos2^tm1Lau/Nos2^tm1Lau
• Genetic Background: B6.Cg-Nos2^tm1Lau Apc^Min

neoplasm

decreased tumor growth/size ( J:73152 )

• polyp size reduced

decreased tumor incidence ( J:73152 )

• 29% of tumor incidence observed in controls

• multiplicity of tumors reduced to about 9% of control level

Genotype
MGI:4358774

cx40

• Allelic Composition: Apc^Min/Apc⁺; Pla2g4a^tm1Jvb/Pla2g4a^tm1Jvb
• Genetic Background: B6.Cg-Pla2g4a^tm1Jvb Apc^Min

digestive/alimentary system

intestine polyps ( J:68495 )

• mice exhibit a 83% reduction in small intestine polyp number with a 22% decrease in size compared with polyps in Apc^Min heterozygotes

• mice exhibit the same number of polyps in the large intestine as in Apc^Min heterozygotes

Genotype
MGI:4440864

cx41

• Allelic Composition: Apc^Min/Apc⁺; Rab25^tm1Jrgo/Rab25⁺
• Genetic Background: B6.Cg-Rab25^tm1Jrgo Apc^Min

neoplasm

increased intestinal adenoma incidence ( J:158733 )

• 2-fold increase in tumor number in the middle and distal intestines compared with heterozygous Apc^min mice

digestive/alimentary system

increased intestinal adenoma incidence ( J:158733 )

• 2-fold increase in tumor number in the middle and distal intestines compared with heterozygous Apc^min mice

Genotype
MGI:4440863

cx42

• Allelic Composition: Apc^Min/Apc⁺; Rab25^tm1Jrgo/Rab25^tm1Jrgo
• Genetic Background: B6.Cg-Rab25^tm1Jrgo Apc^Min

Rab25^tm1Jrgo/Rab25^tm1Jrgo Apc^Min/Apc⁺ mice exhibit increased intestinal adenoma formation compared to Apc^Min/Apc⁺ mice

neoplasm

increased intestinal adenoma incidence ( J:158733 )

• tubular adenomas in the intestine

• 4-fold increase in tumor number throughout the intestines compared with heterozygous Apc^min mice

increased colon adenoma incidence ( J:158733 )

• tubular adenomas in the colon

digestive/alimentary system

colon polyps ( J:158733 )

• 2-fold increase in colonic polyp number compared with heterozygous Apc^min mice

• increased polyp size

• more widely distributed polyps in the colon

increased intestinal adenoma incidence ( J:158733 )

• tubular adenomas in the intestine

• 4-fold increase in tumor number throughout the intestines compared with heterozygous Apc^min mice

increased colon adenoma incidence ( J:158733 )

• tubular adenomas in the colon

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
familial adenomatous polyposis		DOID:0050424	OMIM:PS175100	J:158733

Genotype
MGI:5426849

cx43

• Allelic Composition: Apc^Min/Apc⁺; Shmt1^{Gt(AD0236)Wtsi}/Shmt1^{Gt(AD0236)Wtsi}
• Genetic Background: B6.Cg-Shmt1^{Gt(AD0236)Wtsi} Apc^Min

neoplasm

neoplasm ( J:183477 )

N • mice exhibit the same tumorigenesis as Apc^Min heterozygotes

Genotype
MGI:3831112

cx44

• Allelic Composition: Apc^Min/Apc⁺; Tgfbr1^tm1Bopa/Tgfbr1⁺
• Genetic Background: B6.Cg-Tgfbr1^tm1Bopa Apc^Min

neoplasm

increased gastrointestinal tumor incidence ( J:143706 )

• mice develop twice as many intestinal tumors as in Apc^Min heterozygotes

• mice develop small and predominantly scattered tumors in the small intestine as well as colonic tumors

increased intestinal adenocarcinoma incidence ( J:143706 )

• 3 mice develop large, polyploidy and ulcerated colonic tumors

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:143706 )

• mice develop twice as many intestinal tumors as in Apc^Min heterozygotes

• mice develop small and predominantly scattered tumors in the small intestine as well as colonic tumors

increased intestinal adenocarcinoma incidence ( J:143706 )

• 3 mice develop large, polyploidy and ulcerated colonic tumors

Genotype
MGI:5881920

cx45

• Allelic Composition: Apc^Min/Apc⁺; Arhgef4^tm1Taki/Arhgef4⁺
• Genetic Background: B6J.Cg-Arhgef4^tm1Taki Apc^Min

neoplasm

decreased intestinal adenoma incidence ( J:157023 )

• at 4 months of age, mice show an intermediate reduction in the total number of intestinal adenomas (polyps) per mouse relative to mice that are homozygous for Arhgef4^tm1Taki and heterozygous for Apc^Min

decreased tumor growth/size ( J:157023 )

• at 4 months of age, mice show an intermediate reduction in the size of intestinal adenomas (polyps) relative to mice that are homozygous for Arhgef4^tm1Taki and heterozygous for Apc^Min

digestive/alimentary system

decreased intestinal adenoma incidence ( J:157023 )

• at 4 months of age, mice show an intermediate reduction in the total number of intestinal adenomas (polyps) per mouse relative to mice that are homozygous for Arhgef4^tm1Taki and heterozygous for Apc^Min

Genotype
MGI:5881919

cx46

• Allelic Composition: Apc^Min/Apc⁺; Arhgef4^tm1Taki/Arhgef4^tm1Taki
• Genetic Background: B6J.Cg-Arhgef4^tm1Taki Apc^Min

neoplasm

decreased intestinal adenoma incidence ( J:157023 )

• at 4 months of age, mice show a significant reduction in the total number of intestinal adenomas (polyps) per mouse relative to Apc^Min heterozygotes

decreased tumor growth/size ( J:157023 )

• at 4 months of age, mice show a significant reduction in the size of intestinal adenomas (polyps) relative to Apc^Min heterozygotes

digestive/alimentary system

decreased intestinal adenoma incidence ( J:157023 )

• at 4 months of age, mice show a significant reduction in the total number of intestinal adenomas (polyps) per mouse relative to Apc^Min heterozygotes

Genotype
MGI:5881925

cx47

• Allelic Composition: Apc^Min/Apc⁺; Arhgef4^tm1Taki/Arhgef4^tm1Taki; Spata13^tm1Taki/Spata13^tm1Taki
• Genetic Background: B6J.Cg-Arhgef4^tm1Taki Spata13^tm1Taki Apc^Min

neoplasm

decreased intestinal adenoma incidence ( J:157023 )

• mice develop only a few small adenomas (polyps) by 4 months of age

abnormal tumor pathology ( J:157023 )

• mice show loss of the wild-type Apc allele in the small adenomas formed

• Rac1 and Cdc42 signaling appears to be reduced

abnormal tumor vascularization ( J:157023 )

• the density of microvessels within adenomas is significantly lower than that in Apc^Min heterozygotes

• however, tumor-associated macrophages are recruited to adenomas and release vascular endothelial growth factor normally

decreased tumor growth/size ( J:157023 )

• mice develop only a few small adenomas (polyps) by 4 months of age

cardiovascular system

abnormal tumor vascularization ( J:157023 )

• the density of microvessels within adenomas is significantly lower than that in Apc^Min heterozygotes

• however, tumor-associated macrophages are recruited to adenomas and release vascular endothelial growth factor normally

homeostasis/metabolism

decreased physiological sensitivity to xenobiotic ( J:157023 )

• treatment of mice with zoledronic acid (a specific inhibitor of MMP9) for 6 weeks fails to result in further suppression of adenoma formation, unlike in Apc^Min heterozygotes

digestive/alimentary system

decreased intestinal adenoma incidence ( J:157023 )

• mice develop only a few small adenomas (polyps) by 4 months of age

Genotype
MGI:5881917

cx48

• Allelic Composition: Apc^Min/Apc⁺; Spata13^tm1Taki/Spata13⁺
• Genetic Background: B6J.Cg-Spata13^tm1Taki Apc^Min

neoplasm

decreased intestinal adenoma incidence ( J:157023 )

• at 4 months of age, mice show an intermediate reduction in the total number of intestinal adenomas (polyps) per mouse relative to mice that are homozygous for Spata13^tm1Taki and heterozygous for Apc^Min

decreased tumor growth/size ( J:157023 )

• at 4 months of age, mice show an intermediate reduction in the size of intestinal adenomas (polyps) relative to mice that are homozygous for Spata13^tm1Taki and heterozygous for Apc^Min

digestive/alimentary system

decreased intestinal adenoma incidence ( J:157023 )

• at 4 months of age, mice show an intermediate reduction in the total number of intestinal adenomas (polyps) per mouse relative to mice that are homozygous for Spata13^tm1Taki and heterozygous for Apc^Min

Genotype
MGI:5881916

cx49

• Allelic Composition: Apc^Min/Apc⁺; Spata13^tm1Taki/Spata13^tm1Taki
• Genetic Background: B6J.Cg-Spata13^tm1Taki Apc^Min

mortality/aging

abnormal survival ( J:157023 )

• mice survive significantly longer than Apc^Min heterozygotes

neoplasm

decreased intestinal adenoma incidence ( J:157023 )

• at 4 months of age, mice show an even greater reduction in the total number of intestinal adenomas (polyps) per mouse than mice that are homozygous for Arhgef4^tm1Taki and heterozygous for Apc^Min

decreased tumor growth/size ( J:157023 )

• at 4 months of age, mice show an even greater reduction in the size of intestinal adenomas (polyps) than mice that are homozygous for Arhgef4^tm1Taki and heterozygous for Apc^Min

digestive/alimentary system

decreased intestinal adenoma incidence ( J:157023 )

• at 4 months of age, mice show an even greater reduction in the total number of intestinal adenomas (polyps) per mouse than mice that are homozygous for Arhgef4^tm1Taki and heterozygous for Apc^Min

Genotype
MGI:7662833

cx50

• Allelic Composition: Apc^Min/Apc⁺; Zfp280c^em1Xss/Zfp280c⁺
• Genetic Background: C57BL/6J-Apc^Min Zfp280c^em1Xss

mortality/aging

increased tumor-free survival time ( J:331404 )

♀ • mice show a prolonged lifespan compared to single Apc^min heterozygotes

Genotype
MGI:7662831

cx51

• Allelic Composition: Apc^Min/Apc⁺; Zfp280c^em1Xss/Zfp280c^em1Xss
• Genetic Background: C57BL/6J-Apc^Min Zfp280c^em1Xss

mortality/aging

increased tumor-free survival time ( J:331404 )

♀ • mice show a prolonged lifespan, with a median survival time of 42.3 weeks compared to 24.6 weeks in single Apc^min heterozygotes

neoplasm

decreased alimentary system tumor incidence ( J:331404 )

♀ • mice show a consistent decrease in the tumor burden across the intestinal tract compared with single Apc^min mice

♀ • mice develop fewer polyps in the small intestine and the colon than single Apc^min mice at 20-24 weeks of age

♀ • the intestinal epithelium is largely normal with fewer Ki-67-positive cells in contrast to frequent carcinoma-like high-grade adenomas in the small intestine and colon in single Apc^min heterozygotes

digestive/alimentary system

decreased alimentary system tumor incidence ( J:331404 )

