Phenotypes associated with this allele

• Allele Symbol: Apc⁺
• Allele Name: wild type
• Allele ID: MGI:2152684
• Summary: 228 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
ht1	Apc^tm2Rfo/Apc^+	129P2/OlaHsd-Apc^tm2Rfo	MGI:4360686
ht2	Apc^Min/Apc^+	(AKR/J x C57BL/6J-Apc^Min)F1	MGI:5449072
ht3	Apc^tm1.1Alew/Apc^+	B6.129-Apc^tm1.1Alew	MGI:5306023
ht4	Apc^tm2.1Alew/Apc^+	B6.129-Apc^tm2.1Alew	MGI:5306025
ht5	Apc^Gt(XA018)Byg/Apc^+	B6.129P2-Apc^Gt(XA018)Byg	MGI:5522758
ht6	Apc^Gt(XA018)Byg/Apc^+	(B6.129P2-Apc^Gt(XA018)Byg x C3H/HeJ)F1	MGI:5522759
ht7	Apc^tm1Rak/Apc^+	B6.129P2-Apc^tm1Rak	MGI:3766127
ht8	Apc^tm2Rfo/Apc^+	B6.129P2-Apc^tm2Rfo	MGI:4360684
ht9	Apc^tm3Mmt/Apc^+	B6.129X1-Apc^tm3Mmt	MGI:3606986
ht10	Apc^tm4Mmt/Apc^+	B6.129X1-Apc^tm4Mmt	MGI:3606966
ht11	Apc^Min/Apc^+	B6(AKR)-Apc^Min	MGI:5446893
ht12	Apc^Min/Apc^+	B6.Cg-Brca2^tm1Mbn Apc^Min	MGI:3814370
ht13	Apc^Min/Apc^+	C57BL/6J-Apc^Min	MGI:2665504
ht14	Apc^Min/Apc^+	C57BL/6J-Apc^Min/J	MGI:6712682
ht15	Apc^tm1Rak/Apc^+	(C57BL/6J x 129P2/OlaHsd)F1	MGI:4360687
ht16	Apc^tm2Rfo/Apc^+	(C57BL/6J x 129P2/OlaHsd)F1	MGI:4360685
ht17	Apc^M1Tno/Apc^+	either: B6JJcl.B6(D2JJcl)-Apc^M1Tno or (involves: C57BL/6 * C57BL/6JJcl * DBA/2JJcl)	MGI:5688288
ht18	Apc^tm1Tno/Apc^+	involves: 129 * 129S4/SvJae * C57BL/6	MGI:4429573
ht19	Apc^Min/Apc^+	involves: 129 * C57BL/6	MGI:4429570
ht20	Apc^tm1.1Rsmi/Apc^+	involves: 129P2/OlaHsd	MGI:3848498
ht21	Apc^tm1Rak/Apc^+	involves: 129P2/OlaHsd * C57BL/6	MGI:2175909
ht22	Apc^tm1Hsa/Apc^+	involves: 129P2/OlaHsd * C57BL/6	MGI:3686784
ht23	Apc^tm1Cip/Apc^+	involves: 129P2/OlaHsd * C57BL/6	MGI:3513849
ht24	Apc^Min/Apc^+	involves: 129P2/OlaHsd * C57BL/6	MGI:3834882
ht25	Apc^tm1.1Rsmi/Apc^+	involves: 129P2/OlaHsd * C57BL/6 * FVB/N	MGI:4456427
ht26	Apc^tm1Rak/Apc^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:3830621
ht27	Apc^tm1Mmt/Apc^+	involves: 129S2/SvPas * C57BL/6J	MGI:2175907
ht28	Apc^tm1.1Tno/Apc^+	involves: 129S4/SvJae * C57BL/6	MGI:3764960
ht29	Apc^tm1.1Tyj/Apc^+	involves: 129S4/SvJaeSor * C57BL/6	MGI:4461184
ht30	Apc^tm2.1Rak/Apc^+	involves: 129/Sv * C57BL/6J * SJL	MGI:3688733
ht31	Apc^tm2Mmt/Apc^+	involves: 129X1/SvJ	MGI:3811534
ht32	Apc^tm3Mmt/Apc^+	involves: 129X1/SvJ * C57BL/6N	MGI:3811542
ht33	Apc^Min/Apc^+	involves: AKR/J * C57BL/6J	MGI:2175903
ht34	Apc^Min/Apc^+	involves: C57BL/6 * C57BL/6J	MGI:3812012
ht35	Apc^M1Tno/Apc^+	involves: C57BL/6 * DBA/2JJcl	MGI:5688286
ht36	Apc^tm2Tno/Apc^+	involves: C57BL/6J	MGI:5521585
ht37	Apc^Min/Apc^+	involves: C57BL/6J	MGI:3513858
ht38	Apc^Min/Apc^+	(MA/MyJ x C57BL/6J-Apc^Min)F1	MGI:5763440
ht39	Apc^tm2Tno/Apc^+	Not Specified	MGI:2678020
cn40	Apc^tm2.1Cip/Apc^+ Lrig1^tm1.1(cre/ERT2)Rjc/Lrig1^+	involves: 129 * 129P2/OlaHsd * C57BL/6	MGI:5432136
cn41	Apc^tm1Tno/Apc^+ Il23a^tm1Ngh/Il23a^tm1Ngh Tg(CDX2-cre)101Erf/0	involves: 129 * 129S4/SvJae * C57BL/6J * SJL/J	MGI:5446624
cn42	Apc^tm1Tno/Apc^+ Il17ra^tm1Koll/Il17ra^tm1Koll Tg(CDX2-cre)101Erf/0	involves: 129 * 129S4/SvJae * C57BL/6J * SJL/J	MGI:5446625
cn43	Apc^Min/Apc^+ Hsd11b2^tm1.1Mzz/Hsd11b2^tm1.1Mzz Tg(Vil1-cre)997Gum/0	involves: 129 * C57BL/6 * C57BL/6J	MGI:5547498
cn44	Apc^Min/Apc^+ Dnmt3b^tm1Jae/Dnmt3b^tm1Jae Tg(Fabp1-cre)1Jig/0	involves: 129 * C57BL/6 * C57BL/6J * FVB/N	MGI:3625330
cn45	Apc^tm1Tno/Apc^+ Pten^tm2Mak/Pten^tm2Mak Tg(Cyp1a1-cre/ERT)1Dwi/0	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA	MGI:3829449
cn46	Apc^tm1Tno/Apc^+ Rac3^tm1.1Bea/Rac3^tm1.1Bea Tg(Vil1-cre/ERT2)23Syr/0	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2	MGI:6715667
cn47	Bmi1^tm1.1Lees/Bmi1^tm1.1Lees Apc^tm2Cip/Apc^+ Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2	MGI:5532577
cn48	Apc^tm2.1Cip/Apc^+ Kras^tm4Tyj/Kras^+ Tg(Fabp1-cre)1Jig/0	involves: 129P2/OlaHsd * 129S4/SvJae * FVB	MGI:3776028
cn49	Bmi1^tm1Brn/Bmi1^tm1Brn Apc^tm2Cip/Apc^+ Cdkn2a^tm1Cjs/Cdkn2a^tm1Cjs Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * DBA/2	MGI:5532576
cn50	Apc^tm2.1Cip/Apc^+ Lgr5^tm1(cre/ERT2)Cle/Lgr5^+	involves: 129P2/OlaHsd * C57BL/6	MGI:5432137
cn51	Apc^tm2.1Cip/Apc^+ Atg7^tm1Tchi/Atg7^tm1Tchi Tg(Vil1-cre/ERT2)23Syr/0	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2	MGI:5702420
cn52	Apc^tm2.1Cip/Apc^+ Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:4461183
cn53	Bmi1^tm1Brn/Bmi1^tm1Brn Apc^tm2Cip/Apc^+ Tg(Vil1-cre)20Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:5532574
cn54	Apc^tm2.1Cip/Apc^+ Tg(Vil1-cre/ERT2)23Syr/0	involves: 129P2/OlaHsd * C57BL/6 * DBA/2	MGI:5702414
cn55	Apc^tm1Rsmi/Apc^+ Ctnnb1^tm1Wvv/Ctnnb1^+ Tg(Fabp1-cre)1Jig/?	involves: 129P2/OlaHsd * C57BL/6J * FVB/N	MGI:5430612
cn56	Apc^tm1Rsmi/Apc^+ Tg(Fabp1-cre)1Jig/0	involves: 129P2/OlaHsd * FVB/N	MGI:4456428
cn57	Apc^tm2.1Cip/Apc^+ Tg(Fabp1-cre)1Jig/0	involves: 129P2/OlaHsd * FVB/N	MGI:3776025
cn58	Apc^Min/Apc^+ Tcf7l2^tm1(EGFP/cre)Mrc/Tcf7l2^tm2.1Mrc	involves: 129S1/Sv * 129S6/SvEvTac * 129X1/SvJ * C57BL/6J * C57BL/6NCrl	MGI:4946926
cn59	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
cn60	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
cn61	Tle5^tm1.1Mmt/Tle5^tm1.1Mmt Apc^tm1Mmt/Apc^+ Tg(Vil1-cre/ERT2)23Syr/0	involves: 129S2/SvPas * C57BL/6 * DBA * SJL	MGI:4888016
cn62	Apc^tm1Tno/Apc^+ Tg(CDX2-cre/ERT)#Erf/0	involves: 129S4/SvJae	MGI:5446623
cn63	Apc^tm2Rak/Apc^+ Kras^tm1.1Khai/Kras^+ Tg(Fabp1-cre)1Jig/0	involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N * SJL	MGI:6505557
cn64	Apc^Min/Apc^+ Pten^tm1Hwu/Pten^tm1Hwu Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL	MGI:4941759
cn65	Apc^Min/Apc^+ Col1a1^tm1(CAG-Sirt1)Dsin/Col1a1^+ Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL	MGI:4430578
cn66	Apc^tm1Tno/Apc^+ Il23r^tm1.2Trin/Il23r^tm1.2Trin Tg(CDX2-cre)101Erf/0	involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL/J	MGI:5446693
cn67	Apc^tm2Rak/Apc^+ Kras^tm4Tyj/Kras^+ Tg(Fabp1-cre)1Jig/0	involves: 129S4/SvJae * C57BL/6 * FVB/N * SJL	MGI:6505558
cn68	Apc^Min/Apc^+ Rab11a^tm1.1Ngao/Rab11a^tm1.1Ngao Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6J * SJL/J	MGI:7642164
cn69	Apc^tm1Tno/Apc^+ Tg(CDX2-cre)101Erf/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:3844311
cn70	Apc^tm1Tno/Apc^+ Tg(Vil1-cre)997Gum/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:3844314
cn71	Apc^tm1Tno/Apc^+ Tg(CDX2-cre*)189Erf/0	involves: 129S4/SvJae * C57BL/6 * SJL	MGI:3844298
cn72	Apc^Min/Apc^+ Dclk1^tm1.1(cre/ERT2)Seno/Dclk1^+ Gt(ROSA)26Sor^tm1Sor/Gt(ROSA)26Sor^tm1(HBEGF)Awai	involves: 129S4/SvJaeSor * C57BL/6	MGI:5475206
cn73	Apc^Min/Apc^+ Erbb3^tm1.1Dwt/Erbb3^tm2.1Dwt Tg(Vil1-cre)997Gum/0	involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL	MGI:4360363
cn74	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
cn75	Apc^Min/Apc^+ Gpa33^tm1(GNAS)Wtsi/Gpa33^+ Hprt1^tm1(CMV-cre)Brd/?	involves: 129S7/SvEvBrd * C57BL/6J	MGI:4889209
cn76	Apc^tm2Rak/Apc^+ Trp53^tm1Brn/Trp53^tm1Brn Tg(Pdx1-cre)6Tuv/0	involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * FVB/N * SJL	MGI:5898453
cn77	Apc^tm2Rak/Apc^+ Tg(Car1-cre)5Flt/0	involves: 129/Sv * C57BL/6J * SJL	MGI:4835054
cn78	Apc^Min/Apc^+ Mapkapk2^tm1.1Gkl/Mapkapk2^tm1.1Gkl Twist2^tm1.1(cre)Dor/Twist2^+	involves: 129X1/SvJ * BALB/cJ * C57BL/6J	MGI:6357723
cn79	Apc^Min/Apc^+ Lmna^tm4Stw/Lmna^tm4Stw Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J	MGI:5774439
cn80	Apc^Min/Apc^+ Elp3^tm1.1Tac/Elp3^tm1.1Tac Tg(Vil1-cre)997Gum/0	involves: C57BL/6 * C57BL/6J * C57BL/6NTac * SJL	MGI:5898003
cn81	Apc^tm1Tno/Apc^+ Brf1^tm1Arte/Brf1^tm1Arte Tg(Cyp1a1-cre)1Dwi/0	involves: C57BL/6 * CBA	MGI:6403689
cn82	Apc^tm1Tyj/Apc^+ Tg(Vil1-cre)20Syr/0	involves: C57BL/6 * DBA/2	MGI:4461182
cn83	Apc^Min/Apc^+ Igf2bp1^tm1Vssp/Igf2bp1^tm1Vssp Tg(Vil1-cre)997Gum/0	involves: C57BL/6J * SJL	MGI:5523866
cx84	Cdx2^tm1Mmt/Cdx2^+ Apc^tm1Mmt/Apc^+	B6.129-Cdx2^tm1Mmt Apc^tm1Mmt	MGI:3715020
cx85	Apc^tm1Rak/Apc^+ Smad4^E6sad/Smad4^+	B6.129P2-Apc^tm1Rak +/+ Smad4^E6sad	MGI:3766126
cx86	Apc^tm1Rak/Apc^+ Smad4^E6sad/Smad4^+	B6.129P2-Apc^tm1Rak Smad4^E6sad/+ +	MGI:3766123
cx87	Apc^Min/Apc^+ Brca2^tm1Mbn/Brca2^+	B6.Cg-Brca2^tm1Mbn Apc^Min	MGI:3814367
cx88	Apc^Min/Apc^+ Gt(ROSA)26Sor/Gt(ROSA)26Sor^+	B6.Cg-Gt(ROSA)26Sor Apc^Min	MGI:5014351
cx89	Apc^Min/Apc^+ Mir10a^tm1.1Ahl/Mir10a^tm1.1Ahl	B6.Cg-Mir10a^tm1.1Ahl Apc^min	MGI:5567980
cx90	Apc^Min/Apc^+ Mthfs^Gt(RRK291)Byg/Mthfs^+	B6.Cg-Mthfs^Gt(RRK291)Byg Apc^Min	MGI:5430745
cx91	Apc^Min/Apc^+ Nos2^tm1Lau/Nos2^+	B6.Cg-Nos2^tm1Lau Apc^Min	MGI:3767792
cx92	Apc^Min/Apc^+ Nos2^tm1Lau/Nos2^tm1Lau	B6.Cg-Nos2^tm1Lau Apc^Min	MGI:3767791
cx93	Apc^Min/Apc^+ Pla2g4a^tm1Jvb/Pla2g4a^tm1Jvb	B6.Cg-Pla2g4a^tm1Jvb Apc^Min	MGI:4358774
cx94	Apc^Min/Apc^+ Rab25^tm1Jrgo/Rab25^tm1Jrgo	B6.Cg-Rab25^tm1Jrgo Apc^Min	MGI:4440863
cx95	Apc^Min/Apc^+ Rab25^tm1Jrgo/Rab25^+	B6.Cg-Rab25^tm1Jrgo Apc^Min	MGI:4440864
cx96	Apc^Min/Apc^+ Shmt1^Gt(AD0236)Wtsi/Shmt1^Gt(AD0236)Wtsi	B6.Cg-Shmt1^Gt(AD0236)Wtsi Apc^Min	MGI:5426849
cx97	Apc^Min/Apc^+ Tgfbr1^tm1Bopa/Tgfbr1^+	B6.Cg-Tgfbr1^tm1Bopa Apc^Min	MGI:3831112
cx98	Apc^Min/Apc^+ Arhgef4^tm1Taki/Arhgef4^tm1Taki	B6J.Cg-Arhgef4^tm1Taki Apc^Min	MGI:5881919
cx99	Apc^Min/Apc^+ Arhgef4^tm1Taki/Arhgef4^+	B6J.Cg-Arhgef4^tm1Taki Apc^Min	MGI:5881920
cx100	Apc^Min/Apc^+ Arhgef4^tm1Taki/Arhgef4^tm1Taki Spata13^tm1Taki/Spata13^tm1Taki	B6J.Cg-Arhgef4^tm1Taki Spata13^tm1Taki Apc^Min	MGI:5881925
cx101	Apc^Min/Apc^+ Spata13^tm1Taki/Spata13^+	B6J.Cg-Spata13^tm1Taki Apc^Min	MGI:5881917
cx102	Apc^Min/Apc^+ Spata13^tm1Taki/Spata13^tm1Taki	B6J.Cg-Spata13^tm1Taki Apc^Min	MGI:5881916
cx103	Apc^Min/Apc^+ Zfp280c^em1Xss/Zfp280c^em1Xss	C57BL/6J-Apc^Min Zfp280c^em1Xss	MGI:7662831
cx104	Apc^Min/Apc^+ Zfp280c^em1Xss/Y	C57BL/6J-Apc^Min Zfp280c^em1Xss	MGI:7662832
cx105	Apc^Min/Apc^+ Zfp280c^em1Xss/Zfp280c^+	C57BL/6J-Apc^Min Zfp280c^em1Xss	MGI:7662833
cx106	Apc^Min/Apc^+ Fxyd5^em1Namje/Fxyd5^em1Namje	C57BL/6J-Fxyd5^em1Namje Apc^min	MGI:7310033
cx107	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
cx108	Apc^Min/Apc^+ Hltf^tm1.1Hdin/Hltf^tm1.1Hdin	involves: 129 * C57BL/6 * FVB/N	MGI:6108175
cx109	Apc^Min/Apc^+ Hpgds^tm1Urad/Hpgds^tm1Urad	involves: 129 * C57BL/6J	MGI:3700064
cx110	Apc^Min/Apc^+ Hpgds^tm1Urad/Hpgds^+	involves: 129 * C57BL/6J	MGI:3700063
cx111	Apc^tm1Rak/Apc^+ Msh2^tm1Rak/Msh2^tm1Rak	involves: 129P2/OlaHsd	MGI:4355516
cx112	Apc^tm1Cip/Apc^+ H19^tm1Lda/H19^+	involves: 129P2/OlaHsd * 129S2/SvPas	MGI:3845818
cx113	Apc^tm1Cip/Apc^+ H19^tm1Lda/H19^+	involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * CBA	MGI:3845817
cx114	Apc^tm1Rak/Apc^+ Pms2^tm1.1Sks/Pms2^tm1.1Sks	involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J	MGI:6764552
cx115	Apc^tm1Cip/Apc^+ Cdhr5^tm1Lex/Cdhr5^tm1Lex	involves: 129P2/OlaHsd * 129S5/SvEvBrd * C57BL/6	MGI:6713511
cx116	Apc^Min/Apc^+ Msh2^tm1Mak/Msh2^tm1Mak Nos2^tm1Mrl/Nos2^tm1Mrl	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J	MGI:5636670
cx117	Apc^Min/Apc^+ Msh2^tm1Mak/Msh2^+ Nos2^tm1Mrl/Nos2^tm1Mrl	involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J	MGI:5636667
cx118	Apc^Min/Apc^+ Blm^tm1Grdn/Blm^+	involves: 129P2/OlaHsd * 129S/SvEv * Black Swiss * C57BL/6J	MGI:3582674
cx119	Apc^Min/Apc^+ Msh2^tm1Htr/Msh2^tm1Htr	involves: 129P2/OlaHsd * BALB/c * C57BL/6J	MGI:4429611
cx120	Apc^Min/Apc^+ Ccdc80^tm1.1Ftk/Ccdc80^tm1.1Ftk	involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 * C57BL/6J * C57BL/6N	MGI:5693797
cx121	Apc^tm1Rak/Apc^+ Hmmr^tm1Baa/Hmmr^tm1Baa	involves: 129P2/OlaHsd * C57BL/6	MGI:2682909
cx122	Apc^tm1Rak/Apc^+ Dcc^tm1.1Mehl/Dcc^tm1.1Mehl	involves: 129P2/OlaHsd * C57BL/6	MGI:5312326
cx123	Apc^tm1Rak/Apc^+ Mlh1^tm1Rak/Mlh1^tm1Rak	involves: 129P2/OlaHsd * C57BL/6	MGI:4412021
cx124	Apc^tm1Rak/Apc^+ Mlh1^tm1Rak/Mlh1^+	involves: 129P2/OlaHsd * C57BL/6	MGI:4412022
cx125	Apc^Min/Apc^+ Foxl1^tm1Khk/Foxl1^tm1Khk	involves: 129P2/OlaHsd * C57BL/6	MGI:3834880
cx126	Apc^Min/Apc^+ Zbtb33^tm1.1Bird/Y	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:3613447
cx127	Apc^Min/Apc^+ Phgdh^tm1.1Shfu/Phgdh^+	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:5426846
cx128	Apc^tm1Cip/Apc^+ Mki67^em1Dfis/Mki67^em1Dfis	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:6715308
cx129	Apc^Min/Apc^+ Mbd2^tm1Bh/Mbd2^+	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:3579839
cx130	Apc^Min/Apc^+ Mbd2^tm1Bh/Mbd2^tm1Bh	involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J	MGI:3579838
cx131	Apc^tm1Cip/Apc^+ Nrip1^tm1Mpk/Nrip1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:5574446
cx132	Apc^Min/Apc^+ Msh2^tm1Mak/Msh2^tm1Mak	involves: 129P2/OlaHsd * C57BL/6J	MGI:5636659
cx133	Apc^tm1Rak/Apc^+ Cdh1^tm1Cbm/Cdh1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:3830619
cx134	Apc^Min/Apc^+ Cd44^tm1Mak/Cd44^tm1Mak	involves: 129P2/OlaHsd * C57BL/6J	MGI:4946621
cx135	Apc^Min/Apc^+ Hp^tm1Skl/Hp^tm1Skl	involves: 129P2/OlaHsd * C57BL/6J	MGI:3610196
cx136	Apc^tm2Rfo/Apc^+ Ctnnb1^tm1.2Wvv/Ctnnb1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:5430611
cx137	Apc^Min/Apc^+ Mom5^129P2/OlaHsd/?	involves: 129P2/OlaHsd * C57BL/6J	MGI:4359622
cx138	Apc^tm1Rak/Apc^+ Ctnnb1^tm1.2Wvv/Ctnnb1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:5430610
cx139	Apc^tm2Rfo/Apc^+ Smad4^E6sad/Smad4^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:4360688
cx140	Apc^Min/Apc^+ Ptgs2^tm1Unc/Ptgs2^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366246
cx141	Apc^Min/Apc^+ Ptgs1^tm1Unc/Ptgs1^tm1Unc	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366247
cx142	Apc^Min/Apc^+ Ptgs1^tm1Unc/Ptgs1^+	involves: 129P2/OlaHsd * C57BL/6J	MGI:4366248
cx143	Apc^Min/Apc^+ Ptgds^tm1Ohy/Ptgds^tm1Ohy	involves: 129P2/OlaHsd * C57BL/6J	MGI:3700062
cx144	Apc^Min/Apc^+ Tcf7^tm1Cle/Tcf7^tm1Cle	involves: 129P2/OlaHsd * C57BL/6J	MGI:5319648
cx145	Apc^Min/Apc^+ Mbd4^tm1Bird/Mbd4^tm1Bird	involves: 129P2/OlaHsd * C57BL/6J	MGI:3719427
cx146	Apc^Min/Apc^+ Trp53^tm1Mlh/Trp53^tm1Mlh	involves: 129P2/OlaHsd * C57BL/6 * SWR	MGI:5448541
cx147	Apc^Min/Apc^+ Dnd1^Ter/Dnd1^+	involves: 129P3/J * C57BL/6J	MGI:5696099
cx148	Apc^tm1Mmt/Apc^+ Mmp7^tm1Lmm/Mmp7^tm1Lmm Smad4^tm1Mmt/Smad4^+	involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ	MGI:4365607
cx149	Apc^Min/Apc^+ Tcf7l2^tm1.1(EGFP/cre)Mrc/Tcf7l2^+	involves: 129S1/Sv * 129X1/SvJ * C57BL/6J	MGI:4946925
cx150	Apc^Min/Apc^+ Tgfbr1^tm1Bopa/Tgfbr1^+	involves: 129S1/SvImJ * C57BL/6J	MGI:3831111
cx151	Apc^tm1Mmt/Apc^+ Smad2^tm2Kato/Smad2^+	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J	MGI:3790616
cx152	Apc^tm1Mmt/Apc^+ Smad2^tm1Kato/Smad2^+	involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J	MGI:3790617
cx153	Apc^tm1Mmt/Apc^+ Ptgs2^tm1Jed/Ptgs2^tm1Jed	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:3603950
cx154	Apc^tm1Mmt/Apc^+ Ptgs2^tm1Jed/Ptgs2^+	involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J	MGI:3603949
cx155	Apc^Min/Apc^+ Il6^tm1Kopf/Il6^tm1Kopf	involves: 129S2/SvPas * C57BL/6	MGI:4365606
cx156	Apc^tm1Mmt/Apc^+ Smad4^tm1Mmt/Smad4^+	involves: 129S2/SvPas * C57BL/6	MGI:2182802
cx157	Apc^Min/Apc^+ Esr2^tm1Mma/Esr2^+	involves: 129S2/SvPas * C57BL/6J	MGI:5298868
cx158	Apc^Min/Apc^+ Esr2^tm1Mma/Esr2^tm1Mma	involves: 129S2/SvPas * C57BL/6J	MGI:5298869
cx159	Apc^Min/Apc^+ Hdac2^Gt(W035F03)Joe/Hdac2^Gt(W035F03)Joe	involves: 129S2/SvPas * C57BL/6J	MGI:4357790
cx160	Apc^Min/Apc^+ Esr1^tm1.1Mma/Esr1^+	involves: 129S2/SvPas * C57BL/6J	MGI:5298871
cx161	Apc^Min/Apc^+ Pms2^tm1Lisk/Pms2^tm1Lisk	involves: 129S2/SvPas * C57BL/6J	MGI:4820588
cx162	Apc^Min/Apc^+ Esr1^tm1.1Mma/Esr1^tm1.1Mma	involves: 129S2/SvPas * C57BL/6J	MGI:5298870
cx163	Apc^tm1.1Tno/Apc^+ Ctnna1^del/Ctnna1^+	involves: 129S4/SvJae * C57BL/6	MGI:3764961
cx164	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
cx165	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
cx166	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
cx167	Apc^Min/Apc^+ Ptprh^tm1.1Mato/Ptprh^tm1.1Mato	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:3839104
cx168	Apc^Min/Apc^+ Col1a1^tm11(tetO-Nup88)Jvd/Col1a1^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:6377634
cx169	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
cx170	Apc^Min/Apc^+ Col1a1^tm1(CAG-Sirt1)Dsin/Col1a1^+	involves: 129S4/SvJae * C57BL/6 * C57BL/6J	MGI:4430577
cx171	Apc^Min/Apc^+ Dnmt1^tm1Pwl/Dnmt1^+	involves: 129S4/SvJae * C57BL/6J	MGI:3848450
cx172	Apc^Min/Apc^+ Dnmt1^tm1Jae/Dnmt1^tm1Pwl	involves: 129S4/SvJae * C57BL/6J	MGI:3848453
cx173	Apc^Min/Apc^+ Dnmt1^tm1Jae/Dnmt1^+	involves: 129S4/SvJae * C57BL/6J	MGI:3848451
cx174	Apc^Min/Apc^+ Map9^tm1.2Bcgen/Map9^tm1.2Bcgen	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6 * C57BL/6J	MGI:6502660
cx175	Apc^Min/Apc^+ Map9^tm1.2Bcgen/Map9^+	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6 * C57BL/6J	MGI:6502661
cx176	Apc^Min/Apc^+ Zfp82^tm1.2Cya/Zfp82^+	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6NTac	MGI:6849776
cx177	Apc^Min/Apc^+ Zfp82^tm1.2Cya/Zfp82^tm1.2Cya	involves: 129S4/SvJaeSor * BALB/cJ * C57BL/6NTac	MGI:6849775
cx178	Apc^Min/Apc^+ Dp(17Nfkbil1-Or2h1)1Cogr/0	involves: 129S6/SvEvTac * C57BL/6J	MGI:5451046
cx179	Apc^Min/Apc^+ Ereg^tm1Dwt/Ereg^tm1Dwt	involves: 129S6/SvEvTac * C57BL/6J	MGI:3512138
cx180	Apc^Min/Apc^+ Il22ra2^tm2Vlcg/Il22ra2^tm2Vlcg	involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac	MGI:5446699
cx181	Apc^Min/Apc^+ Myc^tm1Jlc/Myc^+	involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J	MGI:3812011
cx182	Apc^Min/Apc^+ Recql4^tm1Glu/Recql4^tm1Glu	involves: 129S7/SvEvBrd * C57BL/6J	MGI:3575580
cx183	Apc^tm1Rak/Apc^+ Mbd4^tm1Wed/Mbd4^tm1Wed	involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * SJL	MGI:3719440
cx184	Fen1^tm1Rak/Fen1^+ Apc^tm1Rak/Apc^+	involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * SJL/J	MGI:3843881
cx185	Apc^Min/Apc^+ Ppard^tm1Jps/Ppard^tm1Jps	involves: 129/Sv * AKR/J * C57BL/6 * C57BL/6J	MGI:3510235
cx186	Apc^Min/Apc^+ Il22^tm1Flv/Il22^tm1Flv	involves: 129/Sv * C57BL/6 * C57BL/6J	MGI:5446700
cx187	Apc^tm1Mmt/Apc^+ Nkd1^tm1Tko/Nkd1^tm1Tko	involves: 129X1/SvJ	MGI:3531415
cx188	Apc^Min/Apc^+ Mmom2^129X1/SvJ/Mmom2^C57BL/6J	involves: 129X1/SvJ * C57BL/6J	MGI:3803126
cx189	Apc^Min/Apc^+ Egfr^Wa5/Egfr^+	involves: BALB/cAnN * C3H/HeN * C57BL/6J	MGI:3623317
cx190	Apc^Min/Apc^+ Pla2g2a^Mom1-r/? Prkdc^dxnph/Prkdc^dxnph	involves: BALB/cByJ * C57BL/6	MGI:4461429
cx191	Apc^Min/Apc^+ Mapkapk2^tm1.2Gkl/Mapkapk2^tm1.2Gkl	involves: BALB/cJ * C57BL/6J	MGI:6357720
cx192	Apc^Min/Apc^+ Dclk1^tm1.1(cre/ERT2)Seno/Dclk1^tm1.1(cre/ERT2)Seno	involves: C57BL/6	MGI:5475210
cx193	Apc^Min/Apc^+ Del(15Rr357-Rr303293)2Jta/Del(15Rr357-Rr303293)2Jta	involves: C57BL/6	MGI:7434699
cx194	Apc^Min/Apc^+ Tg(Rorc-EGFP)1Ebe/?	involves: C57BL/6	MGI:3829423
cx195	Apc^Min/Apc^+ Rr21^tm1Jta/Rr21^+	involves: C57BL/6	MGI:5463417
cx196	Apc^Min/Apc^+ Bcl2l14^tm1.1Boui/Bcl2l14^tm1.1Boui	involves: C57BL/6 * C57BL/6J	MGI:6470552
cx197	Apc^Min/Apc^+ Slc5a8^tm1.1Boet/Slc5a8^tm1.1Boet	involves: C57BL/6 * C57BL/6J	MGI:3811523
cx198	Apc^Min/Apc^+ Tnfaip8l1^em1Huwa/Tnfaip8l1^em1Huwa	involves: C57BL/6 * C57BL/6J	MGI:7568795
cx199	Apc^Min/Apc^+ Mmp7^tm1Lmm/Mmp7^tm1Lmm	involves: C57BL/6 * C57BL/6J	MGI:2183289
cx200	Apc^Min/Apc^+ Rr21^tm1.1Jta/Rr21^tm1.1Jta	involves: C57BL/6 * FVB/N	MGI:5463415
cx201	Apc^Min/Apc^+ Tnik^tm1Teya/Tnik^tm1Teya	involves: C57BL/6J	MGI:6113599
cx202	Gata6os^em1Zfa/Gata6os^em1Zfa Apc^Min/Apc^+	involves: C57BL/6J	MGI:6367566
cx203	Apc^Min/Apc^+ Glp2r^tm1Ddr/Glp2r^+	involves: C57BL/6J	MGI:3827117
cx204	Apc^Min/Apc^+ Glp2r^tm1Ddr/Glp2r^tm1Ddr	involves: C57BL/6J	MGI:3827123
cx205	Apc^Min/Apc^+ Cd44^tm1Mak/Cd44^tm1Mak	involves: C57BL/6J	MGI:5544115
cx206	Apc^Min/Apc^+ Cd44^tm1Stpa/Cd44^tm2Stpa	involves: C57BL/6J	MGI:5544114
cx207	Apc^Min/Apc^+ Cd44^tm2Stpa/Cd44^tm2Stpa	involves: C57BL/6J	MGI:5544112
cx208	Apc^Min/Apc^+ Mom5^C57BL/6J/Mom5^C57BL/6J	involves: C57BL/6J	MGI:4359621
cx209	Apc^Min/Apc^+ Dcc^tm1Wbg/Dcc^+	involves: C57BL/6J	MGI:2446655
cx210	Apc^Min/Apc^+ Tcf7l2^tm2.2Mrc/Tcf7l2^+	involves: C57BL/6J	MGI:4946927
cx211	Apc^Min/Apc^+ Ccnd1^tm1Dsn/Ccnd1^tm1Dsn	involves: C57BL/6J	MGI:3045027
cx212	Apc^Min/Apc^+ Thbs1^tm1Hyn/Thbs1^tm1Hyn	involves: C57BL/6J	MGI:3032868
cx213	Apc^Min/Apc^+ Spata18^tm1.2Hifa/Spata18^+	involves: C57BL/6J	MGI:6121393
cx214	Apc^Min/Apc^+ Spata18^tm1.2Hifa/Spata18^tm1.2Hifa	involves: C57BL/6J	MGI:6121392
cx215	Apc^Min/Apc^+ Cd44^tm1Stpa/Cd44^tm1Stpa	involves: C57BL/6J * C57BL/6JIco	MGI:5544111
cx216	Apc^Min/Apc^+ Mir708^tm1Wtsi/Mir708^tm1Wtsi	involves: C57BL/6J * C57BL/6N	MGI:6864129
cx217	Apc^Min/Apc^+ Tmem9^tm1d(EUCOMM)Wtsi/Tmem9^+	involves: C57BL/6J * C57BL/6N	MGI:6806148
cx218	Apc^Min/Apc^+ Tmem9^tm1d(EUCOMM)Wtsi/Tmem9^tm1d(EUCOMM)Wtsi	involves: C57BL/6J * C57BL/6N	MGI:6806147
cx219	Apc^Min/Apc^+ Atp5f1a^Mom2/Atp5f1a^+	involves: C57BL/6J * DBA/2J	MGI:3653360
cx220	Apc^Min/Apc^+ Atp5f1a^Mom2/Atp5f1a^Mom2	involves: C57BL/6J * DBA/2J	MGI:3653359
cx221	Apc^Min/Apc^+ Tg(Vil1-PPARGC1A)#Amos/0	involves: C57BL/6J * FVB/N	MGI:4950747
cx222	Apc^Min/Apc^+ Tg(CAG-PGDS)S-55Hjl/0	involves: C57BL/6J * FVB/N	MGI:3700065
cx223	Apc^Min/Apc^+ Mmom4^C57BL/6J/Mmom4^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803129
cx224	Apc^Min/Apc^+ Mmom1^C57BL/6J/Mmom1^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803123
cx225	Apc^Min/Apc^+ Mmom2^C57BL/6J/Mmom2^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803125
cx226	Apc^Min/Apc^+ Mmom2^C57BL/6J/Mmom2^FVB/NTac Mmom3^C57BL/6J/Mmom3^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803127
cx227	Apc^Min/Apc^+ Mmom2^C57BL/6J/Mmom2^FVB/NTac Mmom4^C57BL/6J/Mmom4^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803128
cx228	Apc^Min/Apc^+ Mmom1^C57BL/6J/Mmom1^FVB/NTac Mmom3^C57BL/6J/Mmom3^FVB/NTac	involves: C57BL/6J * FVB/NTac	MGI:3803124

