Phenotypes associated with this allele

• Allele Symbol: Apc^Min
• Allele Name: multiple intestinal neoplasia
• Allele ID: MGI:1856318
• Summary: 151 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^+ Dclk1^tm1.1(cre/ERT2)Seno/Dclk1^+ Gt(ROSA)26Sor^tm1(HBEGF)Awai/Gt(ROSA)26Sor^+ Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor^+	involves: 129S4/SvJaeSor * C57BL/6	MGI:5475206
cn26	Apc^Min/Apc^+ Erbb3^tm1.1Dwt/Erbb3^tm2.1Dwt Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL	MGI:4360363
cn27	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
cn28	Apc^Min/Apc^+ Gpa33^tm1(GNAS)Wtsi/Gpa33^+ Hprt1^tm1(CMV-cre)Brd/?	involves: 129S7/SvEvBrd * C57BL/6J	MGI:4889209
cn29	Apc^Min/Apc^+ Mapkapk2^tm1.1Gkl/Mapkapk2^tm1.1Gkl Twist2^tm1.1(cre)Dor/Twist2^+	involves: 129X1/SvJ * BALB/cJ * C57BL/6J	MGI:6357723
cn30	Apc^Min/Apc^+ Lmna^tm4Stw/Lmna^tm4Stw Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J	MGI:5774439
cn31	Apc^Min/Apc^+ Elp3^tm1.1Tac/Elp3^tm1.1Tac Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * C57BL/6NTac * SJL	MGI:5898003
cn32	Apc^Min/Apc^+ Igf2bp1^tm1Vssp/Igf2bp1^tm1Vssp Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:5523866
cx33	Apc^Min/Apc^+ Brca2^tm1Mbn/Brca2^+	B6.Cg-Brca2^tm1Mbn Apc^Min	MGI:3814367
cx34	Apc^Min/Apc^+ Gt(ROSA)26Sor/Gt(ROSA)26Sor^+	B6.Cg-Gt(ROSA)26Sor Apc^Min	MGI:5014351
cx35	Apc^Min/Apc^+ Mir10a^tm1.1Ahl/Mir10a^tm1.1Ahl	B6.Cg-Mir10a^tm1.1Ahl Apc^min	MGI:5567980
cx36	Apc^Min/Apc^+ Mthfs^Gt(RRK291)Byg/Mthfs^+	B6.Cg-Mthfs^Gt(RRK291)Byg Apc^Min	MGI:5430745
cx37	Apc^Min/Apc^+ Nos2^tm1Lau/Nos2^+	B6.Cg-Nos2^tm1Lau Apc^Min	MGI:3767792
cx38	Apc^Min/Apc^+ Nos2^tm1Lau/Nos2^tm1Lau	B6.Cg-Nos2^tm1Lau Apc^Min	MGI:3767791
cx39	Apc^Min/Apc^+ Pla2g4a^tm1Jvb/Pla2g4a^tm1Jvb	B6.Cg-Pla2g4a^tm1Jvb Apc^Min	MGI:4358774
cx40	Apc^Min/Apc^+ Rab25^tm1Jrgo/Rab25^+	B6.Cg-Rab25^tm1Jrgo Apc^Min	MGI:4440864
cx41	Apc^Min/Apc^+ Rab25^tm1Jrgo/Rab25^tm1Jrgo	B6.Cg-Rab25^tm1Jrgo Apc^Min	MGI:4440863
cx42	Apc^Min/Apc^+ Shmt1^Gt(AD0236)Wtsi/Shmt1^Gt(AD0236)Wtsi	B6.Cg-Shmt1^Gt(AD0236)Wtsi Apc^Min	MGI:5426849
cx43	Apc^Min/Apc^+ Tgfbr1^tm1Bopa/Tgfbr1^+	B6.Cg-Tgfbr1^tm1Bopa Apc^Min	MGI:3831112
cx44	Apc^Min/Apc^+ Arhgef4^tm1Taki/Arhgef4^tm1Taki	B6J.Cg-Arhgef4^tm1Taki Apc^Min	MGI:5881919
cx45	Apc^Min/Apc^+ Arhgef4^tm1Taki/Arhgef4^+	B6J.Cg-Arhgef4^tm1Taki Apc^Min	MGI:5881920
cx46	Apc^Min/Apc^+ Arhgef4^tm1Taki/Arhgef4^tm1Taki Spata13^tm1Taki/Spata13^tm1Taki	B6J.Cg-Arhgef4^tm1Taki Spata13^tm1Taki Apc^Min	MGI:5881925