♀ • mice show a consistent decrease in the tumor burden across the intestinal tract compared with single Apc^min mice

♀ • mice develop fewer polyps in the small intestine and the colon than single Apc^min mice at 20-24 weeks of age

♀ • the intestinal epithelium is largely normal with fewer Ki-67-positive cells in contrast to frequent carcinoma-like high-grade adenomas in the small intestine and colon in single Apc^min heterozygotes

Genotype
MGI:7662832

cx52

• Allelic Composition: Apc^Min/Apc⁺; Zfp280c^em1Xss/Y
• Genetic Background: C57BL/6J-Apc^Min Zfp280c^em1Xss

mortality/aging

increased tumor-free survival time ( J:331404 )

♂ • mice show a medial survival time of 43.6 weeks which is longer than in single Apc^min heterozygotes with a median survival time of around 42 weeks

Genotype
MGI:7310033

cx53

• Allelic Composition: Apc^Min/Apc⁺; Fxyd5^em1Namje/Fxyd5^em1Namje
• Genetic Background: C57BL/6J-Fxyd5^em1Namje Apc^min

neoplasm

increased gastrointestinal tumor incidence ( J:325989 )

• mice develop intestinal tumors unlike wild-type mice but at a slower rate and with reduced tumor load and invasiveness compared with mice homozygous for the wild-type Fxyd5 allele

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:325989 )

• mice develop intestinal tumors unlike wild-type mice but at a slower rate and with reduced tumor load and invasiveness compared with mice homozygous for the wild-type Fxyd5 allele

Genotype
MGI:5529263

cx54

• Allelic Composition: Apc^Min/Apc⁺; Pla2g2a^Mom1-r/Pla2g2a⁺
• Genetic Background: either: (AKR/J x C57BL/6J-Apc^Min)F1 or (MA/MyJ x C57BL/6J-Apc^Min)F1 or (CAST/EiJ x C57BL/6J-Apc^Min)F1

neoplasm

decreased alimentary system tumor incidence ( J:15703 )

• controlled for age of the mice, the mean tumor incidence was 5.8 +/- 4.3 compared with 28.5 +/-7.9 in mice with a C57BL/6J background

• mice homozygous for Pla2g2a^Mom1-r from AKR/J produced by backcrossing the F1 to AKR/J produced offspring with a lower mean tumor incidence of 1.7 +/- 1.7

• mice heterozygous for Pla2g2a^Mom1-r from C57BL/6J and AKR/J produced by backcrossing the F1 to C57BL/6J show a mean tumor incidence significantly lower than seen in mice having a C57BL/6J background but significantly higher than mice homozygous for Pla2g2a from AKR/J

• inbred srains MA/MyJ and CAST/Ei also carry the tumor suppressing allele Pla2g2a^Mom1-r s

decreased intestinal adenoma incidence ( J:15703 )

• inbred strains AKR/J, MA/MyJ, and CAST/Ei are homozygous for the tumor suppressing allele Pla2g2a

digestive/alimentary system

decreased alimentary system tumor incidence ( J:15703 )

• controlled for age of the mice, the mean tumor incidence was 5.8 +/- 4.3 compared with 28.5 +/-7.9 in mice with a C57BL/6J background

• mice homozygous for Pla2g2a^Mom1-r from AKR/J produced by backcrossing the F1 to AKR/J produced offspring with a lower mean tumor incidence of 1.7 +/- 1.7

• mice heterozygous for Pla2g2a^Mom1-r from C57BL/6J and AKR/J produced by backcrossing the F1 to C57BL/6J show a mean tumor incidence significantly lower than seen in mice having a C57BL/6J background but significantly higher than mice homozygous for Pla2g2a from AKR/J

• inbred srains MA/MyJ and CAST/Ei also carry the tumor suppressing allele Pla2g2a^Mom1-r s

decreased intestinal adenoma incidence ( J:15703 )

• inbred strains AKR/J, MA/MyJ, and CAST/Ei are homozygous for the tumor suppressing allele Pla2g2a

Genotype
MGI:4429574

cx55

• Allelic Composition: Apc^Min/Apc^tm1Tno; Ctnnb1^tm4.1Wbm/Ctnnb1⁺
• Genetic Background: involves: 129 * 129P2/OlaHsd * 129S4/SvJae * C57BL/6

Anterior head defects during embryonic development in Apc^Min/Apc^tm1Tno embryos and rescue of head defects by Ctnnb1^tm4.1Wbm/Ctnnb1⁺

liver/biliary system

increased hepatocellular carcinoma incidence ( J:156864 )

• hepatocellular carcinomas (HCC) in 47% of mutant mice (n=15), including 20% that showed intestinal comorbidity

• mice only have HCC (n=4) live longer than Apc^min/+ mice

nervous system

nervous system phenotype ( J:156864 )

N • normal head morphology

craniofacial

craniofacial phenotype ( J:156864 )

N • normal head morphology

digestive/alimentary system

intestine polyps ( J:156864 )

• reduced tumor multiplicity and incidence, leaving 6 of 15 mice (40%) free of polyps

• the remaining macroscopic lesions are of tubulo-villous structure

• similar size and latency to those observed in age-matched Apc^min/+ mice

neoplasm

increased hepatocellular carcinoma incidence ( J:156864 )

• hepatocellular carcinomas (HCC) in 47% of mutant mice (n=15), including 20% that showed intestinal comorbidity

• mice only have HCC (n=4) live longer than Apc^min/+ mice

Genotype
MGI:4429575

cx56

• Allelic Composition: Apc^Min/Apc^Min; Ctnnb1^tm4.1Wbm/Ctnnb1⁺
• Genetic Background: involves: 129 * 129P2/OlaHsd * C57BL/6

mortality/aging

embryonic lethality between implantation and somite formation, complete penetrance ( J:156864 )

• death immediately after gastrulation

• embryos only detected at embryonic day 4.5 (E4.5) and E5.5 but not at later stages (E6 and E7)

Genotype
MGI:6108175

cx57

• Allelic Composition: Apc^Min/Apc⁺; Hltf^tm1.1Hdin/Hltf^tm1.1Hdin
• Genetic Background: involves: 129 * C57BL/6 * FVB/N

cellular

chromosomal instability ( J:252991 )

• aneuploidy owing to nonreciprocal translocations, chromosomal fusions (dicentric chromosomes, centromeric fusions, missing telomeres) and chromosomal fragments and breaks in cultured colon tumor cells

neoplasm

neoplasm ( J:252991 )

N • average 65 macroscopic intestine adenocarcinoma tumors per mouse, similar to wild-type

N • average 1.5 macroscopic colon adenocarcinoma tumors per mouse, similar to wild-type

increased metastatic potential ( J:252991 )

• invasive intestinal adenocarcinomas (deeper invasion of tumor cells into muscularis propria of small intestine)

• high beta-catenin activity in invaded neoplastic glandular cells in small intestine

• most colon tumors displayed a more severe glandular atypia resulting in formation of many mucin-filled cysts

• most colon tumors displayed strong desmoplastic stromal reaction

• higher beta-catenin activity in colon tumor cells

• transplanted colon tumor cells are malignant

Genotype
MGI:3700063

cx58

• Allelic Composition: Apc^Min/Apc⁺; Hpgds^tm1Urad/Hpgds⁺
• Genetic Background: involves: 129 * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:118232 )

• mice have 44-61% more intestinal adenomas than Apc-heterozygous controls

• 95% of adenomas are in small intestine, while colon adenomas are increased 2-fold

• adenomas tend to be smaller than in wild-type APC mutants (~.5 mm vs 0.68 mm in controls but difference is not significant

digestive/alimentary system

increased intestinal adenoma incidence ( J:118232 )

• mice have 44-61% more intestinal adenomas than Apc-heterozygous controls

• 95% of adenomas are in small intestine, while colon adenomas are increased 2-fold

• adenomas tend to be smaller than in wild-type APC mutants (~.5 mm vs 0.68 mm in controls but difference is not significant

Genotype
MGI:3700064

cx59

• Allelic Composition: Apc^Min/Apc⁺; Hpgds^tm1Urad/Hpgds^tm1Urad
• Genetic Background: involves: 129 * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:118232 )

• mice have 44-61% more intestinal adenomas than Apc-heterozygous controls

• 95% of adenomas are in small intestine, while colon adenomas are increased 2-fold

• adenomas tend to be smaller than in wild-type APC mutants (~.5 mm vs 0.68 mm in controls but difference is not significant

digestive/alimentary system

increased intestinal adenoma incidence ( J:118232 )

• mice have 44-61% more intestinal adenomas than Apc-heterozygous controls

• 95% of adenomas are in small intestine, while colon adenomas are increased 2-fold

• adenomas tend to be smaller than in wild-type APC mutants (~.5 mm vs 0.68 mm in controls but difference is not significant

Genotype
MGI:5636670

cx60

• Allelic Composition: Apc^Min/Apc⁺; Msh2^tm1Mak/Msh2^tm1Mak; Nos2^tm1Mrl/Nos2^tm1Mrl
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J

digestive/alimentary system

intestine polyps ( J:200824 )

• mutants exhibit similar polyp formation in the small intestine and colon as mice heterozygous for Apc^Min and homozygous for Msh2^tm1Mak

Genotype
MGI:5636667

cx61

• Allelic Composition: Apc^Min/Apc⁺; Msh2^tm1Mak/Msh2⁺; Nos2^tm1Mrl/Nos2^tm1Mrl
• Genetic Background: involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J

digestive/alimentary system

intestine polyps ( J:200824 )

• mutants exhibit enhanced polyp number in the small intestine, but not in the colon compared to double Apc^Min Msh2^tm1Mak heterozygotes

Genotype
MGI:3582674

cx62

• Allelic Composition: Apc^Min/Apc⁺; Blm^tm1Grdn/Blm⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S/SvEv * Black Swiss * C57BL/6J

neoplasm

increased gastrointestinal tumor incidence ( J:79058 )

• developed twice as many gastrointestinal adenomas as single heterozygous Apc mutant mice (31.4 tumors/mouse vs. 14.2 tumors/mouse in wildtype), however tumors were similar in size

increased intestinal adenoma incidence ( J:79058 )

• developed low- and high-grade adenomas in the small intestine, whereas only low-grade adenomas were seen in heterozygous Apc mutant mice

increased colon adenoma incidence ( J:79058 )

• all colonic adenomas displayed high-grade dysplasia

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:79058 )

• developed twice as many gastrointestinal adenomas as single heterozygous Apc mutant mice (31.4 tumors/mouse vs. 14.2 tumors/mouse in wildtype), however tumors were similar in size

increased intestinal adenoma incidence ( J:79058 )

• developed low- and high-grade adenomas in the small intestine, whereas only low-grade adenomas were seen in heterozygous Apc mutant mice

increased colon adenoma incidence ( J:79058 )

• all colonic adenomas displayed high-grade dysplasia

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Bloom syndrome		DOID:2717	OMIM:210900	J:79058

Genotype
MGI:4429611

cx63

• Allelic Composition: Apc^Min/Apc⁺; Msh2^tm1Htr/Msh2^tm1Htr
• Genetic Background: involves: 129P2/OlaHsd * BALB/c * C57BL/6J

mortality/aging

premature death ( J:45433 )