Genotype
MGI:4360686

ht1

• Allelic Composition: Apc^tm2Rfo/Apc⁺
• Genetic Background: 129P2/OlaHsd-Apc^tm2Rfo

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

Mammary adenocarcinomas from Apc^tm2Rfo/Apc⁺ mice

mortality/aging

premature death ( J:151494 )

• mice die prior to 18 weeks

neoplasm

increased gastrointestinal tumor incidence ( J:151494 )

♂ • 29% of male mice develop gastrointestinal tumors

increased mammary adenocarcinoma incidence ( J:151494 )

• in 94% of female mice and 50% of male mice

increased liver tumor incidence ( J:151494 )

• in 11% of female mice and 29% of male mice

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:151494 )

• in 94% of female mice and 50% of male mice

liver/biliary system

increased liver tumor incidence ( J:151494 )

• in 11% of female mice and 29% of male mice

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:151494 )

♂ • 29% of male mice develop gastrointestinal tumors

integument

increased mammary adenocarcinoma incidence ( J:151494 )

• in 94% of female mice and 50% of male mice

Genotype
MGI:5449072

ht2

• 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:5306023

ht3

• Allelic Composition: Apc^tm1.1Alew/Apc⁺
• Genetic Background: B6.129-Apc^tm1.1Alew

neoplasm

abnormal tumor morphology ( J:180275 )

• mice exhibit increased incidents and polyp size with more frequent paneth cell differentiation and polyp crypt fission with normal tissue compared with Apc^Min heterozygotes

increased adenoma incidence ( J:180057 )

• gastric and intestinal

increased intestinal adenoma incidence ( J:180057 , J:180275 )

• however, no carcinomas are observed (J:180057)

• adenoma gastrointestinal polyps, greatest in the small intestine (J:180275)

digestive/alimentary system

increased intestinal adenoma incidence ( J:180057 , J:180275 )

• however, no carcinomas are observed (J:180057)

• adenoma gastrointestinal polyps, greatest in the small intestine (J:180275)

gastrointestinal tract polyps ( J:180057 , J:180275 )

• adenoma gastrointestinal polyps, greatest in the small intestine (J:180275)

• severe polyposis with increased incidents and polyp size compared with Apc^Min heterozygotes (J:180275)

cellular

increased apoptosis ( J:180275 )

• in polyps

increased cell proliferation ( J:180275 )

• in polyps

hematopoietic system

anemia ( J:180275 )

• mice are euthanized by 12 weeks of age due to symptoms of anemia

mortality/aging

premature death ( J:180275 )

• mice are euthanized by 12 weeks of age due to symptoms of anemia

Genotype
MGI:5306025

ht4

• Allelic Composition: Apc^tm2.1Alew/Apc⁺
• Genetic Background: B6.129-Apc^tm2.1Alew

neoplasm

abnormal tumor pathology ( J:180057 )

• indistinguishable from Apc^tm1.1Alew heterozygotes

• however, no carcinomas are observed

increased adenoma incidence ( J:180057 )

• gastric and intestinal

increased intestinal adenoma incidence ( J:180057 )

digestive/alimentary system

increased intestinal adenoma incidence ( J:180057 )

gastrointestinal tract polyps ( J:180057 )

• majority in the duodenum and jejunum

behavior/neurological

hunched posture ( J:180057 )

hematopoietic system

anemia ( J:180057 )

Genotype
MGI:5522758

ht5

• Allelic Composition: Apc^Gt(XA018)Byg/Apc⁺
• Genetic Background: B6.129P2-Apc^Gt(XA018)Byg

neoplasm

increased intestinal adenoma incidence ( J:202877 )

• small intestine

increased colon adenoma incidence ( J:202877 )

increased tumor growth/size ( J:202877 )

• increased tumor multiplicity and burden of smaller sized tumors/polyps in the distal small intestine compared with Apc^Min heterozygotes

• Background Sensitivity: mice on a congenic C57BL/6 background develop more polyps than mice with a C57BL6 and C3H/HeJ F1 background