cx47	Apc^Min/Apc^+ Spata13^tm1Taki/Spata13^tm1Taki	B6J.Cg-Spata13^tm1Taki Apc^Min	MGI:5881916
cx48	Apc^Min/Apc^+ Spata13^tm1Taki/Spata13^+	B6J.Cg-Spata13^tm1Taki Apc^Min	MGI:5881917
cx49	Apc^Min/Apc^+ Fxyd5^em1Namje/Fxyd5^em1Namje	C57BL/6J-Fxyd5^em1Namje Apc^min	MGI:7310033
cx50	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
cx51	Apc^Min/Apc^tm1Tno Ctnnb1^tm4.1Wbm/Ctnnb1^+	involves: 129 * 129P2/OlaHsd * 129S4/SvJae * C57BL/6	MGI:4429574
cx52	Apc^Min/Apc^Min Ctnnb1^tm4.1Wbm/Ctnnb1^+	involves: 129 * 129P2/OlaHsd * C57BL/6	MGI:4429575
cx53	Apc^Min/Apc^+ Hltf^tm1.1Hdin/Hltf^tm1.1Hdin	involves: 129 * C57BL/6 * FVB/N	MGI:6108175
cx54	Apc^Min/Apc^+ Hpgds^tm1Urad/Hpgds^tm1Urad	involves: 129 * C57BL/6J	MGI:3700064
cx55	Apc^Min/Apc^+ Hpgds^tm1Urad/Hpgds^+	involves: 129 * C57BL/6J	MGI:3700063
cx56	Apc^Min/Apc^+ Msh2^tm1Mak/Msh2^tm1Mak Nos2^tm1Mrl/Nos2^tm1Mrl	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J	MGI:5636670
cx57	Apc^Min/Apc^+ Msh2^tm1Mak/Msh2^+ Nos2^tm1Mrl/Nos2^tm1Mrl	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J	MGI:5636667
cx58	Apc^Min/Apc^+ Blm^tm1Grdn/Blm^+	involves: 129P2/OlaHsd * 129S/SvEv * Black Swiss * C57BL/6J	MGI:3582674
cx59	Apc^Min/Apc^+ Msh2^tm1Htr/Msh2^tm1Htr	involves: 129P2/OlaHsd * BALB/c * C57BL/6J	MGI:4429611
cx60	Apc^Min/Apc^+ Ccdc80^tm1.1Ftk/Ccdc80^tm1.1Ftk	involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 * C57BL/6J * C57BL/6N	MGI:5693797
cx61	Apc^Min/Apc^+ Foxl1^tm1Khk/Foxl1^tm1Khk	involves: 129P2/OlaHsd * C57BL/6	MGI:3834880
cx62	Apc^Min/Apc^+ Phgdh^tm1.1Shfu/Phgdh^+	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:5426846
cx63	Apc^Min/Apc^+ Mbd2^tm1Bh/Mbd2^+	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:3579839
cx64	Apc^Min/Apc^+ Mbd2^tm1Bh/Mbd2^tm1Bh	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:3579838
cx65	Apc^Min/Apc^+ Zbtb33^tm1.1Bird/Y	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:3613447
cx66	Apc^Min/Apc^+ Hp^tm1Skl/Hp^tm1Skl	involves: 129P2/OlaHsd * C57BL/6J	MGI:3610196
cx67	Apc^Min/Apc^+ Ptgds^tm1Ohy/Ptgds^tm1Ohy	involves: 129P2/OlaHsd * C57BL/6J	MGI:3700062
cx68	Apc^Min/Apc^+ Mbd4^tm1Bird/Mbd4^tm1Bird	involves: 129P2/OlaHsd * C57BL/6J	MGI:3719427
cx69	Apc^Min/Apc^+ Mom5^129P2/OlaHsd/?	involves: 129P2/OlaHsd * C57BL/6J	MGI:4359622
cx70	Apc^Min/Apc^+ Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366246
cx71	Apc^Min/Apc^+ Ptgs1^tm1Unc/Ptgs1^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366247