• survival is reduced 4-fold compared with Apc^Min heterozygotes

• all mice die within 5 months

neoplasm

increased gastrointestinal tumor incidence ( J:45433 )

• mice have an 8-fold increase in intestinal tumor load compared with Apc^Min heterozygotes

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:45433 )

• mice have an 8-fold increase in intestinal tumor load compared with Apc^Min heterozygotes

Genotype
MGI:5693797

cx64

• Allelic Composition: Apc^Min/Apc⁺; Ccdc80^tm1.1Ftk/Ccdc80^tm1.1Ftk
• Genetic Background: involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 * C57BL/6J * C57BL/6N

mortality/aging

premature death ( J:216704 )

• median survival is 94 days compared to 142 days in control Apc^Min heterozygotes

neoplasm

increased gastrointestinal tumor incidence ( J:216704 )

• mice develop tumors in the small intestine with no difference in number, distribution, size and histology from tumors in single Apc^Min heterozygotes

increased colon tumor incidence ( J:216704 )

• mean number of colonic tumors is 11.9 compared to 3.1 in control Apc^Min heterozygotes and mice show an increase in mean tumor multiplicity in both the proximal and distal colon

• by 10 weeks of age, mice show more tumors in the colon than in single Apc^Min heterozygotes, with 29% of tumors being adenocarcinoma

• no metastases to lymph nodes, liver or lungs are seen

increased colon adenoma incidence ( J:216704 )

• 65% of colon tumors are adenomas

increased colon adenocarcinoma incidence ( J:216704 )

• 35% of colon tumors are adenocarcinomas

• 97% of carcinomas are located in the distal colon

digestive/alimentary system

intestine polyps ( J:216704 )

• vast majority of polyps localize to the small intestine

increased gastrointestinal tumor incidence ( J:216704 )

• mice develop tumors in the small intestine with no difference in number, distribution, size and histology from tumors in single Apc^Min heterozygotes

increased colon tumor incidence ( J:216704 )

• mean number of colonic tumors is 11.9 compared to 3.1 in control Apc^Min heterozygotes and mice show an increase in mean tumor multiplicity in both the proximal and distal colon

• by 10 weeks of age, mice show more tumors in the colon than in single Apc^Min heterozygotes, with 29% of tumors being adenocarcinoma

• no metastases to lymph nodes, liver or lungs are seen

increased colon adenoma incidence ( J:216704 )

• 65% of colon tumors are adenomas

increased colon adenocarcinoma incidence ( J:216704 )

• 35% of colon tumors are adenocarcinomas

• 97% of carcinomas are located in the distal colon

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:216704

Genotype
MGI:3834880

cx65

• Allelic Composition: Apc^Min/Apc⁺; Foxl1^tm1Khk/Foxl1^tm1Khk
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

neoplasm

neoplasm ( J:95893 )

N • mutants do not show increased tumor multiplicity up to 90 days in the small intestine compared to heterozygous Apc^Min mice

increased colon adenoma incidence ( J:95893 )

• adenomatous polyps contain a large number of proliferating epithelial cells

• no evidence of invasion or metastases are observed in any tumors in the colon

digestive/alimentary system

colon polyps ( J:95893 )

• mice develop a 7.7-fold higher number of colonic polyps compared to heterozygous Apc^Min mice with wild-type Foxl1

increased colon adenoma incidence ( J:95893 )

• adenomatous polyps contain a large number of proliferating epithelial cells

• no evidence of invasion or metastases are observed in any tumors in the colon

gastric polyps ( J:95893 )

• mice develop an average of 5.5 polyps in the stomach by 3 months of age, compared to no polyps in heterozygous Apc^Min mice with wild-type Foxl1

• adenomatous polyps form in the stomach with disturbed glandular architecture and nuclear atypia; polyps contain large numbers of proliferating epithelial cells

cellular

abnormal cell physiology ( J:95893 )

• cells from adenomatous colonic polyps isolated from 30-day-old mice show loss of heterozygosity (LOH) of the wild-type Apc allele while colonic mucosa from heterozygous Apc^Min mice show no LOH

• cells from gastric adenomas isolated from 30-day-old mice show >90% loss of heterozygosity (LOH) of the wild-type Apc allele similar to LOH observed in adenomas from 79-day-old heterozygous Apc^Min mice

Genotype
MGI:3613447

cx66

• Allelic Composition: Apc^Min/Apc⁺; Zbtb33^tm1.1Bird/Y
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J

mortality/aging

premature death ( J:104155 )

♂ • life span of these animals is an average of 317 days; this is improved over Apc^Min mice alone at an average of 217 days

neoplasm

increased intestinal adenoma incidence ( J:104155 )

♂ • mice exhibit a similar number of intestinal tumors as compared to Apc^Min mice

decreased tumor growth/size ( J:104155 )

♂ • tumors in doubly heterozygous mice significantly smaller at 180 days of age

digestive/alimentary system

increased intestinal adenoma incidence ( J:104155 )

♂ • mice exhibit a similar number of intestinal tumors as compared to Apc^Min mice

Genotype
MGI:3579839

cx67

• Allelic Composition: Apc^Min/Apc⁺; Mbd2^tm1Bh/Mbd2⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J

mortality/aging

premature death ( J:83087 )

• although survival is reduced, they live longer than mice only heterozygous for Apc^Min

neoplasm

decreased tumor incidence ( J:83087 )

• tumor repression specific to the small intestine

Genotype
MGI:3579838

cx68

• Allelic Composition: Apc^Min/Apc⁺; Mbd2^tm1Bh/Mbd2^tm1Bh
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J

mortality/aging

mortality/aging ( J:83087 )

N • homozygotes survive significantly longer than mice only heterozygous for Apc^Min

neoplasm

decreased tumor growth/size ( J:83087 )

• tumors present are smaller in size

decreased tumor incidence ( J:83087 )

• at death, mice have a 10 fold reduction in adenomas

• adenomas that are present are restricted to Brunners gland and the distal 2 cm of the large intestine

Genotype
MGI:5426846

cx69

• Allelic Composition: Apc^Min/Apc⁺; Phgdh^tm1.1Shfu/Phgdh⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J

neoplasm

neoplasm ( J:183477 )

N • mice exhibit the same tumorigenesis as Apc^Min heterozygotes

Genotype
MGI:4946621

cx70

• Allelic Composition: Apc^Min/Apc⁺; Cd44^tm1Mak/Cd44^tm1Mak
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

neoplasm

decreased intestinal adenoma incidence ( J:135025 )

• an almost 50% reduction in intestinal adenoma number at 16 weeks

• strongly reduced number of aberrant crypts both at 8 weeks and at 16 weeks

• no change in mean adenoma diameter

digestive/alimentary system

increased small intestinal crypt cell apoptosis ( J:135025 )

• increased number of apoptotic cells in the intestinal crypt compartments shown by cleaved caspase-3 staining

• majority of these positive cells are localized below the transit-amplifying zone in the basal crypt compartment, between Paneth cells

• no change in proliferation

decreased intestinal adenoma incidence ( J:135025 )

• an almost 50% reduction in intestinal adenoma number at 16 weeks

• strongly reduced number of aberrant crypts both at 8 weeks and at 16 weeks

• no change in mean adenoma diameter

cellular

increased small intestinal crypt cell apoptosis ( J:135025 )

• increased number of apoptotic cells in the intestinal crypt compartments shown by cleaved caspase-3 staining

• majority of these positive cells are localized below the transit-amplifying zone in the basal crypt compartment, between Paneth cells

• no change in proliferation

Genotype
MGI:4359622

cx71

• Allelic Composition: Apc^Min/Apc⁺; Mom5^129P2/OlaHsd/?
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

neoplasm

decreased incidence of induced tumors ( J:152194 )

• significantly reduced incidence of intestinal adenoma (around 20-25)

Genotype
MGI:4366246

cx72

• Allelic Composition: Apc^Min/Apc⁺; Ptgs2^tm1Unc/Ptgs2^tm1Unc
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

premature death ( J:64401 )

• mice survive 1 year unlike Apc^Min heterozygotes that die after 7 to 8 months

neoplasm

decreased tumor incidence ( J:64401 )

• mice form 84% fewer, smaller intestinal tumors compared with Apc^Min heterozygotes

homeostasis/metabolism

decreased prostaglandin level ( J:64401 )

• intestinal tumor tissue fails to exhibit an increase in prostaglandin levels unlike in Apc^Min heterozygotes

digestive/alimentary system

intestine polyps ( J:64401 )

Genotype
MGI:4366247

cx73

• Allelic Composition: Apc^Min/Apc⁺; Ptgs1^tm1Unc/Ptgs1^tm1Unc
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

mortality/aging ( J:64401 )

N • mice live 12 months or longer unlike Apc^Min heterozygotes that die after 7 to 8 months

neoplasm

decreased tumor incidence ( J:64401 )

• mice form 77% fewer, smaller intestinal tumors than in Apc^Min heterozygotes

homeostasis/metabolism

decreased prostaglandin level ( J:64401 )

• prostaglandin levels in normal intestinal tissue is lower than in Apc^Min heterozygotes

• intestinal tumor tissue fails to exhibit an increase in prostaglandin levels unlike in Apc^Min heterozygotes

digestive/alimentary system

intestine polyps ( J:64401 )

Genotype
MGI:4366248

cx74

• Allelic Composition: Apc^Min/Apc⁺; Ptgs1^tm1Unc/Ptgs1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

premature death ( J:64401 )

• mice survive 10 months unlike Apc^Min heterozygotes that die after 7 to 8 months

neoplasm

decreased tumor incidence ( J:64401 )

• mice form 43% fewer tumors than in Apc^Min heterozygotes

digestive/alimentary system

intestine polyps ( J:64401 )

Genotype
MGI:3719427

cx75

• Allelic Composition: Apc^Min/Apc⁺; Mbd4^tm1Bird/Mbd4^tm1Bird
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

premature death ( J:77896 )

• mice exhibit reduced survival

neoplasm

increased intestinal adenoma incidence ( J:77896 )

• mice had a greater intestinal adenoma burden at death with a median of 28 tumors compared to Mbd4^tm1Bird Apc^Min heterozygotes (median of 14 tumors at time of death)

homeostasis/metabolism

abnormal DNA repair ( J:77896 )

• repair of C to T transitions is reduced to 88% efficiency from 96% in Mbd4^tm1Bird Apc^Min heterozygotes

cellular

abnormal DNA repair ( J:77896 )

• repair of C to T transitions is reduced to 88% efficiency from 96% in Mbd4^tm1Bird Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:77896 )

• mice had a greater intestinal adenoma burden at death with a median of 28 tumors compared to Mbd4^tm1Bird Apc^Min heterozygotes (median of 14 tumors at time of death)

Genotype
MGI:5319648

cx76

• Allelic Composition: Apc^Min/Apc⁺; Tcf7^tm1Cle/Tcf7^tm1Cle
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

neoplasm

increased salivary gland tumor incidence ( J:57721 )

• 60% of mice with adenomas and adenoacanthomas of the salivary glands at 6 months of age

increased intestinal adenoma incidence ( J:57721 )

• adenomatous polyps form throughout the intestine

• large in size but showing no signs of tumor progression

increased mammary adenoacanthoma incidence ( J:57721 )