• however, tumor pathology is the same as in Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:202877 )

• small intestine

increased colon adenoma incidence ( J:202877 )

intestine polyps ( J:202877 )

• increased tumor multiplicity and burden of smaller sized tumors/polyps in the small intestine compared with Apc^Min heterozygotes

Genotype
MGI:5522759

ht6

• Allelic Composition: Apc^Gt(XA018)Byg/Apc⁺
• Genetic Background: (B6.129P2-Apc^Gt(XA018)Byg x C3H/HeJ)F1

neoplasm

decreased tumor growth/size ( J:202877 )

• Background Sensitivity: mice with a C57BL6 and C3H/HeJ F1 background exhibit develop fewer polyps than mice in a congenic C57BL/6 background in the small intestine

Genotype
MGI:3766127

ht7

• Allelic Composition: Apc^tm1Rak/Apc⁺
• Genetic Background: B6.129P2-Apc^tm1Rak

mortality/aging

decreased tumor-free survival time ( J:107273 )

• 50% of mice have died by 13 months of age due to intestinal tumors, with the remaining mice dying by 18 months of age

digestive/alimentary system

intestine polyps ( J:107273 )

• 100% incidence of low to high dysplastic polyps in 6-18 months of age

colon polyps ( J:107273 )

• 19% incidence of low to high dysplastic polyps in 6-18 months of age

gastric polyps ( J:107273 )

• 25% incidence of polyps in the gastric mucosa of mice 6-18 months of age

• 88% incidence of polyps in the periampullar region

Genotype
MGI:4360684

ht8

• Allelic Composition: Apc^tm2Rfo/Apc⁺
• Genetic Background: B6.129P2-Apc^tm2Rfo

Mammary adenocarcinomas from Apc^tm2Rfo/Apc⁺ mice

mortality/aging

premature death ( J:151494 )

• mice die prior to 16 weeks

neoplasm

increased mammary gland tumor incidence ( J:151494 )

• in 100% of virgin females and 29% of males

• all tumors exhibit squamous metaplasia

• however, mice do not exhibit an increased susceptibility to intestinal tumors

increased mammary adenocarcinoma incidence ( J:151494 )

• primary mammary adenocarcinomas metastasize to the lungs

increased liver tumor incidence ( J:151494 )

• in 29% of male mice

• all tumors exhibit squamous metaplasia

integument

increased mammary gland tumor incidence ( J:151494 )

• in 100% of virgin females and 29% of males

• all tumors exhibit squamous metaplasia

• however, mice do not exhibit an increased susceptibility to intestinal tumors

increased mammary adenocarcinoma incidence ( J:151494 )

• primary mammary adenocarcinomas metastasize to the lungs

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:151494 )

• in 100% of virgin females and 29% of males

• all tumors exhibit squamous metaplasia

• however, mice do not exhibit an increased susceptibility to intestinal tumors

increased mammary adenocarcinoma incidence ( J:151494 )

• primary mammary adenocarcinomas metastasize to the lungs

liver/biliary system

increased liver tumor incidence ( J:151494 )

• in 29% of male mice

• all tumors exhibit squamous metaplasia

Genotype
MGI:3606986

ht9

• Allelic Composition: Apc^tm3Mmt/Apc⁺
• Genetic Background: B6.129X1-Apc^tm3Mmt

digestive/alimentary system

increased intestinal adenoma incidence ( J:101604 )

• intesinal polyps are dysplastic adenomas

intestine polyps ( J:101604 )

• an average of 0.26 polyps per mouse at 15 months of age

neoplasm

increased intestinal adenoma incidence ( J:101604 )

• intesinal polyps are dysplastic adenomas

Genotype
MGI:3606966

ht10

• Allelic Composition: Apc^tm4Mmt/Apc⁺
• Genetic Background: B6.129X1-Apc^tm4Mmt

digestive/alimentary system

increased intestinal adenoma incidence ( J:101604 )

• intesinal polyps are dysplastic adenomas

intestine polyps ( J:101604 )

• an average of 1.09 polyps per mouse at 15 months of age

neoplasm

increased intestinal adenoma incidence ( J:101604 )

• intesinal polyps are dysplastic adenomas

Genotype
MGI:5446893

ht11

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

mortality/aging

premature death ( J:10209 )

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

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

neoplasm

increased intestinal adenocarcinoma incidence ( J:10209 )

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

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

increased intestinal adenoma incidence ( J:10209 )

increased mammary gland tumor incidence ( J:15101 )

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

reproductive system

abnormal pregnancy ( J:10209 )

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

hematopoietic system

anemia ( J:10209 )

• anemia is diagnosed by 60 days of age

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

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:15101 )

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

mammary gland hyperplasia ( J:15101 )

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

integument

increased mammary gland tumor incidence ( J:15101 )

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

mammary gland hyperplasia ( J:15101 )

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

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:10209 )

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

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

increased intestinal adenoma incidence ( J:10209 )

Genotype
MGI:3814370

ht12

• 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

ht13

• 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:85142 , J:158733 , J:241611 , 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)

• 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)

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

• tubular adenomas in the colon (J:158733)

digestive/alimentary system

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

• 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)

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

ht14

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

mortality/aging

premature death ( J:331404 )

• mice show a median survival time of 24.6 weeks

neoplasm

increased intestinal adenoma incidence ( J:331404 )

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

increased colon adenoma incidence ( J:331404 )

immune system

abnormal interleukin secretion ( J:305794 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:331404 )

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

increased colon adenoma incidence ( J:331404 )

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

Genotype
MGI:4360687

ht15

• Allelic Composition: Apc^tm1Rak/Apc⁺
• Genetic Background: (C57BL/6J x 129P2/OlaHsd)F1

mortality/aging

premature death ( J:151494 )

• mice die prior to 16 weeks

neoplasm

increased gastrointestinal tumor incidence ( J:151494 )

• mice develop multiple gastro-intestinal tumors

increased stomach tumor incidence ( J:151494 )

• mice develop pyloric tumors

increased desmoid tumor incidence ( J:151494 )

• mice develop desmoid with increased mutliplicity in males

integument

epidermal cyst ( J:151494 )

• with increased multiplicity in males

growth/size/body

epidermal cyst ( J:151494 )

• with increased multiplicity in males

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:151494 )

• mice develop multiple gastro-intestinal tumors

increased stomach tumor incidence ( J:151494 )

• mice develop pyloric tumors

Genotype
MGI:4360685

ht16

• Allelic Composition: Apc^tm2Rfo/Apc⁺
• Genetic Background: (C57BL/6J x 129P2/OlaHsd)F1

Mammary adenocarcinomas from Apc^tm2Rfo/Apc⁺ mice

mortality/aging

premature death ( J:151494 )

• mice die prior to 21 weeks

neoplasm

increased metastatic potential ( J:204440 )

• lung micro- and macro-metastases

increased tumor incidence ( J:151494 )

♂ • mice develop epidermal cysts with increased multiplicity in male mice

♂ • however, mice do not exhibit an increased susceptibility to intestinal tumors

♂ • all tumors exhibit squamous metaplasia

increased mammary gland tumor incidence ( J:151494 )

• in 86% of virgin females and 31% of males

increased mammary adenocarcinoma incidence ( J:151494 , J:204440 )

• primary mammary adenocarcinomas metastasize to the lungs (J:151494)

• mice develop metaplastic mammary adenocarcinoma, a subtype of triple-negative breast cancer (J:204440)

increased liver tumor incidence ( J:151494 )

♂ • 31% of male mice develop liver tumors

♂ • however, female mice do not develop liver tumors

♂ • all tumors exhibit squamous metaplasia

increased desmoid tumor incidence ( J:151494 )

♂ • mice develop desmoids with increased multiplicity in male mice

integument

increased mammary gland tumor incidence ( J:151494 )

• in 86% of virgin females and 31% of males

increased mammary adenocarcinoma incidence ( J:151494 , J:204440 )

• primary mammary adenocarcinomas metastasize to the lungs (J:151494)

• mice develop metaplastic mammary adenocarcinoma, a subtype of triple-negative breast cancer (J:204440)

epidermal cyst ( J:151494 )

♂ • with increased mutliplicity in males

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:151494 )

• in 86% of virgin females and 31% of males

increased mammary adenocarcinoma incidence ( J:151494 , J:204440 )

• primary mammary adenocarcinomas metastasize to the lungs (J:151494)

• mice develop metaplastic mammary adenocarcinoma, a subtype of triple-negative breast cancer (J:204440)

growth/size/body

epidermal cyst ( J:151494 )

♂ • with increased mutliplicity in males

liver/biliary system

increased liver tumor incidence ( J:151494 )

♂ • 31% of male mice develop liver tumors

♂ • however, female mice do not develop liver tumors

♂ • all tumors exhibit squamous metaplasia

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
breast cancer		DOID:1612	OMIM:114480	J:204440

Genotype
MGI:5688288

ht17

• Allelic Composition: Apc^M1Tno/Apc⁺
• Genetic Background: either: B6JJcl.B6(D2JJcl)-Apc^M1Tno or (involves: C57BL/6 * C57BL/6JJcl * DBA/2JJcl)

neoplasm

increased mammary gland tumor incidence ( J:218227 )

• 100% of females but only 10.1% of males develop breast cancers

• breast cancers arise from 2 months of age

increased mammary adenocarcinoma incidence ( J:218227 )

• breast cancers are adenosquamous carcinoma with ductal structures, invasive foci, and poorly differentiated features

increased skin tumor incidence ( J:218227 )

• 86.5% of males, but only 12.2% of females, exhibit trichogenic tumors

• trichogenic tumors in males arise from 9 months of age

increased pilomatricoma incidence ( J:218227 )

• trichogenic tumors are trichoepithelioma and pilomatricoma

increased trichoepithelioma incidence ( J:218227 )

• trichogenic tumors are trichoepithelioma and pilomatricoma

increased osteosarcoma incidence ( J:218227 )

• some mice develop bone tumors containing proliferating spindle cells indicating osteosarcomas

increased osteoma incidence ( J:218227 )

• 54.2% of females and 93.3% of males exhibit osteomas

• osteomas are mainly seen in the skulls and mandibular bones, with some in the ribs and scapulas

• osteomas in males arise from 9 months of age

mortality/aging

premature death ( J:218227 )

• females become moribund as early as 9 weeks of age

integument

increased mammary gland tumor incidence ( J:218227 )

• 100% of females but only 10.1% of males develop breast cancers

• breast cancers arise from 2 months of age

increased mammary adenocarcinoma incidence ( J:218227 )

• breast cancers are adenosquamous carcinoma with ductal structures, invasive foci, and poorly differentiated features

increased skin tumor incidence ( J:218227 )

• 86.5% of males, but only 12.2% of females, exhibit trichogenic tumors

• trichogenic tumors in males arise from 9 months of age

increased pilomatricoma incidence ( J:218227 )

• trichogenic tumors are trichoepithelioma and pilomatricoma

increased trichoepithelioma incidence ( J:218227 )

• trichogenic tumors are trichoepithelioma and pilomatricoma

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:218227 )

• 100% of females but only 10.1% of males develop breast cancers

• breast cancers arise from 2 months of age

increased mammary adenocarcinoma incidence ( J:218227 )

• breast cancers are adenosquamous carcinoma with ductal structures, invasive foci, and poorly differentiated features

skeleton

increased osteosarcoma incidence ( J:218227 )

• some mice develop bone tumors containing proliferating spindle cells indicating osteosarcomas

increased osteoma incidence ( J:218227 )

• 54.2% of females and 93.3% of males exhibit osteomas

• osteomas are mainly seen in the skulls and mandibular bones, with some in the ribs and scapulas

• osteomas in males arise from 9 months of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
familial adenomatous polyposis		DOID:0050424	OMIM:PS175100	J:218227

Genotype
MGI:4429573

ht18

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

neoplasm

increased hepatocellular carcinoma incidence ( J:156864 )

• low incidence (<10%)

• hepatic tumor volumes are smaller than in homozygous mice

liver/biliary system

increased hepatocellular carcinoma incidence ( J:156864 )

• low incidence (<10%)

• hepatic tumor volumes are smaller than in homozygous mice

Genotype
MGI:4429570

ht19

• 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:3848498

ht20

• Allelic Composition: Apc^tm1.1Rsmi/Apc⁺
• Genetic Background: involves: 129P2/OlaHsd

neoplasm

increased gastrointestinal tumor incidence ( J:149225 )

• mice develop multiple intestinal tumors at an early age

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:149225 )

• mice develop multiple intestinal tumors at an early age

Genotype
MGI:2175909

ht21

• Allelic Composition: Apc^tm1Rak/Apc⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

Neoplastic lesions in an Apc^tm1Rak/Apc⁺ mouse

mortality/aging

premature death ( J:20443 )

• began dying around 32 weeks of age

• 70% were dead before 1 year of age

neoplasm

increased intestinal adenocarcinoma incidence ( J:20443 )

• found in the colon and in the duodenum and jejunum of the small intestine

• moderately to highly differentiated with infiltration into the muscularis mucosa, submucosa, or inner layer of the muscularis

increased intestinal adenoma incidence ( J:20443 )

• intestinal tumors were polypoid hyperplastic lesions

• benign villous or tubulovillous adenomas

increased hepatocellular carcinoma incidence ( J:20443 )

• focal lesions of the glandular epithelium of the liver seen at 1 year of age

cardiovascular system

rectal hemorrhage ( J:20443 )

• rectal bleeding in older mice

digestive/alimentary system

rectal hemorrhage ( J:20443 )

• rectal bleeding in older mice

increased intestinal adenocarcinoma incidence ( J:20443 )

• found in the colon and in the duodenum and jejunum of the small intestine

• moderately to highly differentiated with infiltration into the muscularis mucosa, submucosa, or inner layer of the muscularis

increased intestinal adenoma incidence ( J:20443 )

• intestinal tumors were polypoid hyperplastic lesions

• benign villous or tubulovillous adenomas

liver/biliary system

increased hepatocellular carcinoma incidence ( J:20443 )

• focal lesions of the glandular epithelium of the liver seen at 1 year of age

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
familial adenomatous polyposis		DOID:0050424	OMIM:PS175100	J:20443

Genotype
MGI:3686784

ht22

• Allelic Composition: Apc^tm1Hsa/Apc⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

integument

increased mammary gland tumor incidence ( J:61978 )

• some develop tumors in the mammary gland at 8 weeks of age

increased mammary adenocarcinoma incidence ( J:61978 )

• 18.5% develop a characteristic mammary tumor between 3 and 5 months of age, indicated as adenoacanthoma

mortality/aging

premature death ( J:61978 )

• die within 6 months of age due to severe anemia

cardiovascular system

intestinal hemorrhage ( J:61978 )

• develop normally until 2-3 months of age, when develop intestinal hemorrhage

hematopoietic system

anemia ( J:61978 )

• develop anemia after 2-3 months of age due to intestinal hemorrhage

neoplasm

increased gastrointestinal tumor incidence ( J:61978 )

• start to develop tumors mainly in the small intestine and some develop them in the colon, stomach, and duodenum at 8 weeks of age

• number of tumors in the intestine is variable and they appear sessile shaped with a central depression

increased stomach tumor incidence ( J:61978 )

increased mammary gland tumor incidence ( J:61978 )

• some develop tumors in the mammary gland at 8 weeks of age

increased mammary adenocarcinoma incidence ( J:61978 )

• 18.5% develop a characteristic mammary tumor between 3 and 5 months of age, indicated as adenoacanthoma

digestive/alimentary system

intestinal hemorrhage ( J:61978 )

• develop normally until 2-3 months of age, when develop intestinal hemorrhage

abnormal digestive system morphology ( J:61978 )

• large tumors sometimes cause stenosis of the gut and hemorrhage

abnormal crypts of Lieberkuhn morphology ( J:61978 )

• exhibit hyperproliferation of intestinal glands and mild cellular and structural abnormalities

colon polyps ( J:61978 )

• develop similar number of intestinal polyps as heterozygous Apc^Min and Apc^tm2Tno mice

increased gastrointestinal tumor incidence ( J:61978 )

• start to develop tumors mainly in the small intestine and some develop them in the colon, stomach, and duodenum at 8 weeks of age

• number of tumors in the intestine is variable and they appear sessile shaped with a central depression

increased stomach tumor incidence ( J:61978 )

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:61978 )

• exhibit hyperproliferation of intestinal glands and mild cellular and structural abnormalities

increased mammary gland tumor incidence ( J:61978 )

• some develop tumors in the mammary gland at 8 weeks of age

increased mammary adenocarcinoma incidence ( J:61978 )

• 18.5% develop a characteristic mammary tumor between 3 and 5 months of age, indicated as adenoacanthoma

Genotype
MGI:3513849

ht23

• Allelic Composition: Apc^tm1Cip/Apc⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

mortality/aging

premature death ( J:94108 )

• heterozygotes begin to die at 4 months of age with 50% dying by 6 months of age

neoplasm

increased intestinal adenocarcinoma incidence ( J:94108 )

• in situ carcinomas are seen in both the small and large intestines

• over 50% of lesions in mutants over 12 months of age are tubular adenomas harboring invasive carcinomas

increased intestinal adenoma incidence ( J:94108 )

• small and large adenomas are seen throughout the intestine

• the number of polyps is increased and the distribution of polyps shifted towards the ileum under specific pathogen-free conditions

increased colon adenoma incidence ( J:94108 )

• compared to Apc^Min heterozygotes more lesions are see in the colon, however the overall number of lesions is the same in both lines

increased mammary adenocarcinoma incidence ( J:94108 )

• 9% of heterozygotes developed mammary adenocanthomas

cardiovascular system

rectal hemorrhage ( J:94108 )

• first seen around 4 months of age, associated with decreased life span

digestive/alimentary system

rectal hemorrhage ( J:94108 )

• first seen around 4 months of age, associated with decreased life span

rectal prolapse ( J:94108 )

• rectal prolapse, associated with more severe polyposis in the colon, is seen as early as 4 months of age and is seen in 61% of surviving mutants by 6 months of age

• the prolapse is highly dysplatic and in 10% of these dysplatic areas adenocarcinoma is also seen

• fewer mutants raised in specific pathogen-free conditions developed rectal prolapse

increased intestinal adenocarcinoma incidence ( J:94108 )

• in situ carcinomas are seen in both the small and large intestines

• over 50% of lesions in mutants over 12 months of age are tubular adenomas harboring invasive carcinomas

increased intestinal adenoma incidence ( J:94108 )

• small and large adenomas are seen throughout the intestine

• the number of polyps is increased and the distribution of polyps shifted towards the ileum under specific pathogen-free conditions

increased colon adenoma incidence ( J:94108 )

• compared to Apc^Min heterozygotes more lesions are see in the colon, however the overall number of lesions is the same in both lines

hematopoietic system

anemia ( J:94108 )

• first seen around 4 months of age, associated with decreased life span

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:94108 )

• 9% of heterozygotes developed mammary adenocanthomas

integument

increased mammary adenocarcinoma incidence ( J:94108 )

• 9% of heterozygotes developed mammary adenocanthomas

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:94108
familial adenomatous polyposis		DOID:0050424	OMIM:PS175100	J:94108

Genotype
MGI:3834882

ht24

• 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:4456427

ht25

• Allelic Composition: Apc^tm1.1Rsmi/Apc⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * FVB/N

growth/size/body

skin cyst ( J:159883 )

• very few cutaneous cysts are observed unlike in wild-type mice

mortality/aging

premature death ( J:159883 )

• primarily due to intestinal obstruction

neoplasm

increased gastrointestinal tumor incidence ( J:159883 )

• mice develop intestinal tumors primarily in the small intestine unlike wild-type mice

increased large intestine adenocarcinoma incidence ( J:159883 )

• mice develop intestinal tumors primarily in the small intestine unlike wild-type mice

increased small intestine adenocarcinoma incidence ( J:159883 )

• mice develop intestinal tumors primarily in the small intestine unlike wild-type mice

increased intestinal adenoma incidence ( J:159883 )

• polyp or flat adenoma

increased desmoid tumor incidence ( J:159883 )

• mice develop infrequent desmoid tumors

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:159883 )

• mice develop intestinal tumors primarily in the small intestine unlike wild-type mice

increased large intestine adenocarcinoma incidence ( J:159883 )