cx72	Apc^Min/Apc^+ Ptgs1^tm1Unc/Ptgs1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366248
cx73	Apc^Min/Apc^+ Cd44^tm1Mak/Cd44^tm1Mak	involves: 129P2/OlaHsd * C57BL/6J	MGI:4946621
cx74	Apc^Min/Apc^+ Tcf7^tm1Cle/Tcf7^tm1Cle	involves: 129P2/OlaHsd * C57BL/6J	MGI:5319648
cx75	Apc^Min/Apc^+ Msh2^tm1Mak/Msh2^tm1Mak	involves: 129P2/OlaHsd * C57BL/6J	MGI:5636659
cx76	Apc^Min/Apc^+ Trp53^tm1Mlh/Trp53^tm1Mlh	involves: 129P2/OlaHsd * C57BL/6 * SWR	MGI:5448541
cx77	Apc^Min/Apc^+ Dnd1^Ter/Dnd1^+	involves: 129P3/J * C57BL/6J	MGI:5696099
cx78	Apc^Min/Apc^Min Rr27^tm1Rohl/Rr27^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:3722288
cx79	Apc^Min/Apc^+ Tcf7l2^tm1.1(EGFP/cre)Mrc/Tcf7l2^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:4946925
cx80	Apc^Min/Apc^+ Tgfbr1^tm1Bopa/Tgfbr1^+	involves: 129S1/SvImJ * C57BL/6J	MGI:3831111
cx81	Apc^Min/Apc^+ Il6^tm1Kopf/Il6^tm1Kopf	involves: 129S2/SvPas * C57BL/6	MGI:4365606
cx82	Apc^Min/Apc^+ Esr1^tm1.1Mma/Esr1^tm1.1Mma	involves: 129S2/SvPas * C57BL/6J	MGI:5298870
cx83	Apc^Min/Apc^+ Esr2^tm1Mma/Esr2^tm1Mma	involves: 129S2/SvPas * C57BL/6J	MGI:5298869
cx84	Apc^Min/Apc^+ Pms2^tm1Lisk/Pms2^tm1Lisk	involves: 129S2/SvPas * C57BL/6J	MGI:4820588
cx85	Apc^Min/Apc^+ Esr2^tm1Mma/Esr2^+	involves: 129S2/SvPas * C57BL/6J	MGI:5298868
cx86	Apc^Min/Apc^+ Hdac2^Gt(W035F03)Joe/Hdac2^Gt(W035F03)Joe	involves: 129S2/SvPas * C57BL/6J	MGI:4357790
cx87	Apc^Min/Apc^+ Esr1^tm1.1Mma/Esr1^+	involves: 129S2/SvPas * C57BL/6J	MGI:5298871
cx88	Apc^Min/Apc^+ Col1a1^tm1(CAG-Sirt1)Dsin/Col1a1^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:4430577
cx89	Apc^Min/Apc^+ Col1a1^tm11(tetO-Nup88)Jvd/Col1a1^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:6377634
cx90	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
cx91	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
cx92	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
cx93	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
cx94	Apc^Min/Apc^+ Ptprh^tm1.1Mato/Ptprh^tm1.1Mato	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:3839104
cx95	Apc^Min/Apc^+ Dnmt1^tm1Jae/Dnmt1^tm1Pwl	involves: 129S4/SvJae * C57BL/6J	MGI:3848453
cx96	Apc^Min/Apc^+ Dnmt1^tm1Jae/Dnmt1^+	involves: 129S4/SvJae * C57BL/6J	MGI:3848451
cx97	Apc^Min/Apc^+ Dnmt1^tm1Pwl/Dnmt1^+	involves: 129S4/SvJae * C57BL/6J	MGI:3848450
cx98	Apc^Min/Apc^+ Map9^tm1.2Bcgen/Map9^tm1.2Bcgen	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6 * C57BL/6J	MGI:6502660