• adenoacanthomas in the mammary glands of all female mice by 8 weeks of age

• also in older male mice

digestive/alimentary system

increased salivary gland tumor incidence ( J:57721 )

• 60% of mice with adenomas and adenoacanthomas of the salivary glands at 6 months of age

increased intestinal adenoma incidence ( J:57721 )

• adenomatous polyps form throughout the intestine

• large in size but showing no signs of tumor progression

endocrine/exocrine glands

increased salivary gland tumor incidence ( J:57721 )

• 60% of mice with adenomas and adenoacanthomas of the salivary glands at 6 months of age

increased mammary adenoacanthoma incidence ( J:57721 )

• adenoacanthomas in the mammary glands of all female mice by 8 weeks of age

• also in older male mice

integument

increased mammary adenoacanthoma incidence ( J:57721 )

• adenoacanthomas in the mammary glands of all female mice by 8 weeks of age

• also in older male mice

growth/size/body

increased salivary gland tumor incidence ( J:57721 )

• 60% of mice with adenomas and adenoacanthomas of the salivary glands at 6 months of age

craniofacial

increased salivary gland tumor incidence ( J:57721 )

• 60% of mice with adenomas and adenoacanthomas of the salivary glands at 6 months of age

Genotype
MGI:3700062

cx77

• Allelic Composition: Apc^Min/Apc⁺; Ptgds^tm1Ohy/Ptgds^tm1Ohy
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:118232 )

• mice with Ptgds deficiency do not show altered adenoma profile compared to Apc heterozygous Ptgds-wild-type mice

digestive/alimentary system

increased intestinal adenoma incidence ( J:118232 )

• mice with Ptgds deficiency do not show altered adenoma profile compared to Apc heterozygous Ptgds-wild-type mice

Genotype
MGI:3610196

cx78

• Allelic Composition: Apc^Min/Apc⁺; Hp^tm1Skl/Hp^tm1Skl
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

neoplasm

increased gastrointestinal tumor incidence ( J:75249 )

• intestinal tumor burden at 60-65 days of age increased by 2-3 fold

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:75249 )

• intestinal tumor burden at 60-65 days of age increased by 2-3 fold

Genotype
MGI:5636659

cx79

• Allelic Composition: Apc^Min/Apc⁺; Msh2^tm1Mak/Msh2^tm1Mak
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

premature death ( J:75393 )

• mice become moribound and die from anemia and intestinal obstruction at a mean age of 82 days

neoplasm

increased intestinal adenoma incidence ( J:75393 )

• mice exhibit accelerated intestinal tumorigenesis compared to single Apc^Min heterozygous mice, with a large increase in number of small and large bowel adenomas that develop

• an average of 333 adenomas are seen in 10 mutants at 47-78 days of age compared to a mean of 48 adenomas in single Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:75393 )

• mice exhibit accelerated intestinal tumorigenesis compared to single Apc^Min heterozygous mice, with a large increase in number of small and large bowel adenomas that develop

• an average of 333 adenomas are seen in 10 mutants at 47-78 days of age compared to a mean of 48 adenomas in single Apc^Min heterozygotes

intestine polyps ( J:200824 )

intestinal obstruction ( J:75393 )

• due to tumors

hematopoietic system

anemia ( J:75393 )

• mutants exhibit enhanced polyp formation in the small intestine and colon at 6 weeks of age compared to double heterozygous mice

• treatment with the Nos2 (iNOS) inhibitor L-NIL has no effect on polyp number

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:75393 , J:200824

Genotype
MGI:5448541

cx80

• Allelic Composition: Apc^Min/Apc⁺; Trp53^tm1Mlh/Trp53^tm1Mlh
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * SWR

neoplasm

increased pancreatic acinar cell carcinoma incidence ( J:29664 )

• 22% of mice with abnormalities of the exocrine pancreas also have pancreatic acinar cell adenocarcinoma

• whole pancreatic lobules are involved implicating a stem cell mutation

endocrine/exocrine glands

abnormal exocrine pancreas morphology ( J:29664 )

• 83% of mice of this genotype show a range of exocrine pancreas abnormalities with dysplasia and preneoplastic foci seen in 61% of the mice

• these tumors have lost the wild-type copy of Apc

• this genotype does not increase the rate or rate of progression of intestinal adenoma

increased pancreatic acinar cell carcinoma incidence ( J:29664 )

• 22% of mice with abnormalities of the exocrine pancreas also have pancreatic acinar cell adenocarcinoma

• whole pancreatic lobules are involved implicating a stem cell mutation

digestive/alimentary system

abnormal exocrine pancreas morphology ( J:29664 )

• 83% of mice of this genotype show a range of exocrine pancreas abnormalities with dysplasia and preneoplastic foci seen in 61% of the mice

• these tumors have lost the wild-type copy of Apc

• this genotype does not increase the rate or rate of progression of intestinal adenoma

Genotype
MGI:5696099

cx81

• Allelic Composition: Apc^Min/Apc⁺; Dnd1^Ter/Dnd1⁺
• Genetic Background: involves: 129P3/J * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:221231 )

• 1.5X increase in intestinal tumor rate relative to Apc single heterozygotes

• significantly elevated polyp mass

digestive/alimentary system

increased intestinal adenoma incidence ( J:221231 )

• 1.5X increase in intestinal tumor rate relative to Apc single heterozygotes

• significantly elevated polyp mass

Genotype
MGI:3722288

cx82

• Allelic Composition: Apc^Min/Apc^Min; Rr27^tm1Rohl/Rr27⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:97083 )

• mice develop twice as many intestinal and colonic adenomas as in Apc^Min homozygotes

increased colon adenoma incidence ( J:97083 )

• mice develop twice as many colonic adenomas as in Apc^Min homozygotes

digestive/alimentary system

abnormal crypts of Lieberkuhn morphology ( J:97083 )

• mice have longer crypts than wild-type mice

increased intestinal adenoma incidence ( J:97083 )

• mice develop twice as many intestinal and colonic adenomas as in Apc^Min homozygotes

increased colon adenoma incidence ( J:97083 )

• mice develop twice as many colonic adenomas as in Apc^Min homozygotes

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:97083 )

• mice have longer crypts than wild-type mice

Genotype
MGI:4946925

cx83

• Allelic Composition: Apc^Min/Apc⁺; Tcf7l2^{tm1.1(EGFP/cre)Mrc}/Tcf7l2⁺
• Genetic Background: involves: 129S1/Sv * 129X1/SvJ * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

Genotype
MGI:3831111

cx84

• Allelic Composition: Apc^Min/Apc⁺; Tgfbr1^tm1Bopa/Tgfbr1⁺
• Genetic Background: involves: 129S1/SvImJ * C57BL/6J

neoplasm

increased gastrointestinal tumor incidence ( J:143706 )

• mice develop twice as many intestinal tumors as in Apc^Min heterozygotes

• mice develop small and predominantly scattered tumors in the small intestine as well as colonic tumors

increased intestinal adenocarcinoma incidence ( J:143706 )

• 3 mice develop large, polyploidy and ulcerated colonic tumors

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:143706 )

• mice develop twice as many intestinal tumors as in Apc^Min heterozygotes

• mice develop small and predominantly scattered tumors in the small intestine as well as colonic tumors

increased intestinal adenocarcinoma incidence ( J:143706 )

• 3 mice develop large, polyploidy and ulcerated colonic tumors

cellular

increased cell proliferation ( J:143706 )

• mouse embryonic fibroblasts treated with TGFbeta exhibit a reduced decrease in proliferation compared to similarly treated wild-type mice

• proliferation of intestinal crypt epithelium is increased compared to in wild-type mice

hematopoietic system

hematopoietic system phenotype ( J:143706 )

N • despite disruptions in cell proliferation, hematopoiesis is normal

Genotype
MGI:4365606

cx85

• Allelic Composition: Apc^Min/Apc⁺; Il6^tm1Kopf/Il6^tm1Kopf
• Genetic Background: involves: 129S2/SvPas * C57BL/6

muscle

muscle phenotype ( J:130429 )

N • no gastrocnemius muscle wasting

adipose tissue

adipose tissue phenotype ( J:130429 )

N • normal epididymal fat pads

neoplasm

abnormal tumor incidence ( J:130429 )

• numbers of gastrointestinal polyps 32% lower at 26 weeks than when both Il6 alleles are wild-type

• polyp sizes are reduced

Genotype
MGI:5298870

cx86

• Allelic Composition: Apc^Min/Apc⁺; Esr1^tm1.1Mma/Esr1^tm1.1Mma
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

mortality/aging

preweaning lethality, complete penetrance ( J:118600 )

• no mice are produced

Genotype
MGI:4820588

cx87

• Allelic Composition: Apc^Min/Apc⁺; Pms2^tm1Lisk/Pms2^tm1Lisk
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

mortality/aging

premature death ( J:46419 )

• mice die earlier than Apc^min heterozygotes

neoplasm

increased intestinal adenoma incidence ( J:46419 )

• mice develop 2.3 times more adenomatous polyps in the intestine compared with Apc^min heterozygotes

• however, no evidence of adenocarcinoma is observed

• tumors exhibit microsatellite instability

digestive/alimentary system

increased intestinal adenoma incidence ( J:46419 )

• mice develop 2.3 times more adenomatous polyps in the intestine compared with Apc^min heterozygotes

• however, no evidence of adenocarcinoma is observed

• tumors exhibit microsatellite instability

intestine polyps ( J:46419 )

• mice develop 2.3 times more adenomatous polyps in the intestine compared with Apc^min heterozygotes

Genotype
MGI:4357790

cx88

• Allelic Composition: Apc^Min/Apc⁺; Hdac2^{Gt(W035F03)Joe}/Hdac2^{Gt(W035F03)Joe}
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

neoplasm

increased small intestine adenocarcinoma incidence ( J:152134 )

• intestinal adenocarcinoma occurs in these mice though not to the extent as in Apc^Min controls

decreased tumor incidence ( J:152134 )

• mice develop fewer intestinal tumors than Apc^Min controls

• the small intestine of female mice had 60% fewer tumors than controls

• mice fail to develop tumors in the colon while they are occasionally found in the colon of Apc^Min controls

digestive/alimentary system

increased small intestine adenocarcinoma incidence ( J:152134 )

• intestinal adenocarcinoma occurs in these mice though not to the extent as in Apc^Min controls

Genotype
MGI:5298871

cx89

• Allelic Composition: Apc^Min/Apc⁺; Esr1^tm1.1Mma/Esr1⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

neoplasm

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

increased colon adenoma incidence ( J:118600 )

• noninvasive

increased carcinoma incidence ( J:118600 )

• all mice develop invasive carcinomas in the intestine and colon unlike Apc^min heterozygotes

digestive/alimentary system

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon

abnormal intestinal mucosa morphology ( J:118600 )

• some mice exhibit abnormal submucosal with thickening of the muscularis mucosae and enrichment of stromal components compared with Apc^min heterozygotes

abnormal large intestine crypts of Lieberkuhn morphology ( J:118600 )

• some mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice

abnormal colon goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevalent pregoblet cells

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

increased colon adenoma incidence ( J:118600 )

• noninvasive

endocrine/exocrine glands

abnormal large intestine crypts of Lieberkuhn morphology ( J:118600 )

