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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
ApcMin
multiple intestinal neoplasia
MGI:1856318
Summary 122 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
ApcMin/ApcMin involves: AKR/J * C57BL/6J MGI:5448316
hm2
ApcMin/ApcMin involves: C57BL/6J MGI:5438590
hm3
ApcMin/ApcMin involves: C57BL/6J * CAST/EiJ MGI:5447942
hm4
ApcMin/ApcMin involves: C57BL/6 * POMOD MGI:5448414
ht5
ApcMin/Apc+ (AKR/J x C57BL/6J)F1 MGI:5449072
ht6
ApcMin/Apc+ B6(AKR)-ApcMin MGI:5446893
ht7
ApcMin/Apc+ B6.Cg-Brca2tm1Mbn ApcMin MGI:3814370
ht8
ApcMin/Apc+ C57BL/6J-ApcMin MGI:2665504
ht9
ApcMin/Apc+ involves: 129P2/OlaHsd * C57BL/6 MGI:3834882
ht10
ApcMin/Apc+ involves: 129/Sv * C57BL/6 MGI:4429570
ht11
ApcMin/Apc+ involves: AKR/J * C57BL/6J MGI:2175903
ht12
ApcMin/Apc+ involves: C57BL/6 * C57BL/6J MGI:3812012
ht13
ApcMin/Apc+ involves: C57BL/6J MGI:3513858
ht14
ApcMin/Apctm1.1Klne B6.Cg-ApcMin/Apctm1.1Klne MGI:5431900
ht15
ApcMin/Apctm1Tno involves: 129/Sv * 129S4/SvJae * C57BL/6 MGI:4429565
cn16
ApcMin/Apc+
Hsd11b2tm1.1Mzz/Hsd11b2tm1.1Mzz
Tg(Vil-cre)997Gum/0
involves: 129 * C57BL/6 * C57BL/6J MGI:5547498
cn17
ApcMin/Apc+
Dnmt3btm1Jae/Dnmt3btm1Jae
Tg(Fabp1-cre)1Jig/0
involves: 129 * C57BL/6 * C57BL/6J * FVB/N MGI:3625330
cn18
ApcMin/Apc+
Ptentm1Hwu/Ptentm1Hwu
Tg(Vil-cre)997Gum/0
involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL MGI:4941759
cn19
ApcMin/Apc+
Col1a1tm1(CAG-Sirt1)Dsin/Col1a1+
Tg(Vil-cre)997Gum/0
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL MGI:4430578
cn20
ApcMin/Apc+
Dclk1tm1.1(cre/ERT2)Seno/Dclk1+
Gt(ROSA)26Sortm1(HBEGF)Awai/Gt(ROSA)26Sor+
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
involves: 129S4/SvJaeSor * C57BL/6 MGI:5475206
cn21
ApcMin/Apc+
Erbb3tm1.1Dwt/Erbb3tm2.1Dwt
Tg(Vil-cre)997Gum/0
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL MGI:4360363
cn22
ApcMin/Apc+
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Tg(Vil-cre)20Syr/0
involves: 129S6/SvEvTac * C57BL/6 * DBA/2 MGI:5013408
cn23
ApcMin/Apc+
Gpa33tm1(GNAS)Wtsi/Gpa33+
Hprttm1(CMV-cre)Brd/?
involves: 129S7/SvEvBrd * C57BL/6J MGI:4889209
cn24
ApcMin/Apc+
Tcf7l2tm1(EGFP/cre)Mrc/Tcf7l2tm2.1Mrc
involves: C57BL/6J MGI:4946926
cn25
ApcMin/Apc+
Igf2bp1tm1Vssp/Igf2bp1tm1Vssp
Tg(Vil-cre)997Gum/0
involves: C57BL/6J * SJL MGI:5523866
cx26
ApcMin/Apc+
Brca2tm1Mbn/Brca2+
B6.Cg-Brca2tm1Mbn ApcMin MGI:3814367
cx27
ApcMin/Apc+
Gt(ROSA)26Sor/Gt(ROSA)26Sor+
B6.Cg-Gt(ROSA)26Sor ApcMin MGI:5014351
cx28
ApcMin/Apc+
Mir10atm1.1Ahl/Mir10atm1.1Ahl
B6.Cg-Mir10atm1.1Ahl Apcmin MGI:5567980
cx29
ApcMin/Apc+
MthfsGt(RRK291)Byg/Mthfs+
B6.Cg-MthfsGt(RRK291)Byg ApcMin MGI:5430745
cx30
ApcMin/Apc+
Nos2tm1Lau/Nos2tm1Lau
B6.Cg-Nos2tm1Lau ApcMin MGI:3767791
cx31
ApcMin/Apc+
Nos2tm1Lau/Nos2+
B6.Cg-Nos2tm1Lau ApcMin MGI:3767792
cx32
ApcMin/Apc+
Pla2g4atm1Jvb/Pla2g4atm1Jvb
B6.Cg-Pla2g4atm1Jvb ApcMin MGI:4358774
cx33
ApcMin/Apc+
Rab25tm1Jrgo/Rab25+
B6.Cg-Rab25tm1Jrgo ApcMin MGI:4440864
cx34
ApcMin/Apc+
Rab25tm1Jrgo/Rab25tm1Jrgo
B6.Cg-Rab25tm1Jrgo ApcMin MGI:4440863
cx35
ApcMin/Apc+
Shmt1Gt(AD0236)Wtsi/Shmt1Gt(AD0236)Wtsi
B6.Cg-Shmt1Gt(AD0236)Wtsi ApcMin MGI:5426849
cx36
ApcMin/Apc+
Tgfbr1tm1Bopa/Tgfbr1+
B6.Cg-Tgfbr1tm1Bopa ApcMin MGI:3831112
cx37
ApcMin/Apc+
Pla2g2aMom1-r/Pla2g2a+
either: (AKR/J x C57BL/6J-ApcMin)F1 or (MA/MyJ x C57BL/6J-ApcMin)F1 or (CAST/EiJ x C57BL/6J-ApcMin)F1 MGI:5529263
cx38
ApcMin/Apc+
Hpgdstm1Urad/Hpgds+
involves: 129 * C57BL/6J MGI:3700063
cx39
ApcMin/Apc+
Hpgdstm1Urad/Hpgdstm1Urad
involves: 129 * C57BL/6J MGI:3700064
cx40
ApcMin/Apc+
Msh2tm1Mak/Msh2+
Nos2tm1Mrl/Nos2tm1Mrl
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J MGI:5636667
cx41
ApcMin/Apc+
Msh2tm1Mak/Msh2tm1Mak