• mice develop intestinal tumors primarily in the small intestine unlike wild-type mice

increased small intestine adenocarcinoma incidence ( J:159883 )

• mice develop intestinal tumors primarily in the small intestine unlike wild-type mice

increased intestinal adenoma incidence ( J:159883 )

• polyp or flat adenoma

intestinal obstruction ( J:159883 )

hematopoietic system

anemia ( J:159883 )

• severe

integument

skin cyst ( J:159883 )

• very few cutaneous cysts are observed unlike in wild-type mice

Genotype
MGI:3830621

ht26

• Allelic Composition: Apc^tm1Rak/Apc⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

neoplasm

increased intestinal adenocarcinoma incidence ( J:65142 )

• mice develop an average of 1.24 tumors per animal in the small intestine unlike wild-type mice

• mice develop fewer tumors than in Apc^tm1Rak Cdh1^tm1Cbm heterozygotes

• tumors are invasive although no metastasis is detected

increased stomach tumor incidence ( J:65142 )

• mice develop fewer gastric tumors than in Apc^tm1Rak Cdh1^tm1Cbm heterozygotes

• unlike wild-type mice, gastric tumors develop

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:65142 )

• mice develop an average of 1.24 tumors per animal in the small intestine unlike wild-type mice

• mice develop fewer tumors than in Apc^tm1Rak Cdh1^tm1Cbm heterozygotes

• tumors are invasive although no metastasis is detected

increased stomach tumor incidence ( J:65142 )

• mice develop fewer gastric tumors than in Apc^tm1Rak Cdh1^tm1Cbm heterozygotes

• unlike wild-type mice, gastric tumors develop

Genotype
MGI:2175907

ht27

• Allelic Composition: Apc^tm1Mmt/Apc⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6J

Nascent intestinal polyps in Apc^tm1Mmt/Apc⁺ mice

neoplasm

increased intestinal adenoma incidence ( J:79668 , J:25200 )

• numerous intestinal tumors develop in homozygotes (J:79668)

• most tumors are small; one animal developed a tumor >6 mm in diameter (J:79668)

• intestinal polyps are polyploid, papillary, or sessile adenoma; every polyp consists of a microadenoma covered with a normal layer of villous epithelium (J:25200)

• increase in incidence follows loss of normal Apc allele in nascent polyps (J:25200)

digestive/alimentary system

increased intestinal adenoma incidence ( J:79668 , J:25200 )

• numerous intestinal tumors develop in homozygotes (J:79668)

• most tumors are small; one animal developed a tumor >6 mm in diameter (J:79668)

• intestinal polyps are polyploid, papillary, or sessile adenoma; every polyp consists of a microadenoma covered with a normal layer of villous epithelium (J:25200)

• increase in incidence follows loss of normal Apc allele in nascent polyps (J:25200)

intestine polyps ( J:79668 )

• multiple polyps develop soon after birth; all heterozygotes develop polyps by 7 weeks of age and numbers increase with age

• polyps are found from duodenum to rectum, mainly in small intestine

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
familial adenomatous polyposis		DOID:0050424	OMIM:PS175100	J:25200

Genotype
MGI:3764960

ht28

• Allelic Composition: Apc^tm1.1Tno/Apc⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

mortality/aging

premature death ( J:127452 )

• average lifespan is 22.5 weeks due to bowel obstructions and bleeding

neoplasm

increased intestinal adenoma incidence ( J:127452 )

• 7 to 50 fold more small intestine tumors as in wild-type controls, with the higher incidences occurring in the more distal portions of the small intestine

digestive/alimentary system

gastrointestinal hemorrhage ( J:127452 )

• severe bleeding often is cause of death

increased intestinal adenoma incidence ( J:127452 )

• 7 to 50 fold more small intestine tumors as in wild-type controls, with the higher incidences occurring in the more distal portions of the small intestine

intestine polyps ( J:127452 )

• occurring frequently in the jejunum and ileum

intestinal obstruction ( J:127452 )

• resulting from the numerous polyps in the small intestines

• major cause of death by 22.5 weeks of age

hematopoietic system

anemia ( J:127452 )

• resulting from intestinal bleeding

cardiovascular system

gastrointestinal hemorrhage ( J:127452 )

• severe bleeding often is cause of death

Genotype
MGI:4461184

ht29

• Allelic Composition: Apc^tm1.1Tyj/Apc⁺
• Genetic Background: involves: 129S4/SvJaeSor * C57BL/6

mortality/aging

premature death ( J:160399 )

• lifespan is decreased compared to mice heterozygous for Apc^Min

neoplasm

increased intestinal adenoma incidence ( J:160399 )

• at 3 months of age small intestinal tumor number is increased compared to mice heterozygous for Apc^Min

• increase in tumor numbers is more pronounced in females

increased colon adenoma incidence ( J:160399 )

• at 3 months of age colonic tumor number is increased compared to mice heterozygous for Apc^Min

• increase in tumor numbers is more pronounced in females

increased tumor growth/size ( J:160399 )

• in females at 3 months of age intestinal tumors are about twice the volume of tumors in female mice heterozygous for Apc^Min

hematopoietic system

anemia ( J:160399 )

• in aged mice

digestive/alimentary system

increased intestinal adenoma incidence ( J:160399 )

• at 3 months of age small intestinal tumor number is increased compared to mice heterozygous for Apc^Min

• increase in tumor numbers is more pronounced in females

increased colon adenoma incidence ( J:160399 )

• at 3 months of age colonic tumor number is increased compared to mice heterozygous for Apc^Min

• increase in tumor numbers is more pronounced in females

Genotype
MGI:3688733

ht30

• Allelic Composition: Apc^tm2.1Rak/Apc⁺
• Genetic Background: involves: 129/Sv * C57BL/6J * SJL

Multiple intestinal neoplasia in Apc^tm2.1Rak/Apc⁺ mice

mortality/aging

premature death ( J:114152 )

• median lifespan is 5 months

behavior/neurological

abnormal nursing ( J:114152 )

♀ • females often become too unhealthy to successfully nurse their pups

neoplasm

increased gastrointestinal tumor incidence ( J:114152 )

• at time of death, mice display average of 100 intestinal tumors

increased intestinal adenoma incidence ( J:114152 )

cardiovascular system

rectal hemorrhage ( J:114152 )

• mice display progressive signs of rectal bleeding

digestive/alimentary system

rectal hemorrhage ( J:114152 )

• mice display progressive signs of rectal bleeding

increased gastrointestinal tumor incidence ( J:114152 )

• at time of death, mice display average of 100 intestinal tumors

increased intestinal adenoma incidence ( J:114152 )

hematopoietic system

anemia ( J:114152 )

• mice display progressive signs of anemia up to time of death

Genotype
MGI:3811534

ht31

• Allelic Composition: Apc^tm2Mmt/Apc⁺
• Genetic Background: involves: 129X1/SvJ

neoplasm

increased intestinal adenoma incidence ( J:81402 )

digestive/alimentary system

increased intestinal adenoma incidence ( J:81402 )

Genotype
MGI:3811542

ht32

• Allelic Composition: Apc^tm3Mmt/Apc⁺
• Genetic Background: involves: 129X1/SvJ * C57BL/6N

digestive/alimentary system

intestine polyps ( J:81402 )

• unlike Apc^tm1Mmt homozygotes, mice display few intestinal polyps

Genotype
MGI:2175903

ht33

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

neoplasm

increased intestinal adenocarcinoma incidence ( J:10209 )

• locally invasive tumors seen in older animals but no metastasis

• sometimes small areas of carcinomas in anemic animals only

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

increased intestinal adenoma incidence ( J:10209 )

• visible tumors of the large and small intestine

• either polyploid, papillary or sessile adenomas

digestive/alimentary system

melena ( J:10209 )

• bloody feces

increased intestinal adenocarcinoma incidence ( J:10209 )

• locally invasive tumors seen in older animals but no metastasis

• sometimes small areas of carcinomas in anemic animals only

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

increased intestinal adenoma incidence ( J:10209 )

• visible tumors of the large and small intestine

• either polyploid, papillary or sessile adenomas

hematopoietic system

anemia ( J:10209 )

• progressive adult onset anemia beconming severe and chronic

• diagnosed in mutant mice by 60 days of age

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

decreased hematocrit ( J:10209 )

• moribund animals with hematocrits around 10-20%

homeostasis/metabolism

hyperlipidemia ( J:10209 )

mortality/aging

premature death ( J:10209 )

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

Genotype
MGI:3812012

ht34

• 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:5688286

ht35

• Allelic Composition: Apc^M1Tno/Apc⁺
• Genetic Background: involves: C57BL/6 * DBA/2JJcl

neoplasm

increased mammary gland tumor incidence ( J:218227 )

♀ • females exhibit multiple breast cancers

increased skin tumor incidence ( J:218227 )

• some mutants of both sexes exhibit multiple trichogenic tumors

increased osteoma incidence ( J:218227 )

♂ • males exhibit multiple osteomas

mortality/aging

premature death ( J:218227 )

• 76% of males survive up to 60 weeks of age

• only 50% of females survive up to 50 weeks of age

integument

increased mammary gland tumor incidence ( J:218227 )

♀ • females exhibit multiple breast cancers

increased skin tumor incidence ( J:218227 )

• some mutants of both sexes exhibit multiple trichogenic tumors

endocrine/exocrine glands

increased mammary gland tumor incidence ( J:218227 )

♀ • females exhibit multiple breast cancers

skeleton

increased osteoma incidence ( J:218227 )

♂ • males exhibit multiple osteomas

Genotype
MGI:5521585

ht36

• Allelic Composition: Apc^tm2Tno/Apc⁺
• Genetic Background: involves: C57BL/6J

digestive/alimentary system

intestine polyps ( J:86036 )

• treatment with pioglitazone or bezafibrate suppresses polyp development

homeostasis/metabolism

increased circulating cholesterol level ( J:86036 )

• total cholesterol levels are increased between 6 and 12 weeks of age

increased circulating free fatty acids level ( J:86036 )

• free fatty acid levels are increased at 12 weeks of age

increased circulating triglyceride level ( J:86036 )

• triglyceride levels are increased after 6 weeks of age, with levels almost 10 times higher at 12 weeks of age than at 6 weeks of age

hyperlipidemia ( J:86036 )

• seen with age

• treatment with pioglitazone or bezafibrate decreases serum lipid levels and reduces severity of hepatic steatosis

liver/biliary system

hepatic steatosis ( J:86036 )

• centrilobular-restricted steatosis is seen in the livers of all mutants at 12 weeks of age, with numerous microvesicular fatty droplets in the cytoplasm of parenchymal cells

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

Genotype
MGI:3513858

ht37

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

mortality/aging

premature death ( J:75393 , J:94108 )

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

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

integument

increased mammary adenocarcinoma incidence ( J:94108 )

• 12% of heterozygotes developed mammary adenocanthomas

neoplasm

decreased intestinal adenoma incidence ( J:268691 )

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

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

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

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

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

increased mammary adenocarcinoma incidence ( J:94108 )

• 12% of heterozygotes developed mammary adenocanthomas

abnormal tumor pathology ( J:268691 )

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

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

decreased tumor growth/size ( J:268691 )

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

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

digestive/alimentary system

abnormal enterocyte proliferation ( J:118600 )

• reduced proliferation of cells in the colon in ovariectomized

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

abnormal intestinal mucosa morphology ( J:118600 )

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

abnormal intestinal goblet cell morphology ( J:118600 )

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

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

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

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

rectal prolapse ( J:94108 )

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

decreased intestinal adenoma incidence ( J:268691 )

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

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

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

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

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

intestine polyps ( J:191217 )

intestinal obstruction ( J:75393 )

• due to tumors

cellular

abnormal intestinal goblet cell morphology ( J:118600 )

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

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

abnormal enterocyte proliferation ( J:118600 )

• reduced proliferation of cells in the colon in ovariectomized

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

endocrine/exocrine glands

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

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

increased mammary adenocarcinoma incidence ( J:94108 )

• 12% of heterozygotes developed mammary adenocanthomas

hematopoietic system

anemia ( J:75393 )

Genotype
MGI:5763440

ht38

• 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:2678020

ht39

• Allelic Composition: Apc^tm2Tno/Apc⁺
• Genetic Background: Not Specified

neoplasm

increased intestinal adenoma incidence ( J:47857 )

• develop multiple intestinal adenomas throughout the duodenal-to-colonic axis

• treatment with piroxicam decreases the size and number of adenomas, while treatment with acarbose decreases only the size of adenomas

mortality/aging

premature death ( J:47857 )

• average lifespan of 120 days

digestive/alimentary system

increased intestinal adenoma incidence ( J:47857 )

• develop multiple intestinal adenomas throughout the duodenal-to-colonic axis

• treatment with piroxicam decreases the size and number of adenomas, while treatment with acarbose decreases only the size of adenomas

Genotype
MGI:5432136

cn40

• Allelic Composition: Apc^tm2.1Cip/Apc⁺; Lrig1^{tm1.1(cre/ERT2)Rjc}/Lrig1⁺
• Genetic Background: involves: 129 * 129P2/OlaHsd * C57BL/6

neoplasm

increased intestinal adenoma incidence ( J:186084 )

• with tamoxifen treatement, colon tumors are observed by day 50 following Apc^fldeletion with cre induction (and stochastic loss of second Apc allele)

• by day 50 there are multiple distal colonic tumors with no proximal colon tumor burden; tumor phenotype is 100% penetrant

• largest tumors are found in distal colon, many having high grade dysplasia; highest tumor number is observed in jejunum

digestive/alimentary system

increased intestinal adenoma incidence ( J:186084 )

• with tamoxifen treatement, colon tumors are observed by day 50 following Apc^fldeletion with cre induction (and stochastic loss of second Apc allele)

• by day 50 there are multiple distal colonic tumors with no proximal colon tumor burden; tumor phenotype is 100% penetrant

• largest tumors are found in distal colon, many having high grade dysplasia; highest tumor number is observed in jejunum

Genotype
MGI:5446624

cn41

• Allelic Composition: Apc^tm1Tno/Apc⁺; Il23a^tm1Ngh/Il23a^tm1Ngh; Tg(CDX2-cre)101Erf/0
• Genetic Background: involves: 129 * 129S4/SvJae * C57BL/6J * SJL/J

neoplasm

decreased tumor growth/size ( J:189226 )

• reduced colorectal tumor multiplicity and grown due to reduced cell proliferation compared with Apc^tm1Tno/Apc⁺ Tg(CDX2-cre)101Erf mice

Genotype
MGI:5446625

cn42

• Allelic Composition: Apc^tm1Tno/Apc⁺; Il17ra^tm1Koll/Il17ra^tm1Koll; Tg(CDX2-cre)101Erf/0
• Genetic Background: involves: 129 * 129S4/SvJae * C57BL/6J * SJL/J

neoplasm

decreased tumor growth/size ( J:189226 )

• reduced colorectal tumor multiplicity and grown compared to in Apc^tm1Tno/Apc⁺ Tg(CDX2-cre)101Erf mice

Genotype
MGI:5547498

cn43

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

neoplasm

increased intestinal adenoma incidence ( J:205456 )

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

decreased tumor growth/size ( J:205456 )

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

homeostasis/metabolism

abnormal corticosterone level ( J:205456 )

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

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:205456 )

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

Genotype
MGI:3625330

cn44

• 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:3829449

cn45

• Allelic Composition: Apc^tm1Tno/Apc⁺; Pten^tm2Mak/Pten^tm2Mak; Tg(Cyp1a1-cre/ERT)1Dwi/0
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * CBA

mortality/aging

premature death ( J:143082 )

• tamoxifen- and beta-naphthoflavone-induced mice median survival is 99 days compared to 405 days for wild-type Pten homozygotes or 409 days for wild-type Apc homozygotes

digestive/alimentary system

abnormal small intestine morphology ( J:143082 )

• 95% of tamoxifen- and beta-naphthoflavone-induced mice exhibit large, flattened, ulcerated lesions in the small intestine unlike control mice homozygous for either a wild-type Pten or Apc allele

increased intestinal adenocarcinoma incidence ( J:143082 )

• tamoxifen- and beta-naphthoflavone-induced mice develop invasive adenocarcinomas in the small intestines with luminal ulceration, and both acute and chronic inflammation compared to control mice that exhibit begnin neoplasms

• invasion and destruction of the small intestinal wall and peritoneal serosa results in localized peritonitis in tamoxifen- and beta-naphthoflavone-induced mice

peritoneal inflammation ( J:143082 )

• invasion and destruction of the small intestinal wall and peritoneal serosa by adenocarcinomas results in localized peritonitis in tamoxifen- and beta-naphthoflavone-induced mice

neoplasm

increased intestinal adenocarcinoma incidence ( J:143082 )

• tamoxifen- and beta-naphthoflavone-induced mice develop invasive adenocarcinomas in the small intestines with luminal ulceration, and both acute and chronic inflammation compared to control mice that exhibit begnin neoplasms

• invasion and destruction of the small intestinal wall and peritoneal serosa results in localized peritonitis in tamoxifen- and beta-naphthoflavone-induced mice

immune system

peritoneal inflammation ( J:143082 )

• invasion and destruction of the small intestinal wall and peritoneal serosa by adenocarcinomas results in localized peritonitis in tamoxifen- and beta-naphthoflavone-induced mice

Genotype
MGI:6715667

cn46

• Allelic Composition: Apc^tm1Tno/Apc⁺; Rac3^tm1.1Bea/Rac3^tm1.1Bea; Tg(Vil1-cre/ERT2)23Syr/0
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2

digestive/alimentary system

decreased alimentary system tumor incidence ( J:306088 )

• reduced number of intestinal tumors in duodenum and jejunum

• normal number of intestinal tumors in ileum and colon

decreased intestinal adenoma incidence ( J:306088 )

• reduced number of intestinal tumors in duodenum and jejunum

neoplasm

decreased tumor growth/size ( J:306088 )

• tumors less proliferative

• reduced ability to form colonies from single tumor cells in vitro

abnormal tumor susceptibility ( J:306088 )

• median intestinal tumor-free survival 138 vs 171 days

decreased alimentary system tumor incidence ( J:306088 )

• reduced number of intestinal tumors in duodenum and jejunum

• normal number of intestinal tumors in ileum and colon

decreased intestinal adenoma incidence ( J:306088 )

• reduced number of intestinal tumors in duodenum and jejunum

Genotype
MGI:5532577

cn47

• Allelic Composition: Bmi1^tm1.1Lees/Bmi1^tm1.1Lees; Apc^tm2Cip/Apc⁺; Tg(Vil1-cre)20Syr/0
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6 * DBA/2

neoplasm

decreased alimentary system tumor incidence ( J:204354 )

• reduced visible and total lesions in the small intestine

decreased colon tumor incidence ( J:204354 )

decreased intestinal adenoma incidence ( J:204354 )

digestive/alimentary system

decreased alimentary system tumor incidence ( J:204354 )

• reduced visible and total lesions in the small intestine

decreased colon tumor incidence ( J:204354 )

decreased intestinal adenoma incidence ( J:204354 )

cellular

cellular phenotype ( J:204354 )

N • no increase in apoptosis is observed in non tumor tissue

Genotype
MGI:3776028

cn48

• Allelic Composition: Apc^tm2.1Cip/Apc⁺; Kras^tm4Tyj/Kras⁺; Tg(Fabp1-cre)1Jig/0
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * FVB

mortality/aging

premature death ( J:132357 )

• animals have greatly reduced life-span compared to mutants expressing wild-type Kras

neoplasm

increased intestinal adenocarcinoma incidence ( J:132357 )

• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio

• mice have more tumors than mutants expressing wild-type Kras

• terminally differentiated cells are absent from tumors

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:132357 )

• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio

• mice have more tumors than mutants expressing wild-type Kras

• terminally differentiated cells are absent from tumors

Genotype
MGI:5532576

cn49

• Allelic Composition: Bmi1^tm1Brn/Bmi1^tm1Brn; Apc^tm2Cip/Apc⁺; Cdkn2a^tm1Cjs/Cdkn2a^tm1Cjs; Tg(Vil1-cre)20Syr/0
• Genetic Background: involves: 129P2/OlaHsd * 129X1/SvJ * C57BL/6 * DBA/2

growth/size/body

cachexia ( J:204354 )

• found in some animals by 90 days of age

behavior/neurological

hunched posture ( J:204354 )