• some mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice

abnormal colon goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevalent pregoblet cells

cellular

abnormal colon goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevalent pregoblet cells

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon

Genotype
MGI:5298868

cx90

• Allelic Composition: Apc^Min/Apc⁺; Esr2^tm1Mma/Esr2⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

neoplasm

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

digestive/alimentary system

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon in ovariectomized

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

cellular

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon in ovariectomized

Genotype
MGI:5298869

cx91

• Allelic Composition: Apc^Min/Apc⁺; Esr2^tm1Mma/Esr2^tm1Mma
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

digestive/alimentary system

abnormal colon goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevalent pregoblet cells

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the large intestine, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

increased colon adenoma incidence ( J:118600 )

• noninvasive

colitis ( J:118600 )

• mononuclear cell infiltrates in the colon

neoplasm

increased gastrointestinal tumor incidence ( J:118600 )

• mice develop increased tumors in the large intestine, including the cecum and one third of the colons, compared with Apc^min heterozygotes

• mice develop sessile and pedunculated forms of colonic adenomas unlike Apc^min heterozygotes

• while tumor progression is stimulated to a greater extent than in Apc^min heterozygotes, tumor initiation is the same

increased colon adenoma incidence ( J:118600 )

• noninvasive

immune system

colitis ( J:118600 )

• mononuclear cell infiltrates in the colon

cellular

abnormal colon goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevalent pregoblet cells

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon

endocrine/exocrine glands

abnormal colon goblet cell morphology ( J:118600 )

• fewer mature goblet cells in the colon with prevalent pregoblet cells

Genotype
MGI:6377634

cx92

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm11(tetO-Nup88)Jvd}/Col1a1⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

digestive/alimentary system

increased colon tumor incidence ( J:231166 )

• doxycycline (dox)-treated mice show increased incidence of colon tumors compared to single Apc^Min heterozygotes, but tumor multiplicity or size is unaffected and there is no difference in the multiplicity of small intestinal polyps

• mice in which dox is discontinued 30 days before analysis, show the same incidence of colon tumors as in mice with continuous administration of dox

neoplasm

increased colon tumor incidence ( J:231166 )

• doxycycline (dox)-treated mice show increased incidence of colon tumors compared to single Apc^Min heterozygotes, but tumor multiplicity or size is unaffected and there is no difference in the multiplicity of small intestinal polyps

• mice in which dox is discontinued 30 days before analysis, show the same incidence of colon tumors as in mice with continuous administration of dox

Genotype
MGI:4430577

cx93

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm1(CAG-Sirt1)Dsin}/Col1a1⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

increased gastrointestinal tumor incidence ( J:134301 )

• mice develop intestinal tumors in the duodenum and ileum

growth/size/body

cachexia ( J:134301 )

• at 16 weeks

hematopoietic system

anemia ( J:134301 )

• at 16 weeks

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:134301 )

• mice develop intestinal tumors in the duodenum and ileum

Genotype
MGI:3839104

cx94

• Allelic Composition: Apc^Min/Apc⁺; Ptprh^tm1.1Mato/Ptprh^tm1.1Mato
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

decreased incidence of induced tumors ( J:146871 )

• mice develop fewer small intestinal macroadenomas compared to Apc^Min heterozygotes

• however, proliferation and apoptosis within the tumor mass is the same as in Apc^Min heterozygotes

Genotype
MGI:5313419

cx95

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm9(tetO-Dnmt3b_i1)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:127808 )

• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apc^min heterozygotes

increased tumor growth/size ( J:127808 )

• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apc^min heterozygotes

• doxycycline-treated mice exhibit increased size of microadenomas compared with Apc^min heterozygotes

cellular

abnormal DNA methylation ( J:127808 )

• doxycycline-treated mice exhibit loss of imprinting and increased expression of Igf2 compared with control mice

• doxycycline-treated mice exhibit biallelic methylation of H19 differentially methylated region in tumors and normal colon epithelial cells compared with control mice

• doxycycline-treated mice exhibit hypermethylation of Sfrp2, Sfrp4 and Sfrp5 in tumors and normal colon epithelial cells unlike control mice

• however, mice exhibit normal methylation of of Snrpn differentially methylated region in tumors and normal colon epithelial cells, and global DNA methylation

digestive/alimentary system

increased intestinal adenoma incidence ( J:127808 )

• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apc^min heterozygotes

Genotype
MGI:5313420

cx96

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm10(tetO-Dnmt3b_i3)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

neoplasm ( J:127808 )

N • doxycycline-treated mice develop intestinal adenomas at the same rate as in Apc^min heterozygotes

Genotype
MGI:5313421

cx97

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm11(tetO-Dnmt3b_i6)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

neoplasm ( J:127808 )

N • doxycycline-treated mice develop intestinal adenomas at the same rate as in Apc^min heterozygotes

Genotype
MGI:5313423

cx98

• Allelic Composition: Apc^Min/Apc⁺; Col1a1^{tm12(tetO-Dnmt3a_i1)Jae}/Col1a1⁺; Gt(ROSA)26Sor^{tm1(rtTA*M2)Jae}/Gt(ROSA)26Sor⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J

neoplasm

neoplasm ( J:127808 )

N • doxycycline-treated mice develop intestinal adenomas at the same rate as in Apc^min heterozygotes

Genotype
MGI:3848451

cx99

• Allelic Composition: Apc^Min/Apc⁺; Dnmt1^tm1Jae/Dnmt1⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6J

digestive/alimentary system

intestine polyps ( J:75230 )

• mice exhibit fewer intestinal polyps compared with Apc^Min heterozygotes

• polyps are smaller than in Apc^Min heterozygotes

Genotype
MGI:3848450

cx100

• Allelic Composition: Apc^Min/Apc⁺; Dnmt1^tm1Pwl/Dnmt1⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6J

digestive/alimentary system

intestine polyps ( J:75230 )

• mice exhibit fewer intestinal polyps compared with Apc^Min heterozygotes

• polyps are smaller than in Apc^Min heterozygotes

Genotype
MGI:3848453

cx101

• Allelic Composition: Apc^Min/Apc⁺; Dnmt1^tm1Jae/Dnmt1^tm1Pwl
• Genetic Background: involves: 129S4/SvJae * C57BL/6J

digestive/alimentary system

digestive/alimentary phenotype ( J:75230 )

N • no intestinal polyps are observed unlike in Apc^Min heterozygotes

Genotype
MGI:6502661

cx102

• Allelic Composition: Apc^Min/Apc⁺; Map9^tm1.2Bcgen/Map9⁺
• Genetic Background: involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6 * C57BL/6J

neoplasm

increased colon tumor incidence ( J:299895 )

• nearly all mice develop intestinal tumors at 3 months of age, with 2 of 10 mice showing multiple tumors

digestive/alimentary system

increased colon tumor incidence ( J:299895 )

• nearly all mice develop intestinal tumors at 3 months of age, with 2 of 10 mice showing multiple tumors

Genotype
MGI:6502660

cx103

• Allelic Composition: Apc^Min/Apc⁺; Map9^tm1.2Bcgen/Map9^tm1.2Bcgen
• Genetic Background: involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6 * C57BL/6J

mortality/aging

premature death ( J:299895 )

neoplasm

increased colon tumor incidence ( J:299895 )

• nearly all mice develop intestinal tumors at 3 months of age, with 5 of 8 mice showing multiple tumors

• mice have 3-fold more tumors that heterozygous Apc^Min heterozygotes, accompanied by significant weight loss

• average tumor burden (sum of all tumor size per mouse) is 2x greater than in Apc^Min heterozygotes

• colon tumors harbor chromosomal abnormalities, with tumors having more somatic structural variations, interchromosomal translocations, and intrachromosomal translocations

digestive/alimentary system

increased colon tumor incidence ( J:299895 )

• mice have 3-fold more tumors that heterozygous Apc^Min heterozygotes, accompanied by significant weight loss

• average tumor burden (sum of all tumor size per mouse) is 2x greater than in Apc^Min heterozygotes

• nearly all mice develop intestinal tumors at 3 months of age, with 5 of 8 mice showing multiple tumors

• colon tumors harbor chromosomal abnormalities, with tumors having more somatic structural variations, interchromosomal translocations, and intrachromosomal translocations

Genotype
MGI:6849775

cx104

• Allelic Composition: Apc^Min/Apc⁺; Zfp82^tm1.2Cya/Zfp82^tm1.2Cya
• Genetic Background: involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6NTac

digestive/alimentary system

increased colon tumor incidence ( J:316087 )

• 4-fold increase compared with mice heterozygous for Apc^Min

neoplasm

increased colon tumor incidence ( J:316087 )

• 4-fold increase compared with mice heterozygous for Apc^Min

Genotype
MGI:6849776

cx105

• Allelic Composition: Apc^Min/Apc⁺; Zfp82^tm1.2Cya/Zfp82⁺
• Genetic Background: involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6NTac

digestive/alimentary system

increased colon tumor incidence ( J:316087 )

• 4-fold increase compared with mice heterozygous for Apc^Min

neoplasm

increased colon tumor incidence ( J:316087 )

• 4-fold increase compared with mice heterozygous for Apc^Min

Genotype
MGI:2653701

cx106

• Allelic Composition: Apc^Min/Apc^Min; Asph^tm1Jed/Asph^tm1Jed
• Genetic Background: involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6J * C57BL/6NTac

mortality/aging

premature death ( J:75888 )

• double mutants become morbidly ill and were sacrificed at an average age of 89 days unlike single homozyous Apc^Min mice that all survive to 110 days of age (the experimental end point)

neoplasm

increased gastrointestinal tumor incidence ( J:75888 )

• approximately 2-fold increase in small intestinal tumor number and increase in tumor size compared to single homozygous Apc^Min mice

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:75888 )

• approximately 2-fold increase in small intestinal tumor number and increase in tumor size compared to single homozygous Apc^Min mice

Genotype
MGI:5451046

cx107

• Allelic Composition: Apc^Min/Apc⁺; Dp(17Nfkbil1-Or2h1)1Cogr/0
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6J

neoplasm

neoplasm ( J:190754 )

N • mice exhibit the same tumor-free survival as Apc^Min heterozygotes

Genotype
MGI:3512138

cx108

• Allelic Composition: Apc^Min/Apc⁺; Ereg^tm1Dwt/Ereg^tm1Dwt
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:93327 )

• the number, average size, and location of intestinal polyps is similar to Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:93327 )

• the number, average size, and location of intestinal polyps is similar to Apc^Min heterozygotes

Genotype
MGI:5446699

cx109

• Allelic Composition: Apc^Min/Apc⁺; Il22ra2^tm2Vlcg/Il22ra2^tm2Vlcg
• Genetic Background: involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac

neoplasm

increased intestinal adenoma incidence ( J:189217 )

• in the colon but not the small intestine compared to compared to mice heterozygous for Apc^Min alone

increased tumor growth/size ( J:189217 )

• in the colon but not the small intestine compared to compared to mice heterozygous for Apc^Min alone

digestive/alimentary system

increased intestinal adenoma incidence ( J:189217 )

• in the colon but not the small intestine compared to compared to mice heterozygous for Apc^Min alone

Genotype
MGI:3812011

cx110

• Allelic Composition: Apc^Min/Apc⁺; Myc^tm1Jlc/Myc⁺
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J

mortality/aging

mortality/aging ( J:134087 )