Nos2tm1Mrl/Nos2tm1Mrl
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J MGI:5636670
cx42
ApcMin/Apc+
Blmtm1Grdn/Blm+
involves: 129P2/OlaHsd * 129S/SvEv * Black Swiss * C57BL/6J MGI:3582674
cx43
ApcMin/Apc+
Msh2tm1Htr/Msh2tm1Htr
involves: 129P2/OlaHsd * BALB/c * C57BL/6J MGI:4429611
cx44
ApcMin/Apc+
Ccdc80tm1.1Ftk/Ccdc80tm1.1Ftk
involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 * C57BL/6J * C57BL/6N MGI:5693797
cx45
ApcMin/Apc+
Mom5129P2/?
involves: 129P2/OlaHsd * C57BL/6 MGI:4359622
cx46
ApcMin/Apc+
Foxl1tm1Khk/Foxl1tm1Khk
involves: 129P2/OlaHsd * C57BL/6 MGI:3834880
cx47
ApcMin/Apc+
Zbtb33tm1.1Bird/Y
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J MGI:3613447
cx48
ApcMin/Apc+
Mbd2tm1Bh/Mbd2tm1Bh
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J MGI:3579838
cx49
ApcMin/Apc+
Mbd2tm1Bh/Mbd2+
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J MGI:3579839
cx50
ApcMin/Apc+
Phgdhtm1.1Shfu/Phgdh+
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J MGI:5426846
cx51
ApcMin/Apc+
Ptgs1tm1Unc/Ptgs1tm1Unc
involves: 129P2/OlaHsd * C57BL/6J MGI:4366247
cx52
ApcMin/Apc+
Cd44tm1Mak/Cd44tm1Mak
involves: 129P2/OlaHsd * C57BL/6J MGI:4946621
cx53
ApcMin/Apc+
Mbd4tm1Bird/Mbd4tm1Bird
involves: 129P2/OlaHsd * C57BL/6J MGI:3719427
cx54
ApcMin/Apc+
Tcf7tm1Cle/Tcf7tm1Cle
involves: 129P2/OlaHsd * C57BL/6J MGI:5319648
cx55
ApcMin/Apc+
Ptgdstm1Ohy/Ptgdstm1Ohy
involves: 129P2/OlaHsd * C57BL/6J MGI:3700062
cx56
ApcMin/Apc+
Ptgs1tm1Unc/Ptgs1+
involves: 129P2/OlaHsd * C57BL/6J MGI:4366248
cx57
ApcMin/Apc+
Hptm1Skl/Hptm1Skl
involves: 129P2/OlaHsd * C57BL/6J MGI:3610196
cx58
ApcMin/Apc+
Msh2tm1Mak/Msh2tm1Mak
involves: 129P2/OlaHsd * C57BL/6J MGI:5636659
cx59
ApcMin/Apc+
Ptgs2tm1Unc/Ptgs2tm1Unc
involves: 129P2/OlaHsd * C57BL/6J MGI:4366246
cx60
ApcMin/Apc+
Trp53tm1Mlh/Trp53tm1Mlh
involves: 129P2/OlaHsd * C57BL/6 * SWR MGI:5448541
cx61
ApcMin/Apc+
Dnd1Ter/Dnd1+
involves: 129P3/J * C57BL/6J MGI:5696099
cx62
ApcMin/ApcMin
Rr27tm1Rohl/Rr27+
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J MGI:3722288
cx63
ApcMin/Apc+
Tgfbr1tm1Bopa/Tgfbr1+
involves: 129S1/SvImJ * C57BL/6J MGI:3831111
cx64
ApcMin/Apc+
Il6tm1Kopf/Il6tm1Kopf
involves: 129S2/SvPas * C57BL/6 MGI:4365606
cx65
ApcMin/Apc+
Esr2tm1Mma/Esr2tm1Mma
involves: 129S2/SvPas * C57BL/6J MGI:5298869
cx66
ApcMin/Apc+
Pms2tm1Lisk/Pms2tm1Lisk
involves: 129S2/SvPas * C57BL/6J MGI:4820588
cx67
ApcMin/Apc+
Esr1tm1.1Mma/Esr1tm1.1Mma
involves: 129S2/SvPas * C57BL/6J MGI:5298870
cx68
ApcMin/Apc+
Hdac2Gt(W035F03)Joe/Hdac2Gt(W035F03)Joe
involves: 129S2/SvPas * C57BL/6J MGI:4357790
cx69
ApcMin/Apc+
Esr1tm1.1Mma/Esr1+
involves: 129S2/SvPas * C57BL/6J MGI:5298871
cx70
ApcMin/Apc+
Esr2tm1Mma/Esr2+
involves: 129S2/SvPas * C57BL/6J MGI:5298868
cx71
ApcMin/Apc+
Col1a1tm11(tetO-Dnmt3b_i6)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5313421
cx72
ApcMin/Apc+
Col1a1tm12(tetO-Dnmt3a_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5313423
cx73
ApcMin/Apc+
Col1a1tm1(CAG-Sirt1)Dsin/Col1a1+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:4430577
cx74
ApcMin/Apc+
Ptprhtm1.1Mato/Ptprhtm1.1Mato
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:3839104
cx75
ApcMin/Apc+
Col1a1tm10(tetO-Dnmt3b_i3)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5313420
cx76
ApcMin/Apc+
Col1a1tm9(tetO-Dnmt3b_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
involves: 129S4/SvJae * C57BL/6 * C57BL/6J MGI:5313419
cx77
ApcMin/Apc+
Dnmt1tm1Jae/Dnmt1tm1Pwl
involves: 129S4/SvJae * C57BL/6J MGI:3848453
cx78
ApcMin/Apc+
Dnmt1tm1Pwl/Dnmt1+
involves: 129S4/SvJae * C57BL/6J MGI:3848450
cx79
ApcMin/Apc+
Dnmt1tm1Jae/Dnmt1+
involves: 129S4/SvJae * C57BL/6J MGI:3848451
cx80
ApcMin/ApcMin
Asphtm1Jed/Asphtm1Jed