• hunching appears in some animals at 90 days of age

neoplasm

increased intestinal adenoma incidence ( J:204354 )

• increased size and number of small intestine adenomas

digestive/alimentary system

increased intestinal adenoma incidence ( J:204354 )

• increased size and number of small intestine adenomas

Genotype
MGI:5432137

cn50

• Allelic Composition: Apc^tm2.1Cip/Apc⁺; Lgr5^{tm1(cre/ERT2)Cle}/Lgr5⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

neoplasm

neoplasm ( J:186084 )

N • following tamoxifen treatment, no intestinal tumors are observed

Genotype
MGI:5702420

cn51

• Allelic Composition: Apc^tm2.1Cip/Apc⁺; Atg7^tm1Tchi/Atg7^tm1Tchi; Tg(Vil1-cre/ERT2)23Syr/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * C57BL/6NCrlj * CBA/JNCrlj * DBA/2

neoplasm

decreased intestinal adenoma incidence ( J:227287 )

• tamoxifen treated mice show fewer and smaller colonic tumors that develop more slowly and have a lower proliferation rate than in single conditional Apc heterozygous mice

• however, prolonged antibiotic treatment of tamoxifen treated mice induces numerous intestinal tumor foci and tamoxifen treated mice administered anti-CD8 antibodies to induce partial depletion of Treg show increased tumor development

digestive/alimentary system

abnormal intestinal goblet cell morphology ( J:227287 )

• abnormal accumulation of granules of mucus in goblet cells in the tumor-free mucosa of tamoxifen treated mice

abnormal Paneth cell morphology ( J:227287 )

• unusually small in tumor-free mucosa of tamoxifen treated mice

decreased intestinal adenoma incidence ( J:227287 )

• tamoxifen treated mice show fewer and smaller colonic tumors that develop more slowly and have a lower proliferation rate than in single conditional Apc heterozygous mice

• however, prolonged antibiotic treatment of tamoxifen treated mice induces numerous intestinal tumor foci and tamoxifen treated mice administered anti-CD8 antibodies to induce partial depletion of Treg show increased tumor development

abnormal gut flora balance ( J:227287 )

• tamoxifen treated mice show altered distribution of gut bacteria, with bacteria occasionally seen within the crypt compartment of the small intestine

• tamoxifen treated mice show a difference in the overall composition of both fecal and ileal microbiota compared to single conditional Apc heterozygotes, with mice showing a high level of Gram+ bacteria related to Firmicutes and low levels of Proteobacteria in feces

• ileal mucosa of tamoxifen treated mice has a higher bacterial diversity than single conditional Apc heterozygotes

abnormal intestine physiology ( J:227287 )

• intestinal permeability is high in tamoxifen treated mice

endocrine/exocrine glands

abnormal Paneth cell morphology ( J:227287 )

• unusually small in tumor-free mucosa of tamoxifen treated mice

hematopoietic system

increased CD103-positive CD11b-low dendritic cell number ( J:227287 )

• proportion of CD103+CD11b- dendritic cell subset involved in T-cell priming is higher in tamoxifen treated mice than in single conditional Apc heterozygous mice

increased CD8-positive, alpha-beta T cell number ( J:227287 )

• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice

• administration of IL-1beta receptor antagonist, anakinra, to tamoxifen treated mice is sufficient to prevent the expansion of cytotoxic CD8+ T cells

increased regulatory T cell number ( J:227287 )

• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice

immune system

increased CD103-positive CD11b-low dendritic cell number ( J:227287 )

• proportion of CD103+CD11b- dendritic cell subset involved in T-cell priming is higher in tamoxifen treated mice than in single conditional Apc heterozygous mice

increased CD8-positive, alpha-beta T cell number ( J:227287 )

• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice

• administration of IL-1beta receptor antagonist, anakinra, to tamoxifen treated mice is sufficient to prevent the expansion of cytotoxic CD8+ T cells

increased regulatory T cell number ( J:227287 )

• the number of Treg and CD8 IFN-gamma T cells in the lamina propria is higher than in single conditional Apc heterozygous mice

abnormal immune system physiology ( J:227287 )

• tamoxifen treated mice show marked infiltration of lymphocytes within the normal mucosa, higher numbers of CD45 and T cells in the small intestine and colon mucosa, influx of CD11c+ cells in the intestinal mucosa compared to single conditional Apc heterozygous mice, indicating promotion of anti-tumor immune responses

increased interleukin-1 beta secretion ( J:227287 )

• immune cells isolated from the lamina propria of tamoxifen treated mice produce high amounts of IL-1beta

increased interleukin-10 secretion ( J:227287 )

• immune cells isolated from the lamina propria of tamoxifen treated mice produce high amounts of IL-10

cellular

abnormal intestinal goblet cell morphology ( J:227287 )

• abnormal accumulation of granules of mucus in goblet cells in the tumor-free mucosa of tamoxifen treated mice

Genotype
MGI:4461183

cn52

• Allelic Composition: Apc^tm2.1Cip/Apc⁺; Tg(Vil1-cre)20Syr/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * DBA/2

neoplasm

increased intestinal adenoma incidence ( J:160399 )

increased colon adenoma incidence ( J:160399 )

digestive/alimentary system

increased intestinal adenoma incidence ( J:160399 )

increased colon adenoma incidence ( J:160399 )

Genotype
MGI:5532574

cn53

• Allelic Composition: Bmi1^tm1Brn/Bmi1^tm1Brn; Apc^tm2Cip/Apc⁺; Tg(Vil1-cre)20Syr/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * DBA/2

neoplasm

decreased alimentary system tumor incidence ( J:204354 )

• tumors in small intestine are almost absent at 120 days of age

• fewer and smaller tumors at 90 days of age as well

• decrease in numbers of tumors between 90 and 120 days

• no increase in tumor size between 90 and 120 days

decreased colon tumor incidence ( J:204354 )

• also reduced at 120 days

decreased intestinal adenoma incidence ( J:204354 )

• adenomas are one tenth the size of those found in controls at 120 days of age

• increased cell proliferation in adenomas at 90 days

• increased apoptosis in smaller adenomas but not larger ones at 90 days

• apoptosis is also increased in non tumor tissue

cellular

increased apoptosis ( J:204354 )

• increased apoptosis in smaller adenomas but not larger ones at 90 days

• apoptosis is also increased in non tumor tissue

digestive/alimentary system

decreased alimentary system tumor incidence ( J:204354 )

• tumors in small intestine are almost absent at 120 days of age

• fewer and smaller tumors at 90 days of age as well

• decrease in numbers of tumors between 90 and 120 days

• no increase in tumor size between 90 and 120 days

decreased colon tumor incidence ( J:204354 )

• also reduced at 120 days

decreased intestinal adenoma incidence ( J:204354 )

• adenomas are one tenth the size of those found in controls at 120 days of age

• increased cell proliferation in adenomas at 90 days

• increased apoptosis in smaller adenomas but not larger ones at 90 days

• apoptosis is also increased in non tumor tissue

Genotype
MGI:5702414

cn54

• Allelic Composition: Apc^tm2.1Cip/Apc⁺; Tg(Vil1-cre/ERT2)23Syr/0
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * DBA/2

neoplasm

increased intestinal adenoma incidence ( J:227287 )

• tamoxifen treated mice develop intestinal adenomas after the sporadic loss of the remaining Apc allele

increased colon adenoma incidence ( J:227287 )

• tamoxifen treated mice develop colon adenomas after the sporadic loss of the remaining Apc allele

homeostasis/metabolism

abnormal autophagy ( J:227287 )

• tamoxifen-treated mice show activation of autophagy in tumoral cells

mortality/aging

decreased tumor-free survival time ( J:227287 )

• tamoxifen treated mice show signs of illness and have to be euthanized at 135 days due to large tumor burden

growth/size/body

cachexia ( J:227287 )

• tamoxifen treated mice show loss of body weight, pale feet and hunching

digestive/alimentary system

rectal prolapse ( J:227287 )

• tumors of tamoxifen treated mice in the distal colon and rectum are associated with frequent rectal prolapse

increased intestinal adenoma incidence ( J:227287 )

• tamoxifen treated mice develop intestinal adenomas after the sporadic loss of the remaining Apc allele

increased colon adenoma incidence ( J:227287 )

• tamoxifen treated mice develop colon adenomas after the sporadic loss of the remaining Apc allele

intestine polyps ( J:227287 )

• in tamoxifen treated mice

• prolonged antibiotic administration of tamoxifen treated mice does not affect severity of polyposis

• metaformin treatment impairs the growth of polyps in tamoxifen-treated mice but does not affect adenoma cell proliferation

abnormal gut flora balance ( J:227287 )

• tamoxifen treated mice show a difference in the overall composition of both fecal and ileal microbiota compared to double conditional mice heterozygous for Apc and homozygous for Atg7, with mice showing high levels of Gram- bacteria mostly from Helicobacter in the feces

• ileal mucosa of tamoxifen treated mice has a lower bacterial diversity than in double conditional mice heterozygous for Apc and homozygous for Atg7

• the ratio of Gram- to Gram+ bacteria is lower in tamoxifen treated mice than in double conditional mice heterozygous for Apc and homozygous for Atg7

cellular

abnormal autophagy ( J:227287 )

• tamoxifen-treated mice show activation of autophagy in tumoral cells

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:227287

Genotype
MGI:5430612

cn55

• Allelic Composition: Apc^tm1Rsmi/Apc⁺; Ctnnb1^tm1Wvv/Ctnnb1⁺; Tg(Fabp1-cre)1Jig/?
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J * FVB/N

neoplasm

increased gastrointestinal tumor incidence ( J:185942 )

• significantly increased tumor load in the intestine of males but not females compared to heterozygous Apc^tm1Ecrm

• tumors in both the ilium and colon but smaller in size than in heterozygous Apc^tm1Ecrm

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:185942 )

• significantly increased tumor load in the intestine of males but not females compared to heterozygous Apc^tm1Ecrm

• tumors in both the ilium and colon but smaller in size than in heterozygous Apc^tm1Ecrm

Genotype
MGI:4456428

cn56

• Allelic Composition: Apc^tm1Rsmi/Apc⁺; Tg(Fabp1-cre)1Jig/0
• Genetic Background: involves: 129P2/OlaHsd * FVB/N

mortality/aging

increased tumor-free survival time ( J:159883 )

• mice succumb to intestinal tumors later than Apc^tm1.1Ecrm

neoplasm

increased gastrointestinal tumor incidence ( J:159883 )

• mice develop intestinal tumors unlike wild-type mice with later premature death and fewer tumors than Apc^tm1.1Ecrm heterozygotes

• intestinal tumors develop predominantly in the large intestine that are larger than in Apc^tm1.1Ecrm heterozygotes

• large intestine tumors are pedunculated (polypoid) or sessile

increased intestinal adenocarcinoma incidence ( J:159883 )

• intestinal tumors develop predominantly in the large intestine

increased large intestine adenocarcinoma incidence ( J:159883 )

• intestinal tumors develop predominantly in the large intestine

increased small intestine adenocarcinoma incidence ( J:159883 )

• intestinal tumors develop predominantly in the large intestine

increased intestinal adenoma incidence ( J:159883 )

• low and high grade

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:159883 )

• mice develop intestinal tumors unlike wild-type mice with later premature death and fewer tumors than Apc^tm1.1Ecrm heterozygotes

• intestinal tumors develop predominantly in the large intestine that are larger than in Apc^tm1.1Ecrm heterozygotes

• large intestine tumors are pedunculated (polypoid) or sessile

increased intestinal adenocarcinoma incidence ( J:159883 )

• intestinal tumors develop predominantly in the large intestine

increased large intestine adenocarcinoma incidence ( J:159883 )

• intestinal tumors develop predominantly in the large intestine

increased small intestine adenocarcinoma incidence ( J:159883 )

• intestinal tumors develop predominantly in the large intestine

increased intestinal adenoma incidence ( J:159883 )

• low and high grade

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:159883

Genotype
MGI:3776025

cn57

• Allelic Composition: Apc^tm2.1Cip/Apc⁺; Tg(Fabp1-cre)1Jig/0
• Genetic Background: involves: 129P2/OlaHsd * FVB/N

neoplasm

increased intestinal adenocarcinoma incidence ( J:132357 )

• focal, pedunculated adencarcinomas develop in the colon; lesions are typically heterogeneous showing both low grade and malignant epithelium

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:132357 )

• focal, pedunculated adencarcinomas develop in the colon; lesions are typically heterogeneous showing both low grade and malignant epithelium

Genotype
MGI:4946926

cn58

• 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

cn59

• 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

cn60

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

neoplasm

increased intestinal adenoma incidence ( J:291671 )

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

increased colon adenoma incidence ( J:291671 )

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

decreased alimentary system tumor incidence ( J:291671 )

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

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:291671 )

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

increased colon adenoma incidence ( J:291671 )

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

decreased alimentary system tumor incidence ( J:291671 )

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

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

Genotype
MGI:4888016

cn61

• Allelic Composition: Tle5^tm1.1Mmt/Tle5^tm1.1Mmt; Apc^tm1Mmt/Apc⁺; Tg(Vil1-cre/ERT2)23Syr/0
• Genetic Background: involves: 129S2/SvPas * C57BL/6 * DBA * SJL

neoplasm

increased colon adenocarcinoma incidence ( J:168065 )

• adenocarcinomas by histopathological definition

• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apc^tm1Mmt adenomas, without a very malignant appearance

increased small intestine adenocarcinoma incidence ( J:168065 )

• adenocarcinomas by histopathological definition

• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apc^tm1Mmt adenomas, without a very malignant appearance

increased metastatic potential ( J:168065 )

• treated with 4-hydroxytamoxifen to activate Cre recombinase at 3 weeks of age

• tumor invasion and intravasation into the smooth muscle layer of the small intestine and colon at 17 weeks of age

• in polyps larger than 2 mm in diameter, about half of them is found invading into the submucosa or beyond

• often seen inside vessels that are distended, reminiscent of tumor embolism

digestive/alimentary system

increased colon adenocarcinoma incidence ( J:168065 )

• adenocarcinomas by histopathological definition

• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apc^tm1Mmt adenomas, without a very malignant appearance

increased small intestine adenocarcinoma incidence ( J:168065 )

• adenocarcinomas by histopathological definition

• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apc^tm1Mmt adenomas, without a very malignant appearance

Genotype
MGI:5446623

cn62

• Allelic Composition: Apc^tm1Tno/Apc⁺; Tg(CDX2-cre/ERT)#Erf/0
• Genetic Background: involves: 129S4/SvJae

neoplasm

increased gastrointestinal tumor incidence ( J:189226 )

• transformed colonic tissue in tamoxifen-treated mice

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:189226 )

• transformed colonic tissue in tamoxifen-treated mice

Genotype
MGI:6505557

cn63

• Allelic Composition: Apc^tm2Rak/Apc⁺; Kras^tm1.1Khai/Kras⁺; Tg(Fabp1-cre)1Jig/0
• Genetic Background: involves: 129S4/SvJae * 129S6/SvEvTac * C57BL/6 * FVB/N * SJL

neoplasm

increased colon adenoma incidence ( J:276349 )

• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

mortality/aging

premature death ( J:276349 )

• mice show slightly longer survival than conditional mice carrying the Kras^tm4Tyj allele

digestive/alimentary system

increased colon adenoma incidence ( J:276349 )

• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

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

Genotype
MGI:4941759

cn64

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

mortality/aging

premature death ( J:150553 )

• all mutants die within 80 days

neoplasm

increased intestinal adenoma incidence ( J:150553 )

• adenomas in the small intestine

digestive/alimentary system

increased intestinal adenoma incidence ( J:150553 )

• adenomas in the small intestine

intestine polyps ( J:150553 )

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

Genotype
MGI:4430578

cn65

• 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:5446693

cn66

• Allelic Composition: Apc^tm1Tno/Apc⁺; Il23r^tm1.2Trin/Il23r^tm1.2Trin; Tg(CDX2-cre)101Erf/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL/J

neoplasm

decreased tumor growth/size ( J:189226 )

• reduced colorectal tumor multiplicity and grown compared to in Apc^tm1Tno/Apc⁺ Tg(CDX2-cre)101Erf mice

Genotype
MGI:6505558

cn67

• Allelic Composition: Apc^tm2Rak/Apc⁺; Kras^tm4Tyj/Kras⁺; Tg(Fabp1-cre)1Jig/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * FVB/N * SJL

neoplasm

increased colon adenoma incidence ( J:276349 )

• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

mortality/aging

premature death ( J:276349 )

• mice show 100% lethality before 150 days of age

digestive/alimentary system

increased colon adenoma incidence ( J:276349 )

• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia

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

Genotype
MGI:7642164

cn68

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

mortality/aging

decreased tumor-free survival time ( J:278932 )

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

neoplasm

increased intestinal adenoma incidence ( J:278932 )

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

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:278932 )

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

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

Genotype
MGI:3844311

cn69

• Allelic Composition: Apc^tm1Tno/Apc⁺; Tg(CDX2-cre)101Erf/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * SJL

mortality/aging

premature death ( J:126018 )

• 36% (13/36) animals survived to 300 days of observation; 3 died and 20 were euthanized upon signs of distress

growth/size/body

decreased body weight ( J:126018 )

• males show inhibited weight gain after 120 days

neoplasm

increased tumor incidence ( J:126018 )

• mice show around 10 tumors

increased gastrointestinal tumor incidence ( J:126018 )

• an average of 5-8 tumors are found in colon and rectum, wit some tumors being observed in the cecum and distal small intestine

• colorectal tumors may be observed at early time points

• male mice have about 60% more colon tumors than controls

increased mammary adenocarcinoma incidence ( J:126018 )

• a small number of mice also develop mammary tumors

digestive/alimentary system

rectal prolapse ( J:126018 )

• greater than half the animals observed developed rectal prolapse with intermittent bleeding

increased gastrointestinal tumor incidence ( J:126018 )

• an average of 5-8 tumors are found in colon and rectum, wit some tumors being observed in the cecum and distal small intestine

• colorectal tumors may be observed at early time points

• male mice have about 60% more colon tumors than controls

intestinal obstruction ( J:126018 )

• some (3) animals died during the observation period from intestinal obstruction by tumor

hematopoietic system

anemia ( J:126018 )

• mice exhibit mild anemia

decreased hematocrit ( J:126018 )

• mice displaying mild anemia show hematocrits in range of 33 to 35% compared to around 45% in controls

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:126018 )

• a small number of mice also develop mammary tumors

integument

increased mammary adenocarcinoma incidence ( J:126018 )

• a small number of mice also develop mammary tumors

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:126018

Genotype
MGI:3844314

cn70

• Allelic Composition: Apc^tm1Tno/Apc⁺; Tg(Vil1-cre)997Gum/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * SJL

growth/size/body

postnatal growth retardation ( J:126018 )

• male and female animals display growth inhibition compared to controls

hematopoietic system

anemia ( J:126018 )

• mice exhibit severe anemia

neoplasm

increased gastrointestinal tumor incidence ( J:126018 )

• about 36 tumors are observed per mouse; most tumors are located in the small intestine

• cecal and colon tumors are small than those in age-matched in CDX2-cre/APC mice

increased small intestine adenocarcinoma incidence ( J:126018 )

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:126018 )

• about 36 tumors are observed per mouse; most tumors are located in the small intestine

• cecal and colon tumors are small than those in age-matched in CDX2-cre/APC mice

increased small intestine adenocarcinoma incidence ( J:126018 )

Genotype
MGI:3844298

cn71

• Allelic Composition: Apc^tm1Tno/Apc⁺; Tg(CDX2-cre*)189Erf/0
• Genetic Background: involves: 129S4/SvJae * C57BL/6 * SJL

neoplasm

neoplasm ( J:148161 )

N • mice show no signs of disease up to 200 days of age

Genotype
MGI:5475206

cn72

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

neoplasm

abnormal tumor morphology ( J:193873 )

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

digestive/alimentary system

digestive/alimentary phenotype ( J:193873 )

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

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:193873 )

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

Genotype
MGI:4360363

cn73

• 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

cn74

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

neoplasm

increased gastrointestinal tumor incidence ( J:173145 )

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

increased tumor growth/size ( J:173145 )

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

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:173145 )

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

Genotype
MGI:4889209

cn75

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

neoplasm

increased intestinal adenoma incidence ( J:168378 )

• compared with Apc^Min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:168378 )