cx99	Apc^Min/Apc^+ Map9^tm1.2Bcgen/Map9^+	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6 * C57BL/6J	MGI:6502661
cx100	Apc^Min/Apc^+ Zfp82^tm1.2Cya/Zfp82^tm1.2Cya	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6NTac	MGI:6849775
cx101	Apc^Min/Apc^+ Zfp82^tm1.2Cya/Zfp82^+	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6NTac	MGI:6849776
cx102	Apc^Min/Apc^Min Asph^tm1Jed/Asph^tm1Jed	involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6J * C57BL/6NTac	MGI:2653701
cx103	Apc^Min/Apc^+ Dp(17Nfkbil1-Or2h1)1Cogr/0	involves: 129S6/SvEvTac * C57BL/6J	MGI:5451046
cx104	Apc^Min/Apc^+ Ereg^tm1Dwt/Ereg^tm1Dwt	involves: 129S6/SvEvTac * C57BL/6J	MGI:3512138
cx105	Apc^Min/Apc^+ Il22ra2^tm2Vlcg/Il22ra2^tm2Vlcg	involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac	MGI:5446699
cx106	Apc^Min/Apc^+ Myc^tm1Jlc/Myc^+	involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J	MGI:3812011
cx107	Apc^Min/Apc^+ Recql4^tm1Glu/Recql4^tm1Glu	involves: 129S7/SvEvBrd * C57BL/6J	MGI:3575580
cx108	Apc^Min/Apc^+ Ppard^tm1Jps/Ppard^tm1Jps	involves: 129/Sv * AKR/J * C57BL/6 * C57BL/6J	MGI:3510235
cx109	Apc^Min/Apc^+ Il22^tm1Flv/Il22^tm1Flv	involves: 129/Sv * C57BL/6 * C57BL/6J	MGI:5446700
cx110	Apc^Min/Apc^Min Sat1^tm1Alh/Y	involves: 129X1/SvJ * C57BL/6J	MGI:3709984
cx111	Apc^Min/Apc^+ Mmom2^129X1/SvJ/Mmom2^C57BL/6J	involves: 129X1/SvJ * C57BL/6J	MGI:3803126
cx112	Apc^Min/Apc^+ Egfr^Wa5/Egfr^+	involves: BALB/cAnN * C3H/HeN * C57BL/6J	MGI:3623317
cx113	Apc^Min/Apc^+ Pla2g2a^Mom1-r/? Prkdc^dxnph/Prkdc^dxnph	involves: BALB/cByJ * C57BL/6	MGI:4461429
cx114	Apc^Min/Apc^+ Mapkapk2^tm1.2Gkl/Mapkapk2^tm1.2Gkl	involves: BALB/cJ * C57BL/6J	MGI:6357720
cx115	Apc^Min/Apc^+ Tg(Rorc-EGFP)1Ebe/?	involves: C57BL/6	MGI:3829423
cx116	Apc^Min/Apc^+ Rr21^tm1Jta/Rr21^+	involves: C57BL/6	MGI:5463417
cx117	Apc^Min/Apc^+ Del(15Rr357-Rr303293)2Jta/Del(15Rr357-Rr303293)2Jta	involves: C57BL/6	MGI:7434699
cx118	Apc^Min/Apc^+ Dclk1^tm1.1(cre/ERT2)Seno/Dclk1^tm1.1(cre/ERT2)Seno	involves: C57BL/6	MGI:5475210
cx119	Apc^Min/Apc^+ Bcl2l14^tm1.1Boui/Bcl2l14^tm1.1Boui	involves: C57BL/6 * C57BL/6J	MGI:6470552
cx120	Apc^Min/Apc^+ Slc5a8^tm1.1Boet/Slc5a8^tm1.1Boet	involves: C57BL/6 * C57BL/6J	MGI:3811523
cx121	Apc^Min/Apc^+ Mmp7^tm1Lmm/Mmp7^tm1Lmm	involves: C57BL/6 * C57BL/6J	MGI:2183289
cx122	Apc^Min/Apc^+ Rr21^tm1.1Jta/Rr21^tm1.1Jta	involves: C57BL/6 * FVB/N	MGI:5463415
cx123	Apc^Min/Apc^+ Mom5^C57BL/6J/Mom5^C57BL/6J	involves: C57BL/6J	MGI:4359621
cx124	Apc^Min/Apc^+ Tcf7l2^tm2.2Mrc/Tcf7l2^+	involves: C57BL/6J	MGI:4946927