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6J * C57BL/6NTac MGI:2653701
cx81
ApcMin/Apc+
Dp(17Nfkbil1-Olfr91)1Cogr/0
involves: 129S6/SvEvTac * C57BL/6J MGI:5451046
cx82
ApcMin/Apc+
Eregtm1Dwt/Eregtm1Dwt
involves: 129S6/SvEvTac * C57BL/6J MGI:3512138
cx83
ApcMin/Apc+
Il22ra2tm2Vlcg/Il22ra2tm2Vlcg
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac MGI:5446699
cx84
ApcMin/Apc+
Myctm1Jlc/Myc+
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J MGI:3812011
cx85
ApcMin/Apc+
Recql4tm1Glu/Recql4tm1Glu
involves: 129S7/SvEvBrd * C57BL/6J MGI:3575580
cx86
ApcMin/Apctm1Tno
Ctnnb1tm4.1Wbm/Ctnnb1+
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6 MGI:4429574
cx87
ApcMin/ApcMin
Ctnnb1tm4.1Wbm/Ctnnb1+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 MGI:4429575
cx88
ApcMin/Apc+
Ppardtm1Jps/Ppardtm1Jps
involves: 129/Sv * AKR/J * C57BL/6 * C57BL/6J MGI:3510235
cx89
ApcMin/Apc+
Il22tm1Flv/Il22tm1Flv
involves: 129/Sv * C57BL/6 * C57BL/6J MGI:5446700
cx90
ApcMin/ApcMin
Sat1tm1Alh/Y
involves: 129X1/SvJ * C57BL/6J MGI:3709984
cx91
ApcMin/Apc+
Mmom2129X1/SvJ/Mmom2C57BL/6J
involves: 129X1/SvJ * C57BL/6J MGI:3803126
cx92
ApcMin/Apc+
EgfrWa5/Egfr+
involves: BALB/cAnN * C3H/HeN * C57BL/6J MGI:3623317
cx93
ApcMin/Apc+
Pla2g2aMom1-r/?
PrkdcBALB/c/PrkdcBALB/c
involves: BALB/cByJ * C57BL/6 MGI:4461429
cx94
ApcMin/Apc+
Rr21tm1Jta/Rr21+
involves: C57BL/6 MGI:5463417
cx95
ApcMin/Apc+
Mom5C57BL/6/Mom5C57BL/6
involves: C57BL/6 MGI:4359621
cx96
ApcMin/Apc+
Dclk1tm1.1(cre/ERT2)Seno/Dclk1tm1.1(cre/ERT2)Seno
involves: C57BL/6 MGI:5475210
cx97
ApcMin/Apc+
Tg(Rorc-EGFP)1Ebe/?
involves: C57BL/6 MGI:3829423
cx98
ApcMin/Apc+
Mmp7tm1Lmm/Mmp7tm1Lmm
involves: C57BL/6 * C57BL/6J MGI:2183289
cx99
ApcMin/Apc+
Slc5a8tm1.1Boet/Slc5a8tm1.1Boet
involves: C57BL/6 * C57BL/6J MGI:3811523
cx100
ApcMin/Apc+
Rr21tm1.1Jta/Rr21tm1.1Jta
involves: C57BL/6 * FVB/N MGI:5463415
cx101
ApcMin/ApcMin
Ppardtm1.1Rev/Ppardtm1.1Rev
involves: C57BL/6J MGI:3715726
cx102
ApcMin/Apc+
Tcf7l2tm2.2Mrc/Tcf7l2+
involves: C57BL/6J MGI:4946927
cx103
ApcMin/Apc+
Cd44tm2Stpa/Cd44tm2Stpa
involves: C57BL/6J MGI:5544112
cx104
ApcMin/Apc+
Cd44tm1Stpa/Cd44tm2Stpa
involves: C57BL/6J MGI:5544114
cx105
ApcMin/Apc+
Cd44tm1Mak/Cd44tm1Mak
involves: C57BL/6J MGI:5544115
cx106
ApcMin/Apc+
Tcf7l2tm1.1(EGFP/cre)Mrc/Tcf7l2+
involves: C57BL/6J MGI:4946925
cx107
ApcMin/Apc+
Ccnd1tm1Dsn/Ccnd1tm1Dsn
involves: C57BL/6J MGI:3045027
cx108
ApcMin/Apc+
Thbs1tm1Hyn/Thbs1tm1Hyn
involves: C57BL/6J MGI:3032868
cx109
ApcMin/Apc+
Glp2rtm1Ddr/Glp2r+
involves: C57BL/6J MGI:3827117
cx110
ApcMin/Apc+
Dcctm1Wbg/Dcc+
involves: C57BL/6J MGI:2446655
cx111
ApcMin/Apc+
Glp2rtm1Ddr/Glp2rtm1Ddr
involves: C57BL/6J MGI:3827123
cx112
ApcMin/Apc+
Cd44tm1Stpa/Cd44tm1Stpa
involves: C57BL/6J * C57BL/6JIco MGI:5544111
cx113
ApcMin/Apc+
Atp5a1Mom2-C57BL/6J/Atp5a1Mom2-C57BL/6J
involves: C57BL/6J * DBA/2J MGI:3653359
cx114
ApcMin/Apc+
Atp5a1Mom2-C57BL/6J/Atp5a1+
involves: C57BL/6J * DBA/2J MGI:3653360
cx115
ApcMin/Apc+
Tg(CAG-PGDS)S-55Hjl/0
involves: C57BL/6J * FVB/N MGI:3700065
cx116
ApcMin/Apc+
Tg(Vil1-PPARGC1A)#Amos/0
involves: C57BL/6J * FVB/N MGI:4950747
cx117
ApcMin/Apc+
Mmom4C57BL/6J/Mmom4FVB/NTac
involves: C57BL/6J * FVB/NTac MGI:3803129
cx118
ApcMin/Apc+
Mmom2C57BL/6J/Mmom2FVB/NTac
Mmom3C57BL/6J/Mmom3FVB/NTac
involves: C57BL/6J * FVB/NTac MGI:3803127
cx119
ApcMin/Apc+
Mmom1C57BL/6J/Mmom1FVB/NTac
involves: C57BL/6J * FVB/NTac MGI:3803123
cx120
ApcMin/Apc+
Mmom1C57BL/6J/Mmom1FVB/NTac
Mmom3C57BL/6J/Mmom3FVB/NTac
involves: C57BL/6J * FVB/NTac MGI:3803124
cx121
ApcMin/Apc+
Mmom2C57BL/6J/Mmom2FVB/NTac
involves: C57BL/6J * FVB/NTac MGI:3803125
cx122
ApcMin/Apc+
Mmom2C57BL/6J/Mmom2FVB/NTac
Mmom4C57BL/6J/Mmom4FVB/NTac
involves: C57BL/6J * FVB/NTac MGI:3803128