• compared with Apc^Min heterozygotes

Genotype
MGI:5898453

cn76

• Allelic Composition: Apc^tm2Rak/Apc⁺; Trp53^tm1Brn/Trp53^tm1Brn; Tg(Pdx1-cre)6Tuv/0
• Genetic Background: involves: 129/Sv * 129P2/OlaHsd * C57BL/6J * FVB/N * SJL

mortality/aging

premature death ( J:234310 )

• survival is shorter than either single conditional mutant; mice can survive up to 32 weeks but most have to be euthanized at 24-26 weeks of age

neoplasm

increased pancreas tumor incidence ( J:234310 )

• all mice develop pancreatic neoplasms between 16 and 24 weeks

• 100% of mice exhibit large cystic pancreata which are mucinous cystadenomas, characterized by the presence of unilocular megacystic lesions with mucoid/watery cyst content, and nodules or peripheral calcification on the cyst wall resembling human mucinous cystic neoplasm

• mucinous cystic neoplasms become malignant pancreatic cancer with nuclear anaplastic features, and show stomach, duodenal or intestinal invasion or liver or lung metastasis, consistent with aggressive pancreatic cystic adenocarcinoma

• 6 week old mice treated with the Wnt inhibitor IWP-2 for 12 weeks show a reduction of or absence of hypertrophic pancreas with cysts

increased metastatic potential ( J:234310 )

• tumors exhibit a high incidence of metastasis and invasion

increased cystadenoma incidence ( J:234310 )

• 100% of mice exhibit large cystic pancreata which are mucinous cystadenomas

endocrine/exocrine glands

increased pancreas tumor incidence ( J:234310 )

• all mice develop pancreatic neoplasms between 16 and 24 weeks

• 100% of mice exhibit large cystic pancreata which are mucinous cystadenomas, characterized by the presence of unilocular megacystic lesions with mucoid/watery cyst content, and nodules or peripheral calcification on the cyst wall resembling human mucinous cystic neoplasm

• mucinous cystic neoplasms become malignant pancreatic cancer with nuclear anaplastic features, and show stomach, duodenal or intestinal invasion or liver or lung metastasis, consistent with aggressive pancreatic cystic adenocarcinoma

• 6 week old mice treated with the Wnt inhibitor IWP-2 for 12 weeks show a reduction of or absence of hypertrophic pancreas with cysts

homeostasis/metabolism

increased circulating cholesterol level ( J:234310 )

increased circulating triglyceride level ( J:234310 )

abnormal cytokine level ( J:234310 )

• cystic fluid of the pancreata shows the induction of the following cytokines: FasL, soluble tumor necrosis factor receptor 1, IL-1beta, IL-6, macrophage inflammatory protein 1gamma, keratinocyte chemoattractant and monocyte chemoattractant protein 1

immune system

abnormal cytokine level ( J:234310 )

• cystic fluid of the pancreata shows the induction of the following cytokines: FasL, soluble tumor necrosis factor receptor 1, IL-1beta, IL-6, macrophage inflammatory protein 1gamma, keratinocyte chemoattractant and monocyte chemoattractant protein 1

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
pancreatic mucinous cystadenoma		DOID:7235		J:234310

Genotype
MGI:4835054

cn77

• Allelic Composition: Apc^tm2Rak/Apc⁺; Tg(Car1-cre)5Flt/0
• Genetic Background: involves: 129/Sv * C57BL/6J * SJL

neoplasm

neoplasm ( J:164247 )

N

increased intestinal adenoma incidence ( J:164247 )

• visible gross tumors are observed by 10 weeks of age with no increase in incidence up to 20 weeks in about 20% of animals; two types of lesions (microadenomas and adenomas) are identifiable microscopically

• both lesion types are overrepresented in the distal colon; microadenomas are present in proximal colon as well

increased incidence of tumors by chemical induction ( J:164247 )

• over 60% of mice receiving dextran sodium sulfate (DSS) for 7 days starting at 10 weeks of age have grossly visible adenomatous lesions in the colon with over 70% of the lesions found in the distal colon; mortality is observed in 55% of animals within 4 days of end of treatment, with remainder of treated mice surviving until end point of study at 15 weeks

• about 50% of mice receiving DSS for 5 days starting at 10 weeks of age develop visible tumors by 20 weeks of age with all lesions in the distal colon; mortality is observed in 20% of animals within 4 days of end of treatment, with remainder of treated mice surviving until end point of study at 15 weeks

• some microadenomas are observed in the cecum after DSS treatment

homeostasis/metabolism

homeostasis/metabolism phenotype ( J:164247 )

N • no differences in body weight are observed relative to wild-type even when animals have tumors

increased incidence of tumors by chemical induction ( J:164247 )

• over 60% of mice receiving dextran sodium sulfate (DSS) for 7 days starting at 10 weeks of age have grossly visible adenomatous lesions in the colon with over 70% of the lesions found in the distal colon; mortality is observed in 55% of animals within 4 days of end of treatment, with remainder of treated mice surviving until end point of study at 15 weeks

• about 50% of mice receiving DSS for 5 days starting at 10 weeks of age develop visible tumors by 20 weeks of age with all lesions in the distal colon; mortality is observed in 20% of animals within 4 days of end of treatment, with remainder of treated mice surviving until end point of study at 15 weeks

• some microadenomas are observed in the cecum after DSS treatment

digestive/alimentary system

melena ( J:164247 )

• some mice with tumors produce bloody stool

colon polyps ( J:164247 )

• some adenomatous polyps are identifiable as sessile or pedunculated

increased intestinal adenoma incidence ( J:164247 )

• visible gross tumors are observed by 10 weeks of age with no increase in incidence up to 20 weeks in about 20% of animals; two types of lesions (microadenomas and adenomas) are identifiable microscopically

• both lesion types are overrepresented in the distal colon; microadenomas are present in proximal colon as well

hematopoietic system

anemia ( J:164247 )

• mice with tumors are mildly anemic

decreased hematocrit ( J:164247 )

• hematocrit of mice is 37% vs 48% in wild-type

Genotype
MGI:6357723

cn78

• 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

cn79

• 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

cn80

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

cellular

abnormal gastrointestinal brush cell morphology ( J:227334 )

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

digestive/alimentary system

digestive/alimentary phenotype ( J:227334 )

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

abnormal gastrointestinal brush cell morphology ( J:227334 )

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

abnormal intestinal epithelium morphology ( J:227334 )

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

• the number of Tuft cells are slightly decreased

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

decreased intestinal adenoma incidence ( J:227334 )

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

neoplasm

decreased intestinal adenoma incidence ( J:227334 )

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

increased tumor latency ( J:227334 )

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

hematopoietic system

hematopoietic system phenotype ( J:227334 )

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

immune system

immune system phenotype ( J:227334 )

N • mice do not exhibit splenomegaly

Genotype
MGI:6403689

cn81

• Allelic Composition: Apc^tm1Tno/Apc⁺; Brf1^tm1Arte/Brf1^tm1Arte; Tg(Cyp1a1-cre)1Dwi/0
• Genetic Background: involves: C57BL/6 * CBA

neoplasm

increased pancreatic ductal adenocarcinoma incidence ( J:285667 )

• mice develop similar tumor number and size as in Apc^tm1aTno Tg(Cyp1a1-cre)1Dwi heterozygotes

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:285667 )

• mice develop similar tumor number and size as in Apc^tm1aTno Tg(Cyp1a1-cre)1Dwi heterozygotes

Genotype
MGI:4461182

cn82

• Allelic Composition: Apc^tm1Tyj/Apc⁺; Tg(Vil1-cre)20Syr/0
• Genetic Background: involves: C57BL/6 * DBA/2

neoplasm

increased intestinal adenoma incidence ( J:160399 )

• develop several lesions in the small intestines and colons by 4 - 5 months of age

increased colon adenoma incidence ( J:160399 )

• develop by 4 - 5 months of age

digestive/alimentary system

increased intestinal adenoma incidence ( J:160399 )

• develop several lesions in the small intestines and colons by 4 - 5 months of age

increased colon adenoma incidence ( J:160399 )

• develop by 4 - 5 months of age

Genotype
MGI:5523866

cn83

• 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:3715020

cx84

• Allelic Composition: Cdx2^tm1Mmt/Cdx2⁺; Apc^tm1Mmt/Apc⁺
• Genetic Background: B6.129-Cdx2^tm1Mmt Apc^tm1Mmt

digestive/alimentary system

abnormal colon morphology ( J:86737 )

• increased anaphase bridge index

• accelerated transition from G1 to S phase

• increased DNA synthesis

• lower apoptotic rates

colon polyps ( J:86737 )

• increased in numbers relative to Apc^tm1Mmt

• mostly in the distal colon

abnormal small intestine morphology ( J:86737 )

• decreased anaphase bridge index

• decreased transition from G1 to S phase

• decreased DNA synthesis

• increased apoptotic rates

• significantly reduced number of polyps relative to Apc^tm1Mmt

cellular

abnormal chromosome morphology ( J:86737 )

• increased anaphase bridge index in the large intestine and decreased in the small intestine

abnormal cell cycle checkpoint function ( J:86737 )

• accelerated transition from G1 to S phase in the large intestine and decreased in the small intestine

• increased DNA synthesis in the large intestine and decreased in the small intestine

decreased apoptosis ( J:86737 )

• lower apoptotic rates in the large intestine

increased apoptosis ( J:86737 )

• in the small intestine

Genotype
MGI:3766126

cx85

• Allelic Composition: Apc^tm1Rak/Apc⁺; Smad4^E6sad/Smad4⁺
• Genetic Background: B6.129P2-Apc^tm1Rak +/+ Smad4^E6sad

mortality/aging

premature death ( J:107273 )

• Background Sensitivity: all mice have died by 8 months of age due to complications arising from intestinal tumors

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:107273 )

• Background Sensitivity: in two of seven mice, adenocarcinomas with invasion of the muscolaris mucosa are observed

increased intestinal adenoma incidence ( J:107273 )

• Background Sensitivity: by 7 months of age, mice present with an average of 20 tumors along the intestinal tract

• Background Sensitivity: tumors are mainly villous or tubulovillous adenomas with foci of severe dysplasia

gastric polyps ( J:107273 )

• Background Sensitivity: in 100% of mice by 7 months of age

neoplasm

increased intestinal adenocarcinoma incidence ( J:107273 )

• Background Sensitivity: in two of seven mice, adenocarcinomas with invasion of the muscolaris mucosa are observed

increased intestinal adenoma incidence ( J:107273 )

• Background Sensitivity: by 7 months of age, mice present with an average of 20 tumors along the intestinal tract

• Background Sensitivity: tumors are mainly villous or tubulovillous adenomas with foci of severe dysplasia

Genotype
MGI:3766123

cx86

• Allelic Composition: Apc^tm1Rak/Apc⁺; Smad4^E6sad/Smad4⁺
• Genetic Background: B6.129P2-Apc^tm1Rak Smad4^E6sad/+ +

mortality/aging

premature death ( J:107273 )

• Background Sensitivity: all mice have died by 3 months of age due to complications arising from intestinal tumors

neoplasm

increased intestinal adenoma incidence ( J:107273 )

• Background Sensitivity: numerous microadenomas in the upper gastrointestinal tract are present upon microscopic inspection

digestive/alimentary system

increased intestinal adenoma incidence ( J:107273 )

• Background Sensitivity: numerous microadenomas in the upper gastrointestinal tract are present upon microscopic inspection

intestine polyps ( J:107273 )

• Background Sensitivity: an average of 60 tumors per mouse by 6 weeks of age

• Background Sensitivity: polyps are either sessile or villous with mild to severe dysplasia

gastric polyps ( J:107273 )

• Background Sensitivity: found in 25% of 3-6 week old mice

hematopoietic system

enlarged spleen ( J:107273 )

• Background Sensitivity: found in moribund mice

anemia ( J:107273 )

• Background Sensitivity: moribund mice have frank anemia

immune system

enlarged spleen ( J:107273 )

• Background Sensitivity: found in moribund mice

growth/size/body

enlarged spleen ( J:107273 )

• Background Sensitivity: found in moribund mice

Genotype
MGI:3814367

cx87

• 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

cx88

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

neoplasm

abnormal tumor susceptibility ( J:66060 )

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

decreased alimentary system tumor incidence ( J:66060 )

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

decreased mammary gland tumor incidence ( J:66060 )

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

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

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

homeostasis/metabolism

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

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

integument

decreased mammary gland tumor incidence ( J:66060 )

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

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:66060 )

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

digestive/alimentary system

decreased alimentary system tumor incidence ( J:66060 )

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

Genotype
MGI:5567980

cx89

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

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

neoplasm

increased gastrointestinal tumor incidence ( J:205135 )

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

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

increased intestinal adenoma incidence ( J:205135 )

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

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

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:205135 )

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

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

increased intestinal adenoma incidence ( J:205135 )

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

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

Genotype
MGI:5430745

cx90

• 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

cx91

• 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

cx92

• 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

cx93

• 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:4440863

cx94

• 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:4440864

cx95

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

neoplasm

increased intestinal adenoma incidence ( J:158733 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:158733 )

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

Genotype
MGI:5426849

cx96

• 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

cx97

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

neoplasm

increased gastrointestinal tumor incidence ( J:143706 )

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

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

increased intestinal adenocarcinoma incidence ( J:143706 )

• 3 mice develop large, polyploidy and ulcerated colonic tumors

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:143706 )

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

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

increased intestinal adenocarcinoma incidence ( J:143706 )

• 3 mice develop large, polyploidy and ulcerated colonic tumors

Genotype
MGI:5881919

cx98

• 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

cx99

• 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

cx100

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

neoplasm

decreased intestinal adenoma incidence ( J:157023 )

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

abnormal tumor pathology ( J:157023 )

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

• Rac1 and Cdc42 signaling appears to be reduced

abnormal tumor vascularization ( J:157023 )

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

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

decreased tumor growth/size ( J:157023 )

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

cardiovascular system

abnormal tumor vascularization ( J:157023 )

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

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

homeostasis/metabolism

decreased physiological sensitivity to xenobiotic ( J:157023 )

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

digestive/alimentary system

decreased intestinal adenoma incidence ( J:157023 )

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

Genotype
MGI:5881917

cx101

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

neoplasm

decreased intestinal adenoma incidence ( J:157023 )

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

decreased tumor growth/size ( J:157023 )

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

digestive/alimentary system

decreased intestinal adenoma incidence ( J:157023 )

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

Genotype
MGI:5881916

cx102

• 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:7662831

cx103

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

mortality/aging

increased tumor-free survival time ( J:331404 )

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

neoplasm

decreased alimentary system tumor incidence ( J:331404 )

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

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

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

digestive/alimentary system

decreased alimentary system tumor incidence ( J:331404 )

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

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

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

Genotype
MGI:7662832

cx104

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

mortality/aging

increased tumor-free survival time ( J:331404 )

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

Genotype
MGI:7662833

cx105

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

mortality/aging

increased tumor-free survival time ( J:331404 )

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

Genotype
MGI:7310033

cx106

• 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

cx107

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

neoplasm

decreased alimentary system tumor incidence ( J:15703 )

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

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

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

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

decreased intestinal adenoma incidence ( J:15703 )

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

digestive/alimentary system

decreased alimentary system tumor incidence ( J:15703 )

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

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

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

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

decreased intestinal adenoma incidence ( J:15703 )

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

Genotype
MGI:6108175

cx108

• 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

cx109

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

neoplasm

increased intestinal adenoma incidence ( J:118232 )

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

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

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:118232 )

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

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

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

Genotype
MGI:3700063

cx110

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

neoplasm

increased intestinal adenoma incidence ( J:118232 )

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

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

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:118232 )

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

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

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

Genotype
MGI:4355516

cx111

• Allelic Composition: Apc^tm1Rak/Apc⁺; Msh2^tm1Rak/Msh2^tm1Rak
• Genetic Background: involves: 129P2/OlaHsd

mortality/aging

premature death ( J:64667 )

• mortality at 2-3 months of age

neoplasm

increased tumor incidence ( J:64667 )

• average of 81 tumors/mouse

Genotype
MGI:3845818

cx112

• Allelic Composition: Apc^tm1Cip/Apc⁺; H19^tm1Lda/H19⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas

neoplasm

increased adenoma incidence ( J:138826 )

• mice exhibit a 1.4-fold increase in the number of adenomas compared to in Apc^tm1Cip heterozygotes

Genotype
MGI:3845817

cx113

• Allelic Composition: Apc^tm1Cip/Apc⁺; H19^tm1Lda/H19⁺
• Genetic Background: involves: 129P2/OlaHsd * 129S2/SvPas * C57BL/6 * CBA

neoplasm

increased intestinal adenocarcinoma incidence ( J:138826 )

• some adenocarcinoma in situ in the intestines

increased adenoma incidence ( J:138826 )

• mice exhibit a 2.2-fold increase in the number of adenomas compared to in Apc^tm1Cip heterozygotes

digestive/alimentary system

colon polyps ( J:138826 )

• mice exhibit a 3-fold increase in the number of small polyps compared to in Apc^tm1Cip heterozygotes

increased intestinal adenocarcinoma incidence ( J:138826 )

• some adenocarcinoma in situ in the intestines

Genotype
MGI:6764552

cx114

• Allelic Composition: Apc^tm1Rak/Apc⁺; Pms2^tm1.1Sks/Pms2^tm1.1Sks
• Genetic Background: involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J

digestive/alimentary system

intestine polyps ( J:310354 )

• mice exhibit increased intestinal polyp formation with microsatellite instability compared with Apc^tm1Rak heterozygotes

• however, morphology of polyps is the same as in Apc^tm1Rak heterozygotes

Genotype
MGI:6713511

cx115

• Allelic Composition: Apc^tm1Cip/Apc⁺; Cdhr5^tm1Lex/Cdhr5^tm1Lex
• Genetic Background: involves: 129P2/OlaHsd * 129S5/SvEvBrd * C57BL/6

digestive/alimentary system

increased intestinal adenoma incidence ( J:301471 )

• at 6-8 months of age, 83% of mice show symptoms of neoplasia (rectal bleeding, anemia, splenomegaly) and 1 or more macroadenomas in the intestinal tract relative to 56% in Apc^tm1Cip heterozygotes

• a greater % of mice develop 51 to 100 or over 100 polyps (all sizes) in the intestinal tract, and the average number of tumors per mouse is ~3-fold higher than that in Apc^tm1Cip heterozygotes

neoplasm

increased intestinal adenoma incidence ( J:301471 )

• at 6-8 months of age, 83% of mice show symptoms of neoplasia (rectal bleeding, anemia, splenomegaly) and 1 or more macroadenomas in the intestinal tract relative to 56% in Apc^tm1Cip heterozygotes

• a greater % of mice develop 51 to 100 or over 100 polyps (all sizes) in the intestinal tract, and the average number of tumors per mouse is ~3-fold higher than that in Apc^tm1Cip heterozygotes

increased tumor growth/size ( J:301471 )

• mice develop more tumors, esp. larger ones, in the intestinal tract; the average number of macroadenomas (>5 mm) per mouse is ~3-fold higher than that in Apc^tm1Cip heterozygotes

• however, no differences in tumor grade, aggressiveness or proliferation are observed

Genotype
MGI:5636670

cx116

• 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

cx117

• 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

cx118

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

neoplasm

increased gastrointestinal tumor incidence ( J:79058 )

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

increased intestinal adenoma incidence ( J:79058 )

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

increased colon adenoma incidence ( J:79058 )

• all colonic adenomas displayed high-grade dysplasia

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:79058 )

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

increased intestinal adenoma incidence ( J:79058 )

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

increased colon adenoma incidence ( J:79058 )

• all colonic adenomas displayed high-grade dysplasia

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

Genotype
MGI:4429611

cx119

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

mortality/aging

premature death ( J:45433 )

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

• all mice die within 5 months

neoplasm

increased gastrointestinal tumor incidence ( J:45433 )

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

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:45433 )

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

Genotype
MGI:5693797

cx120

• 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:2682909

cx121

• Allelic Composition: Apc^tm1Rak/Apc⁺; Hmmr^tm1Baa/Hmmr^tm1Baa
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

neoplasm

decreased tumor incidence ( J:86065 )

• decreased number of aggressive fibromatosis tumors formed relative to Apc^tm1Rak heterozygotes