N • mice exhibit a life span of 291 days compared to 169 days in Apc^Min heterozygotes

digestive/alimentary system

intestine polyps ( J:134087 )

• mice develop fewer and smaller polyps than in Apc^Min heterozygotes

abnormal digestive system physiology ( J:134087 )

• cell proliferation in polyps is decreased compared to in Apc^Min heterozygotes while levels of apoptosis are increased compared to in Apc^Min heterozygotes and wild-type mice

hematopoietic system

hematopoietic system phenotype ( J:134087 )

N • unlike in Apc^Min heterozygotes, hematocrit levels and spleen size are normal

abnormal hematopoietic system morphology/development ( J:134087 )

• expression of angiogenic factors is decreased compared to in Apc^Min heterozygotes

Genotype
MGI:3575580

cx111

• Allelic Composition: Apc^Min/Apc⁺; Recql4^tm1Glu/Recql4^tm1Glu
• Genetic Background: involves: 129S7/SvEvBrd * C57BL/6J

neoplasm

increased tumor growth/size ( J:97101 )

• the average maximal diameter of macroadenomas was larger than in double heterozygous controls

increased adenoma incidence ( J:97101 )

• at 120 days of age, exhibited a 2-fold increase in the multiplicity of macroadenomas along the entire GI tract compared to double heterozygous mutant controls, however no difference in the mean or maximal lifespan compared to controls

increased colon adenoma incidence ( J:97101 )

• mutants always developed tumors in the large intestine, a site that is inconsistently affected in double heterozygous controls

digestive/alimentary system

increased colon adenoma incidence ( J:97101 )

• mutants always developed tumors in the large intestine, a site that is inconsistently affected in double heterozygous controls

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Rothmund-Thomson syndrome		DOID:2732	OMIM:268400	J:97101

Genotype
MGI:3510235

cx112

• Allelic Composition: Apc^Min/Apc⁺; Ppard^tm1Jps/Ppard^tm1Jps
• Genetic Background: involves: 129/Sv * AKR/J * C57BL/6 * C57BL/6J

neoplasm

increased intestinal adenocarcinoma incidence ( J:90337 )

• colon cancer is more severe and mortality occurs earlier than in controls

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:90337 )

• colon cancer is more severe and mortality occurs earlier than in controls

intestine polyps ( J:90337 )

• increased numbers of small intestine polyps as well in females

Genotype
MGI:5446700

cx113

• Allelic Composition: Apc^Min/Apc⁺; Il22^tm1Flv/Il22^tm1Flv
• Genetic Background: involves: 129/Sv * C57BL/6 * C57BL/6J

neoplasm

decreased alimentary system tumor incidence ( J:189217 )

• decrease in tumor numbers in the small intestine and colon compared to mice heterozygous for Apc^Min alone

digestive/alimentary system

decreased alimentary system tumor incidence ( J:189217 )

• decrease in tumor numbers in the small intestine and colon compared to mice heterozygous for Apc^Min alone

Genotype
MGI:3803126

cx114

• Allelic Composition: Apc^Min/Apc⁺; Mmom2^129X1/SvJ/Mmom2^C57BL/6J
• Genetic Background: involves: 129X1/SvJ * C57BL/6J

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

• increased tumor latency

integument

decreased mammary gland tumor incidence ( J:128481 )

• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

• increased tumor latency

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

• increased tumor latency

Genotype
MGI:3709984

cx115

• Allelic Composition: Apc^Min/Apc^Min; Sat1^tm1Alh/Y
• Genetic Background: involves: 129X1/SvJ * C57BL/6J

neoplasm

decreased tumor incidence ( J:99381 )

♂ • total tumor counts in small intestine were reduced by about 75% for both small and large tumors

♂ • however, there is no significant effect on colonic tumor number or size despite the fact that Sat1 over-expression increases tumor number about 6-fold

Genotype
MGI:3623317

cx116

• Allelic Composition: Apc^Min/Apc⁺; Egfr^Wa5/Egfr⁺
• Genetic Background: involves: BALB/cAnN * C3H/HeN * C57BL/6J

neoplasm

decreased tumor incidence ( J:92308 )

• 46% reduction in the number of macroscopic intestinal polyps in comparison to mice heterozygous only for Apc^Min at 3 months of age

• no reduction in tumor size

Genotype
MGI:4461429

cx117

• Allelic Composition: Apc^Min/Apc⁺; Pla2g2a^Mom1-r/?; Prkdc^dxnph/Prkdc^dxnph
• Genetic Background: involves: BALB/cByJ * C57BL/6

neoplasm

increased incidence of tumors by ionizing radiation induction ( J:83497 )

• mice show 2-3 fold increase in adenoma incidence in the small intestine after X-irradiation

Genotype
MGI:6357720

cx118

• Allelic Composition: Apc^Min/Apc⁺; Mapkapk2^tm1.2Gkl/Mapkapk2^tm1.2Gkl
• Genetic Background: involves: BALB/cJ * C57BL/6J

mortality/aging

increased tumor-free survival time ( J:262876 )

• mice exhibit increased survival compared with Apc^min heterozygotes

neoplasm

abnormal tumor vascularization ( J:262876 )

• reduced tumor angiogenesis to in Apc^min heterozygotes

• however, inflammation in tumors is the same as in Apc^min heterozygotes

increased intestinal adenoma incidence ( J:262876 )

• at 8 weeks, mice develop the same number of microadenomas as in Apc^min heterozygotes

• however, fewer microadenomas and adenomas at later time points

decreased tumor growth/size ( J:262876 )

• smaller tumors and microadenomas compared with Apc^min heterozygotes

decreased tumor incidence ( J:262876 )

• mice exhibit reduced number of tumor, adenomas and microadenomas compared with Apc^min heterozygotes

• mice fail to exhibit adenocarcinomas/carcinomas at 22 weeks unlike Apc^min heterozygotes

• due to reduced proliferation and increased apoptosis levels of tumor cells compared with Apc^min heterozygotes

• reduced proliferation compared with Apc^min heterozygotes

• chimera reconstitution experiments indicate that nonhematopoietic cells are responsible for tumor suppression

digestive/alimentary system

increased intestinal adenoma incidence ( J:262876 )

• at 8 weeks, mice develop the same number of microadenomas as in Apc^min heterozygotes

• however, fewer microadenomas and adenomas at later time points

intestine polyps ( J:262876 )

• fewer than in Apc^min heterozygotes

cardiovascular system

abnormal tumor vascularization ( J:262876 )

• reduced tumor angiogenesis to in Apc^min heterozygotes

• however, inflammation in tumors is the same as in Apc^min heterozygotes

hematopoietic system

hematopoietic system phenotype ( J:262876 )

N • mice exhibit normal spleen size unlike Apc^min heterozygotes

immune system

abnormal chemokine secretion ( J:262876 )

• decreased secretion of MIP2 and MMP9 from intestinal mesenchymal cells in culture stimulated with IL1beta, TNF or TGFbeta compared with cells from Apc^min heterozygotes

decreased interleukin-6 secretion ( J:262876 )

• from intestinal mesenchymal cells in culture stimulated with IL1beta, TNF or TGFbeta compared with cells from Apc^min heterozygotes

Genotype
MGI:7434699

cx119

• Allelic Composition: Apc^Min/Apc⁺; Del(15Rr357-Rr303293)2Jta/Del(15Rr357-Rr303293)2Jta
• Genetic Background: involves: C57BL/6

digestive/alimentary system

decreased colon tumor incidence ( J:257088 )

• fewer polyps

neoplasm

decreased colon tumor incidence ( J:257088 )

• fewer polyps

Genotype
MGI:5475210

cx120

• Allelic Composition: Apc^Min/Apc⁺; Dclk1^{tm1.1(cre/ERT2)Seno}/Dclk1^{tm1.1(cre/ERT2)Seno}
• Genetic Background: involves: C57BL/6

digestive/alimentary system

intestine polyps ( J:193873 )

• Dclk1 mutant homozygotes develop polyps in similar numbers and with similar size distribution as Dclk1 wild-type, Apc^Min/+ controls

Genotype
MGI:3829423

cx121

• Allelic Composition: Apc^Min/Apc⁺; Tg(Rorc-EGFP)1Ebe/?
• Genetic Background: involves: C57BL/6

immune system

abnormal effector T cell morphology ( J:137020 )

• in the mesenteric lymph node (MLN), the ratio of IL-17 producing cells to Foxp3-positive cells within the GFP-positive T cell population is significantly decreased compared to controls

• this observation is compared to an induced-colitis control where ratio of the two effector cell populations remain the same in the MLN despite inflammation occuring

enlarged mesenteric lymph nodes ( J:137020 )

• mesenteric lymph nodes are hyperplastic

lymph node hyperplasia ( J:137020 )

• mesenteric lymph nodes are hyperplastic

digestive/alimentary system

intestine polyps ( J:137020 )

• ileal polyps occur in these mice

colon polyps ( J:137020 )

• occur in these mice

hematopoietic system

abnormal effector T cell morphology ( J:137020 )

• in the mesenteric lymph node (MLN), the ratio of IL-17 producing cells to Foxp3-positive cells within the GFP-positive T cell population is significantly decreased compared to controls

• this observation is compared to an induced-colitis control where ratio of the two effector cell populations remain the same in the MLN despite inflammation occuring

Genotype
MGI:5463417

cx122

• Allelic Composition: Apc^Min/Apc⁺; Rr21^tm1Jta/Rr21⁺
• Genetic Background: involves: C57BL/6

digestive/alimentary system

intestine polyps ( J:191217 )

• similar frequency of intestinal polyps compared to mice heterozygous for Apc^Min alone

Genotype
MGI:6470552

cx123

• Allelic Composition: Apc^Min/Apc⁺; Bcl2l14^tm1.1Boui/Bcl2l14^tm1.1Boui
• Genetic Background: involves: C57BL/6 * C57BL/6J

neoplasm

increased colon tumor incidence ( J:296081 )

• mice develop colon tumors but show no difference in overall number or size of colon tumors in the proximal, middle, or distal small intestine compared to single heterozygous Apc^Min mice and no difference in tumor epithelial proliferation

digestive/alimentary system

increased colon tumor incidence ( J:296081 )

• mice develop colon tumors but show no difference in overall number or size of colon tumors in the proximal, middle, or distal small intestine compared to single heterozygous Apc^Min mice and no difference in tumor epithelial proliferation

Genotype
MGI:3811523

cx124

• Allelic Composition: Apc^Min/Apc⁺; Slc5a8^tm1.1Boet/Slc5a8^tm1.1Boet
• Genetic Background: involves: C57BL/6 * C57BL/6J

neoplasm

increased colon adenoma incidence ( J:139883 )

• mice develop colon tumors at the same rate as Apc^Min homozygotes

digestive/alimentary system

increased colon adenoma incidence ( J:139883 )

• mice develop colon tumors at the same rate as Apc^Min homozygotes

Genotype
MGI:2183289

cx125

• Allelic Composition: Apc^Min/Apc⁺; Mmp7^tm1Lmm/Mmp7^tm1Lmm
• Genetic Background: involves: C57BL/6 * C57BL/6J

neoplasm

abnormal tumor morphology ( J:38609 )