Genotype
MGI:5448316
hm1
Allelic
Composition
ApcMin/ApcMin
Genetic
Background
involves: AKR/J * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryogenesis
• at E6.5 there is a range of abnormal development, underdeveloped embryonic tissue and associated maternal cells, with no obvious primitive ectoderm or proamniotic cavity to disorganized embryonic and extraembryonic tissue
• empty space is seen in the distal region where primitive ectoderm is expected

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




Genotype
MGI:5438590
hm2
Allelic
Composition
ApcMin/ApcMin
Genetic
Background
involves: C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cellular
• cultured adenomatous tissue form highly clonogenic spheroids




Genotype
MGI:5447942
hm3
Allelic
Composition
ApcMin/ApcMin
Genetic
Background
involves: C57BL/6J * CAST/EiJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• inferred from no recovery of mice homozygous for embryos typed as homozygous for the identifying, linked B6 D18Mitl4 marker among a significant number of E10.5 and E13.5 progeny
• at E10.5 histological analysis shows trophoblast giant cells and a small cluster of embryonic cells, source unknown
• at E13.5 decidual swellings were necrotic with remnants of trophoblast giant cells




Genotype
MGI:5448414
hm4
Allelic
Composition
ApcMin/ApcMin
Genetic
Background
involves: C57BL/6 * POMOD
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
embryogenesis
• at E7.5 embryos are disorganized,showing significant reduction in embryo growth and reduction of primitive ectoderm
• failure of primitive ectoderm development shortly after implantation
• embryos are small and embedded in maternal tissue

growth/size/body
• embryos are small and embedded in maternal tissue

mortality/aging




Genotype
MGI:5449072
ht5
Allelic
Composition
ApcMin/Apc+
Genetic
Background
(AKR/J x C57BL/6J)F1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• a range of 1 to 12 with an average of 3 adenomas were found per mouse

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

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

homeostasis/metabolism




Genotype
MGI:5446893
ht6
Allelic
Composition
ApcMin/Apc+
Genetic
Background
B6(AKR)-ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 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

mortality/aging
• 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

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

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

hematopoietic system
• anemia is diagnosed by 60 days of age
• follows development of multiple adenomas which bleed into the intestinal lumen

endocrine/exocrine glands
• on this background colony maintenance data show that mammary tumors occasionally develop in heterozygous females but not in wild-type female siblings
• females of this genotype have an increased susceptibility to developing mammary neoplasia

integument
• on this background colony maintenance data show that mammary tumors occasionally develop in heterozygous females but not in wild-type female siblings
• females of this genotype have an increased susceptibility to developing mammary neoplasia




Genotype
MGI:3814370
ht7
Allelic
Composition
ApcMin/Apc+
Genetic
Background
B6.Cg-Brca2tm1Mbn ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
• 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
N
• only observed in 1/9 ENU-treated males, similar to wild-type males (1/9)
• absent in 26% of ENU-treated females
• remaining follicles are degenerating in ENU-treated females
• arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice
• 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
• observed in ENU-treated females displaying ovarian failure (atrophy); endometrium and myometrium appear immature
• reduced in thickness and lined with vacuolated cells indicative of anestrus in ENU-treated females