• the number of gastrointestinal polyps was not altered relative to Apc^tm1Rak heterozygotes

Genotype
MGI:5312326

cx122

• Allelic Composition: Apc^tm1Rak/Apc⁺; Dcc^tm1.1Mehl/Dcc^tm1.1Mehl
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

neoplasm

increased gastrointestinal tumor incidence ( J:181517 )

• all mice have tumors whereas 21.4% of heterozygous Apc^tm1Rak controls are tumor free

• tumor apoptosis rate in adenomas is reduced

increased intestinal adenocarcinoma incidence ( J:181517 )

• 100% have adenocarcenomas

increased metastatic potential ( J:181517 )

• 45.5% of tumors involve serosal invasion compared to 8% in controls

• micrometastatic lesions are found in the liver when serosal invasion occurs

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:181517 )

• all mice have tumors whereas 21.4% of heterozygous Apc^tm1Rak controls are tumor free

• tumor apoptosis rate in adenomas is reduced

increased intestinal adenocarcinoma incidence ( J:181517 )

• 100% have adenocarcenomas

Genotype
MGI:4412021

cx123

• Allelic Composition: Apc^tm1Rak/Apc⁺; Mlh1^tm1Rak/Mlh1^tm1Rak
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

mortality/aging

premature death ( J:53451 )

• all mice die by 4 months of age

neoplasm

increased tumor incidence ( J:53451 )

• all mice develop tumors at an average age of 3.3 months

• all mice develop gastrointestinal tract tumors and 9% develop non-gastrointestinal tract tumors

increased gastrointestinal tumor incidence ( J:53451 )

• all mice develop gastrointestinal tract tumors

• mice exhibit a 30-fold increase in gastrointestinal tumors compared to Mlh1^tm1Rak homozygotes

• mice exhibit a 4- to 5-fold increase in stomach and colon tumors, and a 25- to 100-fold increase in duodenum, jejunum, and ileum compared to in homozygous mice

increased skin tumor incidence ( J:53451 )

• one mouse develops skin carcinoma with lung metastasis

increased adenoma incidence ( J:53451 )

• 34% of mice develop microadenomas and 36% adenomas

increased lymphoma incidence ( J:53451 )

• non-Hodgkin's lymphoma in two mice

increased carcinoma incidence ( J:53451 )

• mice develop gastrointestinal adenocarcinomas, early invasive carcinomas (in 13% of mice), and carcinomas (in 17% of mice)

increased adenocarcinoma incidence ( J:53451 )

digestive/alimentary system

melena ( J:53451 )

• at 2 to 4 weeks of age

increased gastrointestinal tumor incidence ( J:53451 )

• all mice develop gastrointestinal tract tumors

• mice exhibit a 30-fold increase in gastrointestinal tumors compared to Mlh1^tm1Rak homozygotes

• mice exhibit a 4- to 5-fold increase in stomach and colon tumors, and a 25- to 100-fold increase in duodenum, jejunum, and ileum compared to in homozygous mice

integument

increased skin tumor incidence ( J:53451 )

• one mouse develops skin carcinoma with lung metastasis

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
Lynch syndrome		DOID:3883	OMIM:PS120435	J:53451

Genotype
MGI:4412022

cx124

• Allelic Composition: Apc^tm1Rak/Apc⁺; Mlh1^tm1Rak/Mlh1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6

mortality/aging

premature death ( J:53451 )

• all mice die by 14 months of age

neoplasm

increased tumor incidence ( J:53451 )

• 85% of mice develop tumors at an average age of 9.4 months

• 77% of mice develop gastrointestinal tract tumors and 23% of mice develop extra-gastrointestinal tract tumors

increased gastrointestinal tumor incidence ( J:53451 )

• 77% of mice develop gastrointestinal tract tumors

• mice exhibit a 7-fold increase in gastrointestinal tumors compared to Mlh1^tm1Rak heterozygotes

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:53451 )

• 77% of mice develop gastrointestinal tract tumors

• mice exhibit a 7-fold increase in gastrointestinal tumors compared to Mlh1^tm1Rak heterozygotes

Genotype
MGI:3834880

cx125

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

neoplasm

neoplasm ( J:95893 )

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

increased colon adenoma incidence ( J:95893 )

• adenomatous polyps contain a large number of proliferating epithelial cells

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

digestive/alimentary system

colon polyps ( J:95893 )

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

increased colon adenoma incidence ( J:95893 )

• adenomatous polyps contain a large number of proliferating epithelial cells

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

gastric polyps ( J:95893 )

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

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

cellular

abnormal cell physiology ( J:95893 )

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

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

Genotype
MGI:3613447

cx126

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

mortality/aging

premature death ( J:104155 )

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

neoplasm

increased intestinal adenoma incidence ( J:104155 )

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

decreased tumor growth/size ( J:104155 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:104155 )

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

Genotype
MGI:5426846

cx127

• 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:6715308

cx128

• Allelic Composition: Apc^tm1Cip/Apc⁺; Mki67^em1Dfis/Mki67^em1Dfis
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J

neoplasm

decreased incidence of tumors by chemical induction ( J:304800 )

• 6 months after induction of colon tumors by AOM-DSS treatment, mice exhibit a significant decrease both in the number of neoplastic lesions/mouse and in total lesion area (mm2) relative to similarly treated mice heterozygous for Mki67^em1Dfis and Apc^tm1Cip

decreased tumor growth/size ( J:304800 )

• 6 months after AOM-DSS treatment, mice exhibit a significant decrease in total lesion area (mm2) relative to similarly treated mice heterozygous for Mki67^em1Dfis and Apc^tm1Cip

homeostasis/metabolism

decreased incidence of tumors by chemical induction ( J:304800 )

• 6 months after induction of colon tumors by AOM-DSS treatment, mice exhibit a significant decrease both in the number of neoplastic lesions/mouse and in total lesion area (mm2) relative to similarly treated mice heterozygous for Mki67^em1Dfis and Apc^tm1Cip

Genotype
MGI:3579839

cx129

• 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

cx130

• 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:5574446

cx131

• Allelic Composition: Apc^tm1Cip/Apc⁺; Nrip1^tm1Mpk/Nrip1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

premature death ( J:211324 )

♀ • compared with Apc^tm1Cip heterozygotes

Genotype
MGI:5636659

cx132

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

mortality/aging

premature death ( J:75393 )

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

neoplasm

increased intestinal adenoma incidence ( J:75393 )

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

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:75393 )

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

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

intestine polyps ( J:200824 )

intestinal obstruction ( J:75393 )

• due to tumors

hematopoietic system

anemia ( J:75393 )

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

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

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

Genotype
MGI:3830619

cx133

• Allelic Composition: Apc^tm1Rak/Apc⁺; Cdh1^tm1Cbm/Cdh1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

neoplasm

increased intestinal adenocarcinoma incidence ( J:65142 )

• mice develop an average of 11.3 tumors per animal in the small intestine unlike wild-type mice

• mice develop more tumors than in Apc^tm1Rak heterozygotes with tumor size the same as in Apc^tm1Rak heterozygotes

• tumors are invasive although no metastasis is detected

increased stomach tumor incidence ( J:65142 )

• 5-fold more mice develop gastric cancer compared to in Apc^tm1Rak heterozygotes

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:65142 )

• mice develop an average of 11.3 tumors per animal in the small intestine unlike wild-type mice

• mice develop more tumors than in Apc^tm1Rak heterozygotes with tumor size the same as in Apc^tm1Rak heterozygotes

• tumors are invasive although no metastasis is detected

increased stomach tumor incidence ( J:65142 )

• 5-fold more mice develop gastric cancer compared to in Apc^tm1Rak heterozygotes

Genotype
MGI:4946621

cx134

• 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:3610196

cx135

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

neoplasm

increased gastrointestinal tumor incidence ( J:75249 )

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

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:75249 )

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

Genotype
MGI:5430611

cx136

• Allelic Composition: Apc^tm2Rfo/Apc⁺; Ctnnb1^tm1.2Wvv/Ctnnb1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

embryonic lethality, complete penetrance ( J:185942 )

embryo

rostral body truncation ( J:185942 )

• anterior truncation

Genotype
MGI:4359622

cx137

• 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:5430610

cx138

• Allelic Composition: Apc^tm1Rak/Apc⁺; Ctnnb1^tm1.2Wvv/Ctnnb1⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

mortality/aging

embryonic lethality, complete penetrance ( J:185942 )

embryo

rostral body truncation ( J:185942 )

• anterior truncation

nervous system

abnormal telencephalon development ( J:185942 )

• severe reduction in the telencephalic region of the brain

Genotype
MGI:4360688

cx139

• Allelic Composition: Apc^tm2Rfo/Apc⁺; Smad4^E6sad/Smad4⁺
• Genetic Background: involves: 129P2/OlaHsd * C57BL/6J

Phenotypic analysis of the compound in cis Apc^tm2Rfo/Apc⁺ Smad4^E6sad/Smad4⁺ mouse model

neoplasm

increased gastrointestinal tumor incidence ( J:151494 )

• unlike in Apc^tm2Rfo heterozygotes, mice develop multiple gastro-intestinal tumors and adenomatous polyps

increased mammary adenocarcinoma incidence ( J:151494 )

• similar to in Apc^tm2Rfo heterozygotes

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:151494 )

• unlike in Apc^tm2Rfo heterozygotes, mice develop multiple gastro-intestinal tumors and adenomatous polyps

integument

increased mammary adenocarcinoma incidence ( J:151494 )

• similar to in Apc^tm2Rfo heterozygotes

endocrine/exocrine glands

increased mammary adenocarcinoma incidence ( J:151494 )

• similar to in Apc^tm2Rfo heterozygotes

Genotype
MGI:4366246

cx140

• 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

cx141

• 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

cx142

• 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:3700062

cx143

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

neoplasm

increased intestinal adenoma incidence ( J:118232 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:118232 )

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

Genotype
MGI:5319648

cx144

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

neoplasm

increased salivary gland tumor incidence ( J:57721 )

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

increased intestinal adenoma incidence ( J:57721 )

• adenomatous polyps form throughout the intestine

• large in size but showing no signs of tumor progression

increased mammary adenoacanthoma incidence ( J:57721 )

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

• also in older male mice

digestive/alimentary system

increased salivary gland tumor incidence ( J:57721 )

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

increased intestinal adenoma incidence ( J:57721 )

• adenomatous polyps form throughout the intestine

• large in size but showing no signs of tumor progression

endocrine/exocrine glands

increased salivary gland tumor incidence ( J:57721 )

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

increased mammary adenoacanthoma incidence ( J:57721 )

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

• also in older male mice

integument

increased mammary adenoacanthoma incidence ( J:57721 )

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

• also in older male mice

growth/size/body

increased salivary gland tumor incidence ( J:57721 )

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

craniofacial

increased salivary gland tumor incidence ( J:57721 )

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

Genotype
MGI:3719427

cx145

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

mortality/aging

premature death ( J:77896 )

• mice exhibit reduced survival

neoplasm

increased intestinal adenoma incidence ( J:77896 )

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

homeostasis/metabolism

abnormal DNA repair ( J:77896 )

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

cellular

abnormal DNA repair ( J:77896 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:77896 )

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

Genotype
MGI:5448541

cx146

• 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

cx147

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

neoplasm

increased intestinal adenoma incidence ( J:221231 )

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

• significantly elevated polyp mass

digestive/alimentary system

increased intestinal adenoma incidence ( J:221231 )

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

• significantly elevated polyp mass

Genotype
MGI:4365607

cx148

• Allelic Composition: Apc^tm1Mmt/Apc⁺; Mmp7^tm1Lmm/Mmp7^tm1Lmm; Smad4^tm1Mmt/Smad4⁺
• Genetic Background: involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ

neoplasm

decreased tumor growth/size ( J:142797 )

• mice exhibit a decrease in tumors size compared to in Apc^tm1Mmt Smad4^tm1Mmt homozygotes

• the ratio of small tumors is increased compared to in Apc^tm1Mmt Smad4^tm1Mmt homozygotes

• however, mice exhibit the same tumor invasion depth and number of fibroblasts in tumor stroma as in Apc^tm1Mmt Smad4^tm1Mmt homozygotes

decreased tumor incidence ( J:142797 )

• mice develop 50% fewer tumors than in Apc^tm1Mmt Smad4^tm1Mmt homozygotes

Genotype
MGI:4946925

cx149

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

neoplasm

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

Genotype
MGI:3831111

cx150

• 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:3790616

cx151

• Allelic Composition: Apc^tm1Mmt/Apc⁺; Smad2^tm2Kato/Smad2⁺
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J

mortality/aging

decreased tumor-free survival time ( J:79668 )

• a small number of mice die suddenly, before thirty weeks of age, as result of lethal intestinal obstruction by large tumorous polyps

neoplasm

increased intestinal adenoma incidence ( J:79668 )

• numerous intestinal tumors develop in homozygotes: compound mutants have more intestinal tumors >4 mm in diameter than Apc^tm1Mmt heterozygotes

• frequently one or two tumors >6 mm in diameter develop

• 10-15% of intestinal polyps exhibit stromal and vascular invasion

• tubular adenomas vary in size and shape, and solid colonies of poorly differentiated carcinoma cells are sometimes observed

• nuclei display more hyperchromaticity than those in tumors in Apc single heterozygotes; nuclear atypia in tumors is enhanced indicating increased malignancy

digestive/alimentary system

increased intestinal adenoma incidence ( J:79668 )

• numerous intestinal tumors develop in homozygotes: compound mutants have more intestinal tumors >4 mm in diameter than Apc^tm1Mmt heterozygotes

• frequently one or two tumors >6 mm in diameter develop

• 10-15% of intestinal polyps exhibit stromal and vascular invasion

• tubular adenomas vary in size and shape, and solid colonies of poorly differentiated carcinoma cells are sometimes observed

• nuclei display more hyperchromaticity than those in tumors in Apc single heterozygotes; nuclear atypia in tumors is enhanced indicating increased malignancy

Genotype
MGI:3790617

cx152

• Allelic Composition: Apc^tm1Mmt/Apc⁺; Smad2^tm1Kato/Smad2⁺
• Genetic Background: involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J

mortality/aging

decreased tumor-free survival time ( J:79668 )

• a small number of mice die suddenly, before thirty weeks of age, as result of lethal intestinal obstruction by large tumorous polyps

neoplasm

increased intestinal adenoma incidence ( J:79668 )

• numerous intestinal tumors develop in homozygotes: compound mutants have more intestinal tumors >4 mm in diameter than Apc^tm1Mmt heterozygotes

• frequently one or two tumors >6 mm in diameter develop

• 10-15% of intestinal polyps exhibit stromal and vascular invasion

• tubular adenomas vary in size and shape, and solid colonies of poorly differentiated carcinoma cells are sometimes observed

• nuclei display more hyperchromaticity than those in tumors in Apc single heterozygotes; nuclear atypia in tumors is enhanced indicating increased malignancy

digestive/alimentary system

increased intestinal adenoma incidence ( J:79668 )

• numerous intestinal tumors develop in homozygotes: compound mutants have more intestinal tumors >4 mm in diameter than Apc^tm1Mmt heterozygotes

• frequently one or two tumors >6 mm in diameter develop

• 10-15% of intestinal polyps exhibit stromal and vascular invasion

• tubular adenomas vary in size and shape, and solid colonies of poorly differentiated carcinoma cells are sometimes observed

• nuclei display more hyperchromaticity than those in tumors in Apc single heterozygotes; nuclear atypia in tumors is enhanced indicating increased malignancy

Genotype
MGI:3603950

cx153

• Allelic Composition: Apc^tm1Mmt/Apc⁺; Ptgs2^tm1Jed/Ptgs2^tm1Jed
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

digestive/alimentary system

abnormal intestine morphology ( J:36816 )

• at 10 weeks, these mutants develop only ~14% of the polyp number detected in the intestinal tracts of mice heterozygous for Apc^tm1Mmt alone

• the size of intestinal polyps is significantly smaller (<1.0 mm) than that observed in mice heterozygous for Apc^tm1Mmt alone, with no polyps larger than 2.0 mm in diameter

• histologically, well-developed polyps are not covered with the normal intestinal epithelium and appear flatter than polyps found in Apc^tm1Mmt heterozygous controls

• notably, no colonic polyps are observed

Genotype
MGI:3603949

cx154

• Allelic Composition: Apc^tm1Mmt/Apc⁺; Ptgs2^tm1Jed/Ptgs2⁺
• Genetic Background: involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J

digestive/alimentary system

abnormal intestine morphology ( J:36816 )

• at 10 weeks, double heterozygotes develop only ~34% of the polyp number detected in the intestinal tracts of mice heterozygous for Apc^tm1Mmt alone

colon polyps ( J:36816 )

• at 10 weeks, double heterozygotes exhibit only 1.5 1.9 colonic polyps versus 6.8 7.2 detected in mice heterozygous for Apc^tm1Mmt alone

Genotype
MGI:4365606

cx155

• 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:2182802

cx156

• Allelic Composition: Apc^tm1Mmt/Apc⁺; Smad4^tm1Mmt/Smad4⁺
• Genetic Background: involves: 129S2/SvPas * C57BL/6

mortality/aging

premature death ( J:46242 )

• most mutants become moribund before 14-20 weeks and often die of intussusception of the small intestine

neoplasm

increased intestinal adenocarcinoma incidence ( J:46242 )

• polyps in small and large intestine develop into malignant adenocarcinomas, beginning at about 14 weeks

increased pancreatic ductal adenocarcinoma incidence ( J:46242 )

• adenocarcinomas found in ampullary region of the pancreatic duct, incomplete penetrance

integument

epidermal cyst ( J:46242 )

• in 53% of mice older than 10 weeks, skin epidermoid cysts found in left axillary region and/or ventral side of the neck

endocrine/exocrine glands

increased pancreatic ductal adenocarcinoma incidence ( J:46242 )

• adenocarcinomas found in ampullary region of the pancreatic duct, incomplete penetrance

growth/size/body

epidermal cyst ( J:46242 )

• in 53% of mice older than 10 weeks, skin epidermoid cysts found in left axillary region and/or ventral side of the neck

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:46242 )

• polyps in small and large intestine develop into malignant adenocarcinomas, beginning at about 14 weeks

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
colorectal cancer		DOID:9256	OMIM:114500	J:46242

Genotype
MGI:5298868

cx157

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

neoplasm

increased gastrointestinal tumor incidence ( J:118600 )

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

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

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

digestive/alimentary system

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon in ovariectomized

increased gastrointestinal tumor incidence ( J:118600 )

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

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

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

cellular

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon in ovariectomized

Genotype
MGI:5298869

cx158

• 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:4357790

cx159

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

neoplasm

increased small intestine adenocarcinoma incidence ( J:152134 )

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

decreased tumor incidence ( J:152134 )

• mice develop fewer intestinal tumors than Apc^Min controls

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

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

digestive/alimentary system

increased small intestine adenocarcinoma incidence ( J:152134 )

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

Genotype
MGI:5298871

cx160

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

neoplasm

increased gastrointestinal tumor incidence ( J:118600 )

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

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

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

increased colon adenoma incidence ( J:118600 )

• noninvasive

increased carcinoma incidence ( J:118600 )

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

digestive/alimentary system

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon

abnormal intestinal mucosa morphology ( J:118600 )

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

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

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

abnormal colon goblet cell morphology ( J:118600 )

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

increased gastrointestinal tumor incidence ( J:118600 )

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

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

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

increased colon adenoma incidence ( J:118600 )

• noninvasive

endocrine/exocrine glands

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

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

abnormal colon goblet cell morphology ( J:118600 )

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

cellular

abnormal colon goblet cell morphology ( J:118600 )

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

abnormal enterocyte proliferation ( J:118600 )

• increased proliferation of cells in the colon

Genotype
MGI:4820588

cx161

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

mortality/aging

premature death ( J:46419 )

• mice die earlier than Apc^min heterozygotes

neoplasm

increased intestinal adenoma incidence ( J:46419 )

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

• however, no evidence of adenocarcinoma is observed

• tumors exhibit microsatellite instability

digestive/alimentary system

increased intestinal adenoma incidence ( J:46419 )

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

• however, no evidence of adenocarcinoma is observed

• tumors exhibit microsatellite instability

intestine polyps ( J:46419 )