• average diameter of tumors is 20% smaller

increased tumor incidence ( J:38609 )

• although tumor incidence is increased relative to wild-type controls, incidence is reduced in comparison to animals heterozygous for Apc but Mmp7<+/+> by 58% (from 25.4 to 10.5 tumors/animal)

Genotype
MGI:7568795

cx126

• Allelic Composition: Apc^Min/Apc⁺; Tnfaip8l1^em1Huwa/Tnfaip8l1^em1Huwa
• Genetic Background: involves: C57BL/6 * C57BL/6J

mortality/aging

premature death ( J:342074 )

• survival of mice is comparable to that of single heterozygous Apc^Min mice, with mice starting to die by 20 weeks of age and most dying by 30 weeks of age

digestive/alimentary system

increased colon tumor incidence ( J:342074 )

• mice develop colon tumors and show no difference in tumor number or tumor load from that of single heterozygous Apc^Min mice and no difference in formation of sporadic tumors is seen

neoplasm

increased colon tumor incidence ( J:342074 )

• mice develop colon tumors and show no difference in tumor number or tumor load from that of single heterozygous Apc^Min mice and no difference in formation of sporadic tumors is seen

Genotype
MGI:5463415

cx127

• Allelic Composition: Apc^Min/Apc⁺; Rr21^tm1.1Jta/Rr21^tm1.1Jta
• Genetic Background: involves: C57BL/6 * FVB/N

digestive/alimentary system

intestine polyps ( J:191217 )

• decrease in the frequency of intestinal polyps compared to mice heterozygous for Apc^Min alone

Genotype
MGI:2446655

cx128

• Allelic Composition: Apc^Min/Apc⁺; Dcc^tm1Wbg/Dcc⁺
• Genetic Background: involves: C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:39765 )

• heterozygosity for the Dcc allele did not affect the polyp initiation or average size or morphology of the adenomas that occur in the Apc^Min heterozygous mice

digestive/alimentary system

increased intestinal adenoma incidence ( J:39765 )

• heterozygosity for the Dcc allele did not affect the polyp initiation or average size or morphology of the adenomas that occur in the Apc^Min heterozygous mice

Genotype
MGI:3827117

cx129

• Allelic Composition: Apc^Min/Apc⁺; Glp2r^tm1Ddr/Glp2r⁺
• Genetic Background: involves: C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

abnormal tumor morphology ( J:141821 )

• size similar to situation in Apc^Min heterozygous mice

digestive/alimentary system

abnormal intestinal epithelium morphology ( J:141821 )

• villus height is similar to Apc^Min heterozygotes

abnormal crypts of Lieberkuhn morphology ( J:141821 )

• crypt morphology is similar to Apc^Min heterozygotes

increased intestinal adenoma incidence ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

intestine polyps ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:141821 )

• crypt morphology is similar to Apc^Min heterozygotes

Genotype
MGI:3827123

cx130

• Allelic Composition: Apc^Min/Apc⁺; Glp2r^tm1Ddr/Glp2r^tm1Ddr
• Genetic Background: involves: C57BL/6J

digestive/alimentary system

abnormal intestinal epithelium morphology ( J:141821 )

• villus height is similar to Apc^Min heterozygotes

abnormal crypts of Lieberkuhn morphology ( J:141821 )

• crypt morphology is similar to Apc^Min heterozygotes

increased intestinal adenoma incidence ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

intestine polyps ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:141821 )

• crypt morphology is similar to Apc^Min heterozygotes

neoplasm

increased intestinal adenoma incidence ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

abnormal tumor morphology ( J:141821 )

• size similar to situation in Apc^Min heterozygous mice

Genotype
MGI:4359621

cx131

• Allelic Composition: Apc^Min/Apc⁺; Mom5^C57BL/6J/Mom5^C57BL/6J
• Genetic Background: involves: C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:152194 )

• higher numbers of intestinal adenomas in homozygotes than in heterozygotes (around 50-55)

digestive/alimentary system

increased intestinal adenoma incidence ( J:152194 )

• higher numbers of intestinal adenomas in homozygotes than in heterozygotes (around 50-55)

Genotype
MGI:3715726

cx132

• Allelic Composition: Apc^Min/Apc^Min; Ppard^tm1.1Rev/Ppard^tm1.1Rev
• Genetic Background: involves: C57BL/6J

digestive/alimentary system

increased intestinal adenoma incidence ( J:73557 )

• polyps are low grade noninvasive tubular adenomas

intestine polyps ( J:73557 )

• mice harbor conspicuous intestinal polyps; average number is similar to wild-type and heterozygous mice

• there is a decrease in large diameter polyps relative to controls, while small polyp number is similar between all groups

colon polyps ( J:73557 )

• mice harbor conspicuous colonic polyps

neoplasm

increased intestinal adenoma incidence ( J:73557 )

• polyps are low grade noninvasive tubular adenomas

Genotype
MGI:4946927

cx133

• Allelic Composition: Apc^Min/Apc⁺; Tcf7l2^tm2.2Mrc/Tcf7l2⁺
• Genetic Background: involves: C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

Genotype
MGI:5544112

cx134

• Allelic Composition: Apc^Min/Apc⁺; Cd44^tm2Stpa/Cd44^tm2Stpa
• Genetic Background: involves: C57BL/6J

digestive/alimentary system

decreased intestinal adenoma incidence ( J:204874 )

• decreased adenoma and microadenoma compared with Apc^Min heterozygotes without a change in intestinal crypt apoptosis and proliferation rates

mortality/aging

increased tumor-free survival time ( J:204874 )

• mice survive longer than Apc^Min heterozygotes

neoplasm

decreased intestinal adenoma incidence ( J:204874 )

• decreased adenoma and microadenoma compared with Apc^Min heterozygotes without a change in intestinal crypt apoptosis and proliferation rates

Genotype
MGI:5544114

cx135

• Allelic Composition: Apc^Min/Apc⁺; Cd44^tm1Stpa/Cd44^tm2Stpa
• Genetic Background: involves: C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:204874 )

• mice develop the same number of intestinal adenoma and microadenoma as in Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:204874 )

• mice develop the same number of intestinal adenoma and microadenoma as in Apc^Min heterozygotes

Genotype
MGI:5544115

cx136

• Allelic Composition: Apc^Min/Apc⁺; Cd44^tm1Mak/Cd44^tm1Mak
• Genetic Background: involves: C57BL/6J

mortality/aging

increased tumor-free survival time ( J:204874 )

• mice survive longer than Apc^Min heterozygotes

neoplasm

decreased intestinal adenoma incidence ( J:204874 )

• decreased adenoma and microadenoma compared with Apc^Min heterozygotes without a change in intestinal crypt apoptosis and proliferation rates

digestive/alimentary system

increased enterocyte apoptosis ( J:204874 )

• compared with Apc^Min heterozygotes

decreased intestinal adenoma incidence ( J:204874 )

• decreased adenoma and microadenoma compared with Apc^Min heterozygotes without a change in intestinal crypt apoptosis and proliferation rates

cellular

increased enterocyte apoptosis ( J:204874 )

• compared with Apc^Min heterozygotes

Genotype
MGI:6113599

cx137

• Allelic Composition: Apc^Min/Apc⁺; Tnik^tm1Teya/Tnik^tm1Teya
• Genetic Background: involves: C57BL/6J

digestive/alimentary system

decreased alimentary system tumor incidence ( J:241611 )

• mice develop significantly lower number of tumors in the small intestine and colon than single Apc^Min heterozygous mice

neoplasm

decreased alimentary system tumor incidence ( J:241611 )

• mice develop significantly lower number of tumors in the small intestine and colon than single Apc^Min heterozygous mice

Genotype
MGI:6121392

cx138

• Allelic Composition: Apc^Min/Apc⁺; Spata18^tm1.2Hifa/Spata18^tm1.2Hifa
• Genetic Background: involves: C57BL/6J

neoplasm

abnormal tumor susceptibility ( J:254117 )

• compared to Apc controls

increased classified tumor incidence ( J:254117 )

• compared to Apc controls

increased intestinal adenocarcinoma incidence ( J:254117 )

increased colon adenocarcinoma incidence ( J:254117 )

increased small intestine adenocarcinoma incidence ( J:254117 )

• significantly increased cell proliferative potential

increased intestinal adenoma incidence ( J:254117 )

• high grade adenoma

• significantly increased cell proliferative potential in small intestine compared to Apc::Spata18 mutants and to Apc controls

increased colon adenoma incidence ( J:254117 )

• high grade adenoma

• significantly increased cell proliferative potential compared to Apc::Spata18 mutants

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:254117 )

increased colon adenocarcinoma incidence ( J:254117 )

increased small intestine adenocarcinoma incidence ( J:254117 )

• significantly increased cell proliferative potential

increased intestinal adenoma incidence ( J:254117 )

• high grade adenoma

• significantly increased cell proliferative potential in small intestine compared to Apc::Spata18 mutants and to Apc controls

increased colon adenoma incidence ( J:254117 )

• high grade adenoma

• significantly increased cell proliferative potential compared to Apc::Spata18 mutants

intestine polyps ( J:254117 )

• increased number compared to Apc controls

• significantly increased size compared to Apc controls

cellular

abnormal mitochondrial crista morphology ( J:254117 )

• substantial increase in nitrotyrosine and 8-OHdG immunoreactivity in small intestinal adenoma and adenocarcinoma tumors

• significant reduction in internal cristae density in small intestine mucosal epithelium and adenoma and adenocarcinoma tumor cells

hematopoietic system

anemia ( J:254117 )

• more severe compared to Apc controls, caused by increased intestinal hemorrhage

mortality/aging

premature death ( J:254117 )

• reduced lifespan, compared to Apc controls, as a result of severe anemia

Genotype
MGI:6121393

cx139

• Allelic Composition: Apc^Min/Apc⁺; Spata18^tm1.2Hifa/Spata18⁺
• Genetic Background: involves: C57BL/6J

neoplasm

abnormal tumor susceptibility ( J:254117 )

• compared to Apc controls

increased classified tumor incidence ( J:254117 )

• compared to Apc controls

increased intestinal adenocarcinoma incidence ( J:254117 )

increased colon adenocarcinoma incidence ( J:254117 )

increased small intestine adenocarcinoma incidence ( J:254117 )

• significantly increased cell proliferative potential

increased intestinal adenoma incidence ( J:254117 )

• high grade adenoma

• significantly increased cell proliferative potential in small intestine

increased colon adenoma incidence ( J:254117 )

• high grade adenoma

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:254117 )

increased colon adenocarcinoma incidence ( J:254117 )

increased small intestine adenocarcinoma incidence ( J:254117 )

• significantly increased cell proliferative potential

increased intestinal adenoma incidence ( J:254117 )

• high grade adenoma

• significantly increased cell proliferative potential in small intestine

increased colon adenoma incidence ( J:254117 )

• high grade adenoma

intestine polyps ( J:254117 )

• increased number compared to Apc controls

• significantly increased size compared to Apc controls

cellular

abnormal mitochondrial crista morphology ( J:254117 )

• substantial increase in nitrotyrosine and 8-OHdG immunoreactivity in small intestinal adenoma and adenocarcinoma tumors

hematopoietic system

anemia ( J:254117 )