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

endocrine/exocrine glands
• females exhibit some adrenal hyperplasia, while none is observed in males
• 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
• 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 in 26% of ENU-treated females
• remaining follicles are degenerating in ENU-treated females
• arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice
• 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
• 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
• by 65 days after ENU treatment, 100% of females develop mammary tumors with a multiplicity of 6.7 +/- 2.8
• males develop tumors at a very low incidence and with a tumor multiplicity of 0.4 +/- 0.5, whereas no wild-type or Brca2-heterozygous males developed mammary tumors
• tumors in male and female mice are adenoacanthomas, characterized by undifferentiated acini and tubules with centrally confined squamous cells and keratin; most tumors contain proportions of adenomatous and squamous cell types
• tumors with predominantly squamous differentiation, moderate to marked inflammation in and around tumors is observed, with areas of fibrosis; in some cases, squamous component becomes cystic and is filled with keratinous debris
• invasion or metastases into the mammary lymph nodes was not observed during time course of study




Genotype
MGI:2665504
ht8
Allelic
Composition
ApcMin/Apc+
Genetic
Background
C57BL/6J-ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Rab25tm1Jrgo/Rab25tm1Jrgo ApcMin/Apc+ mice exhibit increased intestinal adenoma formation compared to ApcMin/Apc+ mice

digestive/alimentary system
• 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)

tumorigenesis
• 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)
• tubular adenomas in the colon (J:158733)

homeostasis/metabolism
• females exhibit increased free fatty acid levels at 15 weeks of age
• females show increased triglyceride levels at 15 weeks of age
• increase in luminal prostaglandin E2 at 15 weeks of age

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

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

hematopoietic system
• 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
• 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




Genotype
MGI:3834882
ht9
Allelic
Composition
ApcMin/Apc+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• no gastric adenomas are observed
• at 30 days, no colonic adenomas are found and normal colonic architecture and cellular morphology is observed




Genotype
MGI:4429570
ht10
Allelic
Composition
ApcMin/Apc+
Genetic
Background
involves: 129/Sv * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• macroscopic lesions primarily within the proximal portion of the small intestine in mutant (n=22)

hematopoietic system
• decreased DX5+, CD3- NK-cells in the spleen at 17 weeks old
• reduction in splenic CD3+ T cells at 17 weeks old
• 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 DX5+, CD3- NK-cells in the spleen at 17 weeks old
• reduction in splenic CD3+ T cells at 17 weeks old
• 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:2175903
ht11
Allelic
Composition
ApcMin/Apc+
Genetic
Background
involves: AKR/J * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 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
• visible tumors of the large and small intestine
• either polyploid, papillary or sessile adenomas

digestive/alimentary system
• 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
• visible tumors of the large and small intestine
• either polyploid, papillary or sessile adenomas
• bloody feces

hematopoietic system
• 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
• moribund animals with hematocrits around 10-20%

homeostasis/metabolism

mortality/aging

Mouse Models of Human Disease
OMIM ID Ref(s)
Familial Adenomatous Polyposis 1; FAP1 175100 J:830




Genotype
MGI:3812012
ht12
Allelic
Composition
ApcMin/Apc+
Genetic
Background
involves: C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die at 169 days

digestive/alimentary system
• mice develop more and bigger polyps than in ApcMin Myctm1Jlc heterozygotes




Genotype
MGI:3513858
ht13
Allelic
Composition
ApcMin/Apc+
Genetic
Background
involves: C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• 12% of heterozygotes developed mammary adenocanthomas

mortality/aging
• 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)

tumorigenesis
• 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 Apctm1Cip heterozygotes (J:94108)
• 12% of heterozygotes developed mammary adenocanthomas

digestive/alimentary system
• reduced proliferation of cells in the colon in ovariectomized
• however, 17beta-estradiol replacement increases colonocyte proliferation 2-fold
• ovariectomized mice exhibit abnormal submucosal with thickening of the muscularis mucosae and enrichment of stromal components compared with control mice
• ovariectomized mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice
• 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
• rectal prolapse is seen in 28% of surviving mutants at 7 months of age
• 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 Apctm1Cip heterozygotes (J:94108)
• due to tumors

cellular
• reduced proliferation of cells in the colon in ovariectomized
• however, 17beta-estradiol replacement increases colonocyte proliferation 2-fold

endocrine/exocrine glands
• ovariectomized mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice
• 12% of heterozygotes developed mammary adenocanthomas

hematopoietic system




Genotype
MGI:5431900
ht14
Allelic
Composition
ApcMin/Apctm1.1Klne
Genetic
Background
B6.Cg-ApcMin/Apctm1.1Klne
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Apctm1.1Klne mutation (0 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased compared with ApcMin heterozygotes
• mice develop more polyps in the jejunum, ileum, duodenum and stomach compared with ApcMin heterozygotes
• mice exhibit larger polyps in the jejunum and ileum compared with ApcMin heterozygotes
• however, the number of polyps in the colon is the same as in ApcMin heterozygotes

cellular
• increased compared with ApcMin heterozygotes




Genotype
MGI:4429565
ht15
Allelic
Composition
ApcMin/Apctm1Tno
Genetic
Background
involves: 129/Sv * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Apctm1Tno mutation (0 available); any Apc mutation (85 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• no mutant mice found at term
• live embryos could still be detected at embryonic day 17.5 (E17.5), but at less than the expected Mendelian ratio

nervous system
• lack all structures anterior to the hindbrain at E12
• first become visible in E8.5-E9.5

craniofacial
• a prominent cap of neural tissue at the most anterior part of the embryo at E12
• absent mandible at E12
• a prominent cap of neural tissue at the most anterior part of the embryo at E12
• absent cranial structures at E12

skeleton
• a prominent cap of neural tissue at the most anterior part of the embryo at E12
• absent mandible at E12
• a prominent cap of neural tissue at the most anterior part of the embryo at E12
• absent cranial structures at E12