cx125	Apc^Min/Apc^+ Glp2r^tm1Ddr/Glp2r^tm1Ddr	involves: C57BL/6J	MGI:3827123
cx126	Apc^Min/Apc^+ Glp2r^tm1Ddr/Glp2r^+	involves: C57BL/6J	MGI:3827117
cx127	Apc^Min/Apc^+ Cd44^tm2Stpa/Cd44^tm2Stpa	involves: C57BL/6J	MGI:5544112
cx128	Apc^Min/Apc^+ Cd44^tm1Stpa/Cd44^tm2Stpa	involves: C57BL/6J	MGI:5544114
cx129	Apc^Min/Apc^+ Cd44^tm1Mak/Cd44^tm1Mak	involves: C57BL/6J	MGI:5544115
cx130	Apc^Min/Apc^Min Ppard^tm1.1Rev/Ppard^tm1.1Rev	involves: C57BL/6J	MGI:3715726
cx131	Apc^Min/Apc^+ Tnik^tm1Teya/Tnik^tm1Teya	involves: C57BL/6J	MGI:6113599
cx132	Apc^Min/Apc^+ Spata18^tm1.2Hifa/Spata18^tm1.2Hifa	involves: C57BL/6J	MGI:6121392
cx133	Apc^Min/Apc^+ Spata18^tm1.2Hifa/Spata18^+	involves: C57BL/6J	MGI:6121393
cx134	Apc^Min/Apc^+ Ccnd1^tm1Dsn/Ccnd1^tm1Dsn	involves: C57BL/6J	MGI:3045027
cx135	Apc^Min/Apc^+ Thbs1^tm1Hyn/Thbs1^tm1Hyn	involves: C57BL/6J	MGI:3032868
cx136	Gata6os^em1Zfa/Gata6os^em1Zfa Apc^Min/Apc^+	involves: C57BL/6J	MGI:6367566
cx137	Apc^Min/Apc^+ Dcc^tm1Wbg/Dcc^+	involves: C57BL/6J	MGI:2446655
cx138	Apc^Min/Apc^+ Cd44^tm1Stpa/Cd44^tm1Stpa	involves: C57BL/6J * C57BL/6JIco	MGI:5544111
cx139	Apc^Min/Apc^+ Mir708^tm1Wtsi/Mir708^tm1Wtsi	involves: C57BL/6J * C57BL/6N	MGI:6864129
cx140	Apc^Min/Apc^+ Tmem9^tm1d(EUCOMM)Wtsi/Tmem9^+	involves: C57BL/6J * C57BL/6N	MGI:6806148
cx141	Apc^Min/Apc^+ Tmem9^tm1d(EUCOMM)Wtsi/Tmem9^tm1d(EUCOMM)Wtsi	involves: C57BL/6J * C57BL/6N	MGI:6806147
cx142	Apc^Min/Apc^+ Atp5f1a^Mom2/Atp5f1a^+	involves: C57BL/6J * DBA/2J	MGI:3653360
cx143	Apc^Min/Apc^+ Atp5f1a^Mom2/Atp5f1a^Mom2	involves: C57BL/6J * DBA/2J	MGI:3653359
cx144	Apc^Min/Apc^+ Tg(Vil1-PPARGC1A)#Amos/0	involves: C57BL/6J * FVB/N	MGI:4950747
cx145	Apc^Min/Apc^+ Tg(CAG-PGDS)S-55Hjl/0	involves: C57BL/6J * FVB/N	MGI:3700065
cx146	Apc^Min/Apc^+ Mmom1^C57BL/6J/Mmom1^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803123
cx147	Apc^Min/Apc^+ Mmom2^C57BL/6J/Mmom2^FVB/NTac Mmom3^C57BL/6J/Mmom3^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803127
cx148	Apc^Min/Apc^+ Mmom2^C57BL/6J/Mmom2^FVB/NTac Mmom4^C57BL/6J/Mmom4^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803128
cx149	Apc^Min/Apc^+ Mmom4^C57BL/6J/Mmom4^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803129
cx150	Apc^Min/Apc^+ Mmom2^C57BL/6J/Mmom2^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803125
cx151	Apc^Min/Apc^+ Mmom1^C57BL/6J/Mmom1^FVB/NTac Mmom3^C57BL/6J/Mmom3^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803124