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

Genotype
MGI:5298870

cx162

• 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:3764961

cx163

• Allelic Composition: Apc^tm1.1Tno/Apc⁺; Ctnna1^del/Ctnna1⁺
• Genetic Background: involves: 129S4/SvJae * C57BL/6

neoplasm

neoplasm ( J:127452 )

N • the tumorigenic phenotype associated with the Apc^tm1.1Tno allele does not occur when both alleles are in a cis-configuration

Genotype
MGI:5313420

cx164

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

neoplasm

neoplasm ( J:127808 )

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

Genotype
MGI:5313421

cx165

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

neoplasm

neoplasm ( J:127808 )

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

Genotype
MGI:5313419

cx166

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

neoplasm

increased intestinal adenoma incidence ( J:127808 )

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

increased tumor growth/size ( J:127808 )

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

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

cellular

abnormal DNA methylation ( J:127808 )

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

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

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

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:127808 )

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

Genotype
MGI:3839104

cx167

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

neoplasm

decreased incidence of induced tumors ( J:146871 )

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

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

Genotype
MGI:6377634

cx168

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

digestive/alimentary system

increased colon tumor incidence ( J:231166 )

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

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

neoplasm

increased colon tumor incidence ( J:231166 )

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

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

Genotype
MGI:5313423

cx169

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

neoplasm

neoplasm ( J:127808 )

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

Genotype
MGI:4430577

cx170

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

neoplasm

increased gastrointestinal tumor incidence ( J:134301 )

• mice develop intestinal tumors in the duodenum and ileum

growth/size/body

cachexia ( J:134301 )

• at 16 weeks

hematopoietic system

anemia ( J:134301 )

• at 16 weeks

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:134301 )

• mice develop intestinal tumors in the duodenum and ileum

Genotype
MGI:3848450

cx171

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

digestive/alimentary system

intestine polyps ( J:75230 )

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

• polyps are smaller than in Apc^Min heterozygotes

Genotype
MGI:3848453

cx172

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

digestive/alimentary system

digestive/alimentary phenotype ( J:75230 )

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

Genotype
MGI:3848451

cx173

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

digestive/alimentary system

intestine polyps ( J:75230 )

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

• polyps are smaller than in Apc^Min heterozygotes

Genotype
MGI:6502660

cx174

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

mortality/aging

premature death ( J:299895 )

neoplasm

increased colon tumor incidence ( J:299895 )

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

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

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

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

digestive/alimentary system

increased colon tumor incidence ( J:299895 )

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

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

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

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

Genotype
MGI:6502661

cx175

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

neoplasm

increased colon tumor incidence ( J:299895 )

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

digestive/alimentary system

increased colon tumor incidence ( J:299895 )

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

Genotype
MGI:6849776

cx176

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

digestive/alimentary system

increased colon tumor incidence ( J:316087 )

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

neoplasm

increased colon tumor incidence ( J:316087 )

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

Genotype
MGI:6849775

cx177

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

digestive/alimentary system

increased colon tumor incidence ( J:316087 )

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

neoplasm

increased colon tumor incidence ( J:316087 )

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

Genotype
MGI:5451046

cx178

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

neoplasm

neoplasm ( J:190754 )

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

Genotype
MGI:3512138

cx179

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

neoplasm

increased intestinal adenoma incidence ( J:93327 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:93327 )

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

Genotype
MGI:5446699

cx180

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

neoplasm

increased intestinal adenoma incidence ( J:189217 )

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

increased tumor growth/size ( J:189217 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:189217 )

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

Genotype
MGI:3812011

cx181

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

mortality/aging

mortality/aging ( J:134087 )

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

digestive/alimentary system

intestine polyps ( J:134087 )

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

abnormal digestive system physiology ( J:134087 )

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

hematopoietic system

hematopoietic system phenotype ( J:134087 )

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

abnormal hematopoietic system morphology/development ( J:134087 )

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

Genotype
MGI:3575580

cx182

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

neoplasm

increased tumor growth/size ( J:97101 )

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

increased adenoma incidence ( J:97101 )

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

increased colon adenoma incidence ( J:97101 )

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

digestive/alimentary system

increased colon adenoma incidence ( J:97101 )

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

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

Genotype
MGI:3719440

cx183

• Allelic Composition: Apc^tm1Rak/Apc⁺; Mbd4^tm1Wed/Mbd4^tm1Wed
• Genetic Background: involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * SJL

Microadenoma in Mbd4^tm1Wed/Mbd4^tm1Wed Apc^tm1Rak/Apc⁺ gastrointestinal tract

neoplasm

increased gastrointestinal tumor incidence ( J:80319 )

• the multiplicity of gastro-intestinal tumors is increased 2.4 times relative to Apc^tm1Rak heterozygotes

• mice have greater number of tumors in the jejunum and ileum than in Apc^tm1Rak heterozygotes

• mice have 10-fold increase in microadenomas compared to Apc^tm1Rak heterozygotes

• tumor progression is accelerated relative to Apc^tm1Rak heterozygotes

cellular

abnormal cell physiology ( J:80319 )

• mice tumors have more CG to TA transition mutations in the Apc gene than in Apc^tm1Rak heterozygotes

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:80319 )

• the multiplicity of gastro-intestinal tumors is increased 2.4 times relative to Apc^tm1Rak heterozygotes

• mice have greater number of tumors in the jejunum and ileum than in Apc^tm1Rak heterozygotes

• mice have 10-fold increase in microadenomas compared to Apc^tm1Rak heterozygotes

• tumor progression is accelerated relative to Apc^tm1Rak heterozygotes

Genotype
MGI:3843881

cx184

• Allelic Composition: Fen1^tm1Rak/Fen1⁺; Apc^tm1Rak/Apc⁺
• Genetic Background: involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * SJL/J

mortality/aging

premature death ( J:77962 )

• median survival of 9 months as compared to 13 months for Apc^tm1Rak single heterozygotes

neoplasm

increased gastrointestinal tumor incidence ( J:77962 )

• 100% develop gastrointestinal tumors by 1 year of age

increased malignant tumor incidence ( J:77962 )

• incidence of malignant tumors is higher than in Apc^tm1Rak single heterozygotes

cellular

abnormal cell physiology ( J:77962 )

• extensive microsatellite instability in tumor DNA

digestive/alimentary system

increased gastrointestinal tumor incidence ( J:77962 )

• 100% develop gastrointestinal tumors by 1 year of age

Genotype
MGI:3510235

cx185

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

neoplasm

increased intestinal adenocarcinoma incidence ( J:90337 )

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

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:90337 )

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

intestine polyps ( J:90337 )

• increased numbers of small intestine polyps as well in females

Genotype
MGI:5446700

cx186

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

neoplasm

decreased alimentary system tumor incidence ( J:189217 )

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

digestive/alimentary system

decreased alimentary system tumor incidence ( J:189217 )

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

Genotype
MGI:3531415

cx187

• Allelic Composition: Apc^tm1Mmt/Apc⁺; Nkd1^tm1Tko/Nkd1^tm1Tko
• Genetic Background: involves: 129X1/SvJ

digestive/alimentary system

abnormal small intestine morphology ( J:95901 )

• the number and size distribution of small intestinal polyps is not different from mice heterozygous for Apc^tm1Mmt alone

Genotype
MGI:3803126

cx188

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

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

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

• increased tumor latency

integument

decreased mammary gland tumor incidence ( J:128481 )

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

• increased tumor latency

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

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

• increased tumor latency

Genotype
MGI:3623317

cx189

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

neoplasm

decreased tumor incidence ( J:92308 )

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

• no reduction in tumor size

Genotype
MGI:4461429

cx190

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

neoplasm

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

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

Genotype
MGI:6357720

cx191

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

mortality/aging

increased tumor-free survival time ( J:262876 )

• mice exhibit increased survival compared with Apc^min heterozygotes

neoplasm

abnormal tumor vascularization ( J:262876 )

• reduced tumor angiogenesis to in Apc^min heterozygotes

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

increased intestinal adenoma incidence ( J:262876 )

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

• however, fewer microadenomas and adenomas at later time points

decreased tumor growth/size ( J:262876 )

• smaller tumors and microadenomas compared with Apc^min heterozygotes

decreased tumor incidence ( J:262876 )

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

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

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

• reduced proliferation compared with Apc^min heterozygotes

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:262876 )

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

• however, fewer microadenomas and adenomas at later time points

intestine polyps ( J:262876 )

• fewer than in Apc^min heterozygotes

cardiovascular system

abnormal tumor vascularization ( J:262876 )

• reduced tumor angiogenesis to in Apc^min heterozygotes

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

hematopoietic system

hematopoietic system phenotype ( J:262876 )

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

immune system

abnormal chemokine secretion ( J:262876 )

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

decreased interleukin-6 secretion ( J:262876 )

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

Genotype
MGI:5475210

cx192

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

digestive/alimentary system

intestine polyps ( J:193873 )

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

Genotype
MGI:7434699

cx193

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

digestive/alimentary system

decreased colon tumor incidence ( J:257088 )

• fewer polyps

neoplasm

decreased colon tumor incidence ( J:257088 )

• fewer polyps

Genotype
MGI:3829423

cx194

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

immune system

abnormal effector T cell morphology ( J:137020 )

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

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

enlarged mesenteric lymph nodes ( J:137020 )

• mesenteric lymph nodes are hyperplastic

lymph node hyperplasia ( J:137020 )

• mesenteric lymph nodes are hyperplastic

digestive/alimentary system

intestine polyps ( J:137020 )

• ileal polyps occur in these mice

colon polyps ( J:137020 )

• occur in these mice

hematopoietic system

abnormal effector T cell morphology ( J:137020 )

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

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

Genotype
MGI:5463417

cx195

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

digestive/alimentary system

intestine polyps ( J:191217 )

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

Genotype
MGI:6470552

cx196

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

neoplasm

increased colon tumor incidence ( J:296081 )

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

digestive/alimentary system

increased colon tumor incidence ( J:296081 )

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

Genotype
MGI:3811523

cx197

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

neoplasm

increased colon adenoma incidence ( J:139883 )

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

digestive/alimentary system

increased colon adenoma incidence ( J:139883 )

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

Genotype
MGI:7568795

cx198

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

mortality/aging

premature death ( J:342074 )

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

digestive/alimentary system

increased colon tumor incidence ( J:342074 )

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

neoplasm

increased colon tumor incidence ( J:342074 )

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

Genotype
MGI:2183289

cx199

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

neoplasm

abnormal tumor morphology ( J:38609 )

• average diameter of tumors is 20% smaller

increased tumor incidence ( J:38609 )

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

Genotype
MGI:5463415

cx200

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

digestive/alimentary system

intestine polyps ( J:191217 )

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

Genotype
MGI:6113599

cx201

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

digestive/alimentary system

decreased alimentary system tumor incidence ( J:241611 )

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

neoplasm

decreased alimentary system tumor incidence ( J:241611 )

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

Genotype
MGI:6367566

cx202

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

mortality/aging

extended life span ( J:268724 )

• compared with Apc^Min heterozygotes

neoplasm

decreased intestinal adenoma incidence ( J:268724 )

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

digestive/alimentary system

decreased intestinal adenoma incidence ( J:268724 )

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

Genotype
MGI:3827117

cx203

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

neoplasm

increased intestinal adenoma incidence ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

abnormal tumor morphology ( J:141821 )

• size similar to situation in Apc^Min heterozygous mice

digestive/alimentary system

abnormal intestinal epithelium morphology ( J:141821 )

• villus height is similar to Apc^Min heterozygotes

abnormal crypts of Lieberkuhn morphology ( J:141821 )

• crypt morphology is similar to Apc^Min heterozygotes

increased intestinal adenoma incidence ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

intestine polyps ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:141821 )

• crypt morphology is similar to Apc^Min heterozygotes

Genotype
MGI:3827123

cx204

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

digestive/alimentary system

abnormal intestinal epithelium morphology ( J:141821 )

• villus height is similar to Apc^Min heterozygotes

abnormal crypts of Lieberkuhn morphology ( J:141821 )

• crypt morphology is similar to Apc^Min heterozygotes

increased intestinal adenoma incidence ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

intestine polyps ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

endocrine/exocrine glands

abnormal crypts of Lieberkuhn morphology ( J:141821 )

• crypt morphology is similar to Apc^Min heterozygotes

neoplasm

increased intestinal adenoma incidence ( J:141821 )

• number similar to situation in Apc^Min heterozygous mice

abnormal tumor morphology ( J:141821 )

• size similar to situation in Apc^Min heterozygous mice

Genotype
MGI:5544115

cx205

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

mortality/aging

increased tumor-free survival time ( J:204874 )

• mice survive longer than Apc^Min heterozygotes

neoplasm

decreased intestinal adenoma incidence ( J:204874 )

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

digestive/alimentary system

increased enterocyte apoptosis ( J:204874 )

• compared with Apc^Min heterozygotes

decreased intestinal adenoma incidence ( J:204874 )

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

cellular

increased enterocyte apoptosis ( J:204874 )

• compared with Apc^Min heterozygotes

Genotype
MGI:5544114

cx206

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

neoplasm

increased intestinal adenoma incidence ( J:204874 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:204874 )

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

Genotype
MGI:5544112

cx207

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

digestive/alimentary system

decreased intestinal adenoma incidence ( J:204874 )

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

mortality/aging

increased tumor-free survival time ( J:204874 )

• mice survive longer than Apc^Min heterozygotes

neoplasm

decreased intestinal adenoma incidence ( J:204874 )

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

Genotype
MGI:4359621

cx208

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

neoplasm

increased intestinal adenoma incidence ( J:152194 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:152194 )

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

Genotype
MGI:2446655

cx209

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

neoplasm

increased intestinal adenoma incidence ( J:39765 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:39765 )

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

Genotype
MGI:4946927

cx210

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

neoplasm

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

digestive/alimentary system

increased intestinal adenoma incidence ( J:170088 )

• mice develop colorectal tubular adenomas unlike Apc^min heterozygotes

Genotype
MGI:3045027

cx211

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

neoplasm

increased intestinal adenoma incidence ( J:78500 )

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

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

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:78500 )

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

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

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

Genotype
MGI:3032868

cx212

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

mortality/aging

premature death ( J:79641 )

neoplasm

increased tumor incidence ( J:79641 )

increased intestinal adenoma incidence ( J:79641 )

increased carcinoma incidence ( J:79641 )

• intestinal carcinoma in situ

digestive/alimentary system

abnormal intestine morphology ( J:79641 )

• intestinal dysplasia

increased intestinal adenoma incidence ( J:79641 )

growth/size/body

weight loss ( J:79641 )

hematopoietic system

anemia ( J:79641 )

skeleton

lordosis ( J:79641 )

Genotype
MGI:6121393

cx213

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

neoplasm

abnormal tumor susceptibility ( J:254117 )

• compared to Apc controls

increased classified tumor incidence ( J:254117 )

• compared to Apc controls

increased intestinal adenocarcinoma incidence ( J:254117 )

increased colon adenocarcinoma incidence ( J:254117 )

increased small intestine adenocarcinoma incidence ( J:254117 )

• significantly increased cell proliferative potential

increased intestinal adenoma incidence ( J:254117 )

• high grade adenoma

• significantly increased cell proliferative potential in small intestine

increased colon adenoma incidence ( J:254117 )

• high grade adenoma

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:254117 )

increased colon adenocarcinoma incidence ( J:254117 )

increased small intestine adenocarcinoma incidence ( J:254117 )

• significantly increased cell proliferative potential

increased intestinal adenoma incidence ( J:254117 )

• high grade adenoma

• significantly increased cell proliferative potential in small intestine

increased colon adenoma incidence ( J:254117 )

• high grade adenoma

intestine polyps ( J:254117 )

• increased number compared to Apc controls

• significantly increased size compared to Apc controls

cellular

abnormal mitochondrial crista morphology ( J:254117 )

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

hematopoietic system

anemia ( J:254117 )

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

mortality/aging

premature death ( J:254117 )

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

Genotype
MGI:6121392

cx214

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

neoplasm

abnormal tumor susceptibility ( J:254117 )

• compared to Apc controls

increased classified tumor incidence ( J:254117 )

• compared to Apc controls

increased intestinal adenocarcinoma incidence ( J:254117 )

increased colon adenocarcinoma incidence ( J:254117 )

increased small intestine adenocarcinoma incidence ( J:254117 )

• significantly increased cell proliferative potential

increased intestinal adenoma incidence ( J:254117 )

• high grade adenoma

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

increased colon adenoma incidence ( J:254117 )

• high grade adenoma

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

digestive/alimentary system

increased intestinal adenocarcinoma incidence ( J:254117 )

increased colon adenocarcinoma incidence ( J:254117 )

increased small intestine adenocarcinoma incidence ( J:254117 )

• significantly increased cell proliferative potential

increased intestinal adenoma incidence ( J:254117 )

• high grade adenoma

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

increased colon adenoma incidence ( J:254117 )

• high grade adenoma

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

intestine polyps ( J:254117 )

• increased number compared to Apc controls

• significantly increased size compared to Apc controls

cellular

abnormal mitochondrial crista morphology ( J:254117 )

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

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

hematopoietic system

anemia ( J:254117 )

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

mortality/aging

premature death ( J:254117 )

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

Genotype
MGI:5544111

cx215

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

mortality/aging

premature death ( J:204874 )

• as in Apc^Min heterozygotes

neoplasm

increased intestinal adenoma incidence ( J:204874 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:204874 )

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

Genotype
MGI:6864129

cx216

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

mortality/aging

premature death ( J:317482 )

• not as much as in Apc^Min heterozygotes

neoplasm

increased colon adenoma incidence ( J:317482 )

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

digestive/alimentary system

increased colon adenoma incidence ( J:317482 )

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

abnormal intestinal epithelium physiology ( J:317482 )

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

Genotype
MGI:6806148

cx217

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

mortality/aging

extended life span ( J:268691 )

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

neoplasm

decreased intestinal adenoma incidence ( J:268691 )

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

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

digestive/alimentary system

decreased intestinal adenoma incidence ( J:268691 )

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

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

Genotype
MGI:6806147

cx218

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

mortality/aging

extended life span ( J:268691 )

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

neoplasm

decreased intestinal adenoma incidence ( J:268691 )

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

abnormal tumor pathology ( J:268691 )

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

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

decreased tumor growth/size ( J:268691 )

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

digestive/alimentary system

decreased intestinal adenoma incidence ( J:268691 )

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

Genotype
MGI:3653360

cx219

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

neoplasm

decreased tumor incidence ( J:73854 )

• resistance to intestinal polyps

Genotype
MGI:3653359

cx220

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

neoplasm

decreased tumor incidence ( J:73854 )

• resistance to intestinal polyps

Genotype
MGI:4950747

cx221

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

neoplasm

decreased alimentary system tumor incidence ( J:171361 )

• fewer intestinal tumors form than in controls

• tumors are smaller in size than in controls

decreased tumor growth/size ( J:171361 )

• fewer intestinal tumors form

• average size of intestinal tumors is reduced

• higher apoptosis rates in intestinal tumors

digestive/alimentary system

decreased alimentary system tumor incidence ( J:171361 )

• fewer intestinal tumors form than in controls

• tumors are smaller in size than in controls

Genotype
MGI:3700065

cx222

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

neoplasm

increased intestinal adenoma incidence ( J:118232 )

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

digestive/alimentary system

increased intestinal adenoma incidence ( J:118232 )

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

Genotype
MGI:3803129

cx223

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

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

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

integument

decreased mammary gland tumor incidence ( J:128481 )

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

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

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

Genotype
MGI:3803123

cx224

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

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

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

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

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

integument

decreased mammary gland tumor incidence ( J:128481 )

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

Genotype
MGI:3803125

cx225

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

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

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

• increased tumor latency

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

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

• increased tumor latency

integument

decreased mammary gland tumor incidence ( J:128481 )

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

• increased tumor latency

Genotype
MGI:3803127

cx226

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

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

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

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

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

integument

decreased mammary gland tumor incidence ( J:128481 )

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

Genotype
MGI:3803128

cx227

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

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

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

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

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

integument

decreased mammary gland tumor incidence ( J:128481 )

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

Genotype
MGI:3803124

cx228

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

neoplasm

decreased mammary gland tumor incidence ( J:128481 )

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

endocrine/exocrine glands

decreased mammary gland tumor incidence ( J:128481 )

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

integument

decreased mammary gland tumor incidence ( J:128481 )

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