Genotype
MGI:5547498
cn16
Allelic
Composition
ApcMin/Apc+
Hsd11b2tm1.1Mzz/Hsd11b2tm1.1Mzz
Tg(Vil-cre)997Gum/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Hsd11b2tm1.1Mzz mutation (0 available); any Hsd11b2 mutation (5 available)
Tg(Vil-cre)997Gum mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• fewer total intestinal adenoma at 20 weeks with prevented initiation of polyp formation compared with ApcMin heterozygotes

tumorigenesis
• fewer total intestinal adenoma at 20 weeks with prevented initiation of polyp formation compared with ApcMin heterozygotes
• reduced proliferation and increased apoptosis compared with tumors from ApcMin heterozygotes

homeostasis/metabolism
• 10-fold higher corticosterone (active glucocorticoid) levels in the intestine compared with ApcMin heterozygotes
• 11-keto-corticosterone (inactive glucocorticoid) levels is lower in the intestine compared with ApcMin heterozygotes




Genotype
MGI:3625330
cn17
Allelic
Composition
ApcMin/Apc+
Dnmt3btm1Jae/Dnmt3btm1Jae
Tg(Fabp1-cre)1Jig/0
Genetic
Background
involves: 129 * C57BL/6 * C57BL/6J * FVB/N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Dnmt3btm1Jae mutation (1 available); any Dnmt3b mutation (28 available)
Tg(Fabp1-cre)1Jig mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• significant decrease in the formation of macroscopic colonic adenomas in ApcMin/+ mice
• no impact on microadenoma formation
• no noticeable effect on later stages of tumor growth




Genotype
MGI:4941759
cn18
Allelic
Composition
ApcMin/Apc+
Ptentm1Hwu/Ptentm1Hwu
Tg(Vil-cre)997Gum/0
Genetic
Background
involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Ptentm1Hwu mutation (3 available); any Pten mutation (40 available)
Tg(Vil-cre)997Gum mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mutants die within 80 days

tumorigenesis
• adenomas in the small intestine

digestive/alimentary system
• mutants develop an average of 20.1 intestinal polyps per mouse, an 11.17-fold increase over the numbers seen in heterozygous Apc mice
• adenomas in the small intestine




Genotype
MGI:4430578
cn19
Allelic
Composition
ApcMin/Apc+
Col1a1tm1(CAG-Sirt1)Dsin/Col1a1+
Tg(Vil-cre)997Gum/0
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Col1a1tm1(CAG-Sirt1)Dsin mutation (1 available); any Col1a1 mutation (88 available)
Tg(Vil-cre)997Gum mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mice do not develop tumors morbidities, including anemia and cachaxia, unlike Col1a1tm1(CAG-Sirt1)Dsin ApcMin heterozygotes
• mice develop fewer intestinal tumors than Col1a1tm1(CAG-Sirt1)Dsin ApcMin heterozygotes




Genotype
MGI:5475206
cn20
Allelic
Composition
ApcMin/Apc+
Dclk1tm1.1(cre/ERT2)Seno/Dclk1+
Gt(ROSA)26Sortm1(HBEGF)Awai/Gt(ROSA)26Sor+
Gt(ROSA)26Sortm1Sor/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJaeSor * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Dclk1tm1.1(cre/ERT2)Seno mutation (0 available); any Dclk1 mutation (16 available)
Gt(ROSA)26Sortm1(HBEGF)Awai mutation (3 available); any Gt(ROSA)26Sor mutation (317 available)
Gt(ROSA)26Sortm1Sor mutation (7 available); any Gt(ROSA)26Sor mutation (317 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 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
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
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
cn21
Allelic
Composition
ApcMin/Apc+
Erbb3tm1.1Dwt/Erbb3tm2.1Dwt
Tg(Vil-cre)997Gum/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Erbb3tm1.1Dwt mutation (1 available); any Erbb3 mutation (22 available)
Erbb3tm2.1Dwt mutation (0 available); any Erbb3 mutation (22 available)
Tg(Vil-cre)997Gum mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• unlike ApcMin heterozygotes, mice do not develop colonic polyps
• mice develop fewer intestinal polyps compared to in ApcMin heterozygotes

tumorigenesis
• the number and size of microadenomas in the intestine are decreased compared to in ApcMin heterozygotes due to an increased in Caspase-3 dependent apoptosis
• mice fail to develop colon tumors unlike ApcMin heterozygotes




Genotype
MGI:5013408
cn22
Allelic
Composition
ApcMin/Apc+
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Tg(Vil-cre)20Syr/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6 * DBA/2
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Gt(ROSA)26Sortm2(Rnf187)Jhai mutation (0 available); any Gt(ROSA)26Sor mutation (317 available)
Tg(Vil-cre)20Syr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• intestinal tumors are increased in number compared to in ApcMin/Apc+ Tg(Vil-cre)20Syr

tumorigenesis
• intestinal tumors are increased in number compared to in ApcMin/Apc+ Tg(Vil-cre)20Syr
• intestinal tumors exhibit increased cell proliferation and size compared to in ApcMin/Apc+ Tg(Vil-cre)20Syr




Genotype
MGI:4889209
cn23
Allelic
Composition
ApcMin/Apc+
Gpa33tm1(GNAS)Wtsi/Gpa33+
Hprttm1(CMV-cre)Brd/?
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Gpa33tm1(GNAS)Wtsi mutation (0 available); any Gpa33 mutation (115 available)
Hprttm1(CMV-cre)Brd mutation (0 available); any Hprt mutation (1256 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• compared with ApcMin heterozygotes

tumorigenesis
• compared with ApcMin heterozygotes




Genotype
MGI:4946926
cn24
Allelic
Composition
ApcMin/Apc+
Tcf7l2tm1(EGFP/cre)Mrc/Tcf7l2tm2.1Mrc
Genetic
Background
involves: C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Tcf7l2tm1(EGFP/cre)Mrc mutation (0 available); any Tcf7l2 mutation (21 available)
Tcf7l2tm2.1Mrc mutation (0 available); any Tcf7l2 mutation (21 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• mice do not exhibit develop intestinal adenomas