• more severe compared to Apc controls, caused by increased intestinal hemorrhage

mortality/aging

premature death ( J:254117 )

• reduced lifespan, compared to Apc controls, as a result of severe anemia

Genotype
MGI:3045027

cx140

• Allelic Composition: Apc^Min/Apc⁺; Ccnd1^tm1Dsn/Ccnd1^tm1Dsn
• Genetic Background: involves: C57BL/6J

neoplasm

increased intestinal adenoma incidence ( J:78500 )

• mice heterozygous for "multiple intestinal neoplasia" (F2 Min) and homozygous null for Ccnd1^tm1Dsn developed significantly fewer tumors (tumor range: 1-39) than mice doubly heterozygous for Min and Ccnd1^tm1Dsn (tumor range: 3-129) or mice heterozygous for Min and wild-type for Ccnd1 (tumor range: 2-112)

• no difference in tumor size was observed between the various Ccnd1 genotypes in heterozygous F2 Min mice

• also, no association was found between tumor number and animal weight

digestive/alimentary system

increased intestinal adenoma incidence ( J:78500 )

• mice heterozygous for "multiple intestinal neoplasia" (F2 Min) and homozygous null for Ccnd1^tm1Dsn developed significantly fewer tumors (tumor range: 1-39) than mice doubly heterozygous for Min and Ccnd1^tm1Dsn (tumor range: 3-129) or mice heterozygous for Min and wild-type for Ccnd1 (tumor range: 2-112)

• no difference in tumor size was observed between the various Ccnd1 genotypes in heterozygous F2 Min mice

• also, no association was found between tumor number and animal weight

Genotype
MGI:3032868

cx141

• Allelic Composition: Apc^Min/Apc⁺; Thbs1^tm1Hyn/Thbs1^tm1Hyn
• Genetic Background: involves: C57BL/6J

mortality/aging

premature death ( J:79641 )

neoplasm

increased tumor incidence ( J:79641 )

increased intestinal adenoma incidence ( J:79641 )

increased carcinoma incidence ( J:79641 )

• intestinal carcinoma in situ

digestive/alimentary system

abnormal intestine morphology ( J:79641 )

• intestinal dysplasia

increased intestinal adenoma incidence ( J:79641 )

growth/size/body

weight loss ( J:79641 )

hematopoietic system

anemia ( J:79641 )

skeleton

lordosis ( J:79641 )

Genotype
MGI:6367566

cx142

• Allelic Composition: Gata6os^em1Zfa/Gata6os^em1Zfa; Apc^Min/Apc⁺
• Genetic Background: involves: C57BL/6J

mortality/aging

extended life span ( J:268724 )

• compared with Apc^Min heterozygotes

neoplasm

decreased intestinal adenoma incidence ( J:268724 )

• fewer adenoma and increased survival compared with Apc^Min heterozygotes

digestive/alimentary system

decreased intestinal adenoma incidence ( J:268724 )

• fewer adenoma and increased survival compared with Apc^Min heterozygotes

Genotype
MGI:5544111

cx143

• Allelic Composition: Apc^Min/Apc⁺; Cd44^tm1Stpa/Cd44^tm1Stpa
• Genetic Background: involves: C57BL/6J * C57BL/6JIco

mortality/aging

premature death ( J:204874 )

• as in Apc^Min heterozygotes

neoplasm

increased intestinal adenoma incidence ( J:204874 )

• mice develop the same number of intestinal adenoma and microadenoma as in Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:204874 )

• mice develop the same number of intestinal adenoma and microadenoma as in Apc^Min heterozygotes

Genotype
MGI:6864129

cx144

• Allelic Composition: Apc^Min/Apc⁺; Mir708^tm1Wtsi/Mir708^tm1Wtsi
• Genetic Background: involves: C57BL/6J * C57BL/6N

mortality/aging

premature death ( J:317482 )

• not as much as in Apc^Min heterozygotes

neoplasm

increased colon adenoma incidence ( J:317482 )

• not as much as in Apc^Min heterozygotes with reduced lethality

digestive/alimentary system

increased colon adenoma incidence ( J:317482 )

• not as much as in Apc^Min heterozygotes with reduced lethality

abnormal intestinal epithelium physiology ( J:317482 )

• reduced organoid formation from crypt cells from AOM/DSS-induced colorectal cancer model mice

Genotype
MGI:6806148

cx145

• Allelic Composition: Apc^Min/Apc⁺; Tmem9^{tm1d(EUCOMM)Wtsi}/Tmem9⁺
• Genetic Background: involves: C57BL/6J * C57BL/6N

mortality/aging

extended life span ( J:268691 )

• mice exhibit a median survival of 199 days versus 124 days in Apc^Min heterozygotes

neoplasm

decreased intestinal adenoma incidence ( J:268691 )

• at 3 months of age, the number of intestinal adenomas is significantly lower than that in Apc^Min heterozygotes

• however, tumor size is not significantly changed despite a reduction in cell proliferation

digestive/alimentary system

decreased intestinal adenoma incidence ( J:268691 )

• at 3 months of age, the number of intestinal adenomas is significantly lower than that in Apc^Min heterozygotes

• however, tumor size is not significantly changed despite a reduction in cell proliferation

Genotype
MGI:6806147

cx146

• Allelic Composition: Apc^Min/Apc⁺; Tmem9^{tm1d(EUCOMM)Wtsi}/Tmem9^{tm1d(EUCOMM)Wtsi}
• Genetic Background: involves: C57BL/6J * C57BL/6N

mortality/aging

extended life span ( J:268691 )

• mice exhibit a median survival of 323 days versus 124 days in Apc^Min heterozygotes

neoplasm

decreased intestinal adenoma incidence ( J:268691 )

• at 3 months of age, the number of intestinal adenomas is significantly lower than that in Apc^Min heterozygotes

abnormal tumor pathology ( J:268691 )

• at 3 months of age, intestinal adenomas show downregulation of Wnt/beta-catenin target genes, reduced cell proliferation, and a decreased number of nuclear beta-catenin-positive cells relative to those in Apc^Min heterozygotes

• however, no differences in apoptosis or epithelial-mesenchymal transition are observed

decreased tumor growth/size ( J:268691 )

• at 3 months of age, the size of intestinal adenomas is slightly smaller than that in Apc^Min heterozygotes

digestive/alimentary system

decreased intestinal adenoma incidence ( J:268691 )

• at 3 months of age, the number of intestinal adenomas is significantly lower than that in Apc^Min heterozygotes

Genotype
MGI:3653360

cx147

• Allelic Composition: Apc^Min/Apc⁺; Atp5f1a^Mom2/Atp5f1a⁺
• Genetic Background: involves: C57BL/6J * DBA/2J

neoplasm

decreased tumor incidence ( J:73854 )

• resistance to intestinal polyps

Genotype
MGI:3653359

cx148

• Allelic Composition: Apc^Min/Apc⁺; Atp5f1a^Mom2/Atp5f1a^Mom2
• Genetic Background: involves: C57BL/6J * DBA/2J

neoplasm

decreased tumor incidence ( J:73854 )

• resistance to intestinal polyps

Genotype
MGI:3700065

cx149

• Allelic Composition: Apc^Min/Apc⁺; Tg(CAG-PGDS)S-55Hjl/0
• Genetic Background: involves: C57BL/6J * FVB/N

neoplasm

increased intestinal adenoma incidence ( J:118232 )

• transgenic mice have 70-80% fewer adenomas than controls

digestive/alimentary system

increased intestinal adenoma incidence ( J:118232 )

• transgenic mice have 70-80% fewer adenomas than controls

Genotype
MGI:4950747

cx150

• Allelic Composition: Apc^Min/Apc⁺; Tg(Vil1-PPARGC1A)#Amos/0
• Genetic Background: involves: C57BL/6J * FVB/N

neoplasm

decreased alimentary system tumor incidence ( J:171361 )

• fewer intestinal tumors form than in controls

• tumors are smaller in size than in controls

decreased tumor growth/size ( J:171361 )

• fewer intestinal tumors form

• average size of intestinal tumors is reduced

• higher apoptosis rates in intestinal tumors

digestive/alimentary system

decreased alimentary system tumor incidence ( J:171361 )

• fewer intestinal tumors form than in controls

• tumors are smaller in size than in controls

Genotype
MGI:3803123

cx151

• Allelic Composition: Apc^Min/Apc⁺; Mmom1^C57BL/6J/Mmom1^FVB/NTac
• Genetic Background: involves: C57BL/6J * FVB/NTac

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

integument

decreased mammary gland tumor incidence ( J:128481 )

• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

Genotype
MGI:3803124

cx152

• Allelic Composition: Apc^Min/Apc⁺; Mmom1^C57BL/6J/Mmom1^FVB/NTac; Mmom3^C57BL/6J/Mmom3^FVB/NTac
• Genetic Background: involves: C57BL/6J * FVB/NTac

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

• 50% decrease in mammary tumor number after ENU mutagenesis compared to C57BL/6J-homozygous females

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

• 50% decrease in mammary tumor number after ENU mutagenesis compared to C57BL/6J-homozygous females

integument

decreased mammary gland tumor incidence ( J:128481 )

• 50% decrease in mammary tumor number after ENU mutagenesis compared to C57BL/6J-homozygous females

Genotype
MGI:3803125

cx153

• Allelic Composition: Apc^Min/Apc⁺; Mmom2^C57BL/6J/Mmom2^FVB/NTac
• Genetic Background: involves: C57BL/6J * FVB/NTac

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

• 24% decrease in mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

• increased tumor latency

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

• 24% decrease in mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

• increased tumor latency

integument

decreased mammary gland tumor incidence ( J:128481 )

• 24% decrease in mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

• increased tumor latency

Genotype
MGI:3803127

cx154

• Allelic Composition: Apc^Min/Apc⁺; Mmom2^C57BL/6J/Mmom2^FVB/NTac; Mmom3^C57BL/6J/Mmom3^FVB/NTac
• Genetic Background: involves: C57BL/6J * FVB/NTac

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

integument

decreased mammary gland tumor incidence ( J:128481 )

• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females

Genotype
MGI:3803128

cx155

• Allelic Composition: Apc^Min/Apc⁺; Mmom2^C57BL/6J/Mmom2^FVB/NTac; Mmom4^C57BL/6J/Mmom4^FVB/NTac
• Genetic Background: involves: C57BL/6J * FVB/NTac

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

• increased tumor latency after ENU treatment compared to C57BL/6J-homozygous females

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

• increased tumor latency after ENU treatment compared to C57BL/6J-homozygous females

integument

decreased mammary gland tumor incidence ( J:128481 )

• increased tumor latency after ENU treatment compared to C57BL/6J-homozygous females

Genotype
MGI:3803129

cx156

• Allelic Composition: Apc^Min/Apc⁺; Mmom4^C57BL/6J/Mmom4^FVB/NTac
• Genetic Background: involves: C57BL/6J * FVB/NTac

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

• increased mammary tumor latency after ENU treatment compared to C57BL/6J-homozygous females

integument

decreased mammary gland tumor incidence ( J:128481 )

• increased mammary tumor latency after ENU treatment compared to C57BL/6J-homozygous females

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

• increased mammary tumor latency after ENU treatment compared to C57BL/6J-homozygous females