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

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 )

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

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

immune system

abnormal interleukin secretion ( J:305794 )

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

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

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

melena ( J:10209 )

• bloody feces

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

intestine polyps ( J:191217 )

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)

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

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

perinatal lethality, complete penetrance ( J:156864 )

• no mutant mice found at term

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

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

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

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

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

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

digestive/alimentary system

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

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

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

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

increased intestinal adenoma incidence ( J:150553 )

• adenomas in the small intestine

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:5475206

cn25

• Allelic Composition: Apc^Min/Apc⁺; Dclk1^{tm1.1(cre/ERT2)Seno}/Dclk1⁺; Gt(ROSA)26Sor^{tm1(HBEGF)Awai}/Gt(ROSA)26Sor⁺; Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor⁺
• 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

cn26

• 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

cn27

• 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

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

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

Genotype
MGI:4889209

cn28

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:168378 )

• compared with Apc^Min heterozygotes

neoplasm

increased intestinal adenoma incidence ( J:168378 )

• compared with Apc^Min heterozygotes

Genotype
MGI:6357723

cn29

• 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

cn30

• 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

cn31

• 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

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 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

cn32

• 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

cx33

• 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

cx34

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

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

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

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

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

Genotype
MGI:5567980

cx35

• 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

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

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

Genotype
MGI:5430745

cx36

• 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

cx37

• 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

cx38

• 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

cx39

• 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

cx40

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

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

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

Genotype
MGI:4440863

cx41

• 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

cx42

• 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

cx43

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

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

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

Genotype
MGI:5881919

cx44

• 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: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:5881925

cx46

• 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:5881916

cx47

• 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: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:7310033

cx49

• 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

cx50

• 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

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

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

Genotype
MGI:4429574

cx51

• 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

cx52

• 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

cx53

• 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:3700064

cx54

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

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

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

Genotype
MGI:3700063

cx55

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

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

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

Genotype
MGI:5636670

cx56

• 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

cx57

• 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

cx58

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

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

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

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

Genotype
MGI:4429611

cx59

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

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:45433 )

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

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

Genotype
MGI:5693797

cx60

• 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

cx61

• 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

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

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

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:5426846

cx62

• 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:3579839

cx63

• 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

cx64

• 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:3613447

cx65

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:104155 )

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

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

Genotype
MGI:3610196

cx66

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

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:75249 )

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

neoplasm

increased gastrointestinal tumor incidence ( J:75249 )

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

Genotype
MGI:3700062

cx67

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

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

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

Genotype
MGI:3719427

cx68

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

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)

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

Genotype
MGI:4359622

cx69

• 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

cx70

• 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

cx71

• 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

cx72

• 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:4946621

cx73

• 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:5319648

cx74

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:57721 )

• adenomatous polyps form throughout the intestine

• large in size but showing no signs of tumor progression

increased salivary gland tumor incidence ( J:57721 )

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

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

neoplasm

increased intestinal adenoma incidence ( J:57721 )

• adenomatous polyps form throughout the intestine

• large in size but showing no signs of tumor progression

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

Genotype
MGI:5636659

cx75

• 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

intestine polyps ( J:200824 )

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

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

cx76

• 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

cx77

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

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

neoplasm

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

cx78

• 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

cx79

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

neoplasm

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

Genotype
MGI:3831111

cx80

• 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

cx81

• 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

cx82

• 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:5298869

cx83

• 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:4820588

cx84

• 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