Genotype
MGI:5523866
cn25
Allelic
Composition
ApcMin/Apc+
Igf2bp1tm1Vssp/Igf2bp1tm1Vssp
Tg(Vil-cre)997Gum/0
Genetic
Background
involves: C57BL/6J * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Igf2bp1tm1Vssp mutation (0 available); any Igf2bp1 mutation (93 available)
Tg(Vil-cre)997Gum mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mice develop reduced number of intestinal tumors compared with Apcmin heterozygotes at 90 days




Genotype
MGI:3814367
cx26
Allelic
Composition
ApcMin/Apc+
Brca2tm1Mbn/Brca2+
Genetic
Background
B6.Cg-Brca2tm1Mbn ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Brca2tm1Mbn mutation (0 available); any Brca2 mutation (60 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
growth/size/body
N
• body weight of mice at time of sacrifice does not differ significantly from Apc-heterozygous, Brca2-heterozygous, or wild-type animals

reproductive system
N
• only observed in 1/8 ENU-treated males, similar to wild-type males (1/9)
• absent in 22% of ENU-treated females
• remaining follicles are degenerating in ENU-treated females
• arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice
• 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
• observed in ENU-treated females displaying ovarian failure (atrophy); endometrium and myometrium appear immature
• reduced in thickness and lined with vacuolated cells indicative of anestrus in ENU-treated females

tumorigenesis
• 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
• multiple intestinal tumors are observed in ENU-treated mice

endocrine/exocrine glands
• 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
• 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 in 22% of ENU-treated females
• remaining follicles are degenerating in ENU-treated females
• arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice
• 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

integument
• 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
• 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
OMIM ID Ref(s)
Breast Cancer 114480 J:67445




Genotype
MGI:5014351
cx27
Allelic
Composition
ApcMin/Apc+
Gt(ROSA)26Sor/Gt(ROSA)26Sor+
Genetic
Background
B6.Cg-Gt(ROSA)26Sor ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Gt(ROSA)26Sor mutation (22 available); any Gt(ROSA)26Sor mutation (317 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• female mice treated with ENU develop significantly fewer mammary tumors than mice carrying either ApcMin alone or C57BL/6 controls

endocrine/exocrine glands
• female mice treated with ENU develop significantly fewer mammary tumors than mice carrying either ApcMin alone or C57BL/6 controls

digestive/alimentary system
• female mice treated with ENU develop significantly fewer intestinal tumors than mice carrying either ApcMin alone or C57BL/6 controls

tumorigenesis
• female mice treated with ENU survive for 86 days as compared to 66-71 days for mice carrying ApcMin alone
• female mice treated with ENU develop significantly fewer intestinal tumors than mice carrying either ApcMin alone or C57BL/6 controls
• female mice treated with ENU develop significantly fewer mammary tumors than mice carrying either ApcMin alone or C57BL/6 controls
• female mice treated with ENU develop significantly fewer mammary or intestinal tumors than mice carrying either ApcMin alone or C57BL/6 controls

homeostasis/metabolism
• female mice treated with ENU develop significantly fewer mammary or intestinal tumors than mice carrying either ApcMin alone or C57BL/6 controls




Genotype
MGI:5567980
cx28
Allelic
Composition
ApcMin/Apc+
Mir10atm1.1Ahl/Mir10atm1.1Ahl
Genetic
Background
B6.Cg-Mir10atm1.1Ahl Apcmin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Mir10atm1.1Ahl mutation (1 available); any Mir10a mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Enhanced intestinal tumorigenesis in ApcMin/Apc+ Mir10atm1.1Ahl/Mir10atm1.1Ahl mice

digestive/alimentary system
• twice as many tumors in the small intestine as in Apcmin heterozygotes
• however, tumor multiplicity in male mice is the same as in Apcmin heterozygotes
• 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 Apcmin heterozygotes

tumorigenesis
• twice as many tumors in the small intestine as in Apcmin heterozygotes
• however, tumor multiplicity in male mice is the same as in Apcmin heterozygotes
• 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 Apcmin heterozygotes




Genotype
MGI:5430745
cx29
Allelic
Composition
ApcMin/Apc+
MthfsGt(RRK291)Byg/Mthfs+
Genetic
Background
B6.Cg-MthfsGt(RRK291)Byg ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
MthfsGt(RRK291)Byg mutation (0 available); any Mthfs mutation (5 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• small intestine and colon tumor incidence is similar to mice heterozygous for ApcMin alone




Genotype
MGI:3767791
cx30
Allelic
Composition
ApcMin/Apc+
Nos2tm1Lau/Nos2tm1Lau
Genetic
Background
B6.Cg-Nos2tm1Lau ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Nos2tm1Lau mutation (6 available); any Nos2 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• polyp size reduced
• 29% of tumor incidence observed in controls
• multiplicity of tumors reduced to about 9% of control level




Genotype
MGI:3767792
cx31
Allelic
Composition
ApcMin/Apc+
Nos2tm1Lau/Nos2+
Genetic
Background
B6.Cg-Nos2tm1Lau ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Nos2tm1Lau mutation (6 available); any Nos2 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• polyp size reduced
• 68% of tumor incidence observed in controls
• multiplicity of tumors reduced to about 33% of control level




Genotype
MGI:4358774
cx32
Allelic
Composition
ApcMin/Apc+
Pla2g4atm1Jvb/Pla2g4atm1Jvb
Genetic
Background
B6.Cg-Pla2g4atm1Jvb ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Pla2g4atm1Jvb mutation (0 available); any Pla2g4a mutation (16 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice exhibit a 83% reduction in small intestine polyp number with a 22% decrease in size compared with polyps in ApcMin heterozygotes
• mice exhibit the same number of polyps in the large intestine as in ApcMin heterozygotes




Genotype
MGI:4440864
cx33
Allelic
Composition
ApcMin/Apc+
Rab25tm1Jrgo/Rab25+
Genetic
Background
B6.Cg-Rab25tm1Jrgo ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Rab25tm1Jrgo mutation (0 available); any Rab25 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 2-fold increase in tumor number in the middle and distal intestines compared with heterozygous Apcmin mice

tumorigenesis
• 2-fold increase in tumor number in the middle and distal intestines compared with heterozygous Apcmin mice




Genotype
MGI:4440863
cx34
Allelic
Composition
ApcMin/Apc+
Rab25tm1Jrgo/Rab25tm1Jrgo
Genetic
Background
B6.Cg-Rab25tm1Jrgo ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Rab25tm1Jrgo mutation (0 available); any Rab25 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Rab25tm1Jrgo/Rab25tm1Jrgo ApcMin/Apc+ mice exhibit increased intestinal adenoma formation compared to ApcMin/Apc+ mice

tumorigenesis
• tubular adenomas in the intestine
• 4-fold increase in tumor number throughout the intestines compared with heterozygous Apcmin mice
• tubular adenomas in the colon

digestive/alimentary system
• more widely distributed polyps in the colon
• 2-fold increase in colonic polyp number compared with heterozygous Apcmin mice
• increased polyp size
• tubular adenomas in the intestine
• 4-fold increase in tumor number throughout the intestines compared with heterozygous Apcmin mice

Mouse Models of Human Disease
OMIM ID Ref(s)
Familial Adenomatous Polyposis 1; FAP1 175100 J:158733




Genotype
MGI:5426849
cx35
Allelic
Composition
ApcMin/Apc+
Shmt1Gt(AD0236)Wtsi/Shmt1Gt(AD0236)Wtsi
Genetic
Background
B6.Cg-Shmt1Gt(AD0236)Wtsi ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Shmt1Gt(AD0236)Wtsi mutation (0 available); any Shmt1 mutation (27 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• mice exhibit the same tumorigenesis as ApcMin heterozygotes




Genotype
MGI:3831112
cx36
Allelic
Composition
ApcMin/Apc+
Tgfbr1tm1Bopa/Tgfbr1+
Genetic
Background
B6.Cg-Tgfbr1tm1Bopa ApcMin
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Tgfbr1tm1Bopa mutation (0 available); any Tgfbr1 mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop twice as many intestinal tumors as in ApcMin heterozygotes
• mice develop small and predominantly scattered tumors in the small intestine as well as colonic tumors
• 3 mice develop large, polyploidy and ulcerated colonic tumors

tumorigenesis
• mice develop twice as many intestinal tumors as in ApcMin heterozygotes
• mice develop small and predominantly scattered tumors in the small intestine as well as colonic tumors
• 3 mice develop large, polyploidy and ulcerated colonic tumors




Genotype
MGI:5529263
cx37
Allelic
Composition
ApcMin/Apc+
Pla2g2aMom1-r/Pla2g2a+
Genetic
Background
either: (AKR/J x C57BL/6J-ApcMin)F1 or (MA/MyJ x C57BL/6J-ApcMin)F1 or (CAST/EiJ x C57BL/6J-ApcMin)F1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Pla2g2aMom1-r mutation (0 available); any Pla2g2a mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 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 Pla2g2aMom1-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 Pla2g2aMom1-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 Pla2g2aMom1-r s
• inbred strains AKR/J, MA/MyJ, and CAST/Ei are homozygous for the tumor suppressing allele Pla2g2a

tumorigenesis
• 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 Pla2g2aMom1-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 Pla2g2aMom1-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 Pla2g2aMom1-r s
• inbred strains AKR/J, MA/MyJ, and CAST/Ei are homozygous for the tumor suppressing allele Pla2g2a




Genotype
MGI:3700063
cx38
Allelic
Composition
ApcMin/Apc+
Hpgdstm1Urad/Hpgds+
Genetic
Background
involves: 129 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Hpgdstm1Urad mutation (0 available); any Hpgds mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 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

tumorigenesis
• mice have 44-61% more intestinal adenomas than Apc-heterozygous controls
• 95% of adenomas are in small intestine, while colon adenomas are increased 2-fold
• adenomas tend to be smaller than in wild-type APC mutants (~.5 mm vs 0.68 mm in controls but difference is not significant




Genotype
MGI:3700064
cx39
Allelic
Composition
ApcMin/Apc+
Hpgdstm1Urad/Hpgdstm1Urad
Genetic
Background
involves: 129 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Hpgdstm1Urad mutation (0 available); any Hpgds mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 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

tumorigenesis
• 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:5636667
cx40
Allelic
Composition
ApcMin/Apc+
Msh2tm1Mak/Msh2+
Nos2tm1Mrl/Nos2tm1Mrl
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Msh2tm1Mak mutation (0 available); any Msh2 mutation (62 available)
Nos2tm1Mrl mutation (4 available); any Nos2 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mutants exhibit enhanced polyp number in the small intestine, but not in the colon compared to double ApcMin Msh2tm1Mak heterozygotes




Genotype
MGI:5636670
cx41
Allelic
Composition
ApcMin/Apc+
Msh2tm1Mak/Msh2tm1Mak
Nos2tm1Mrl/Nos2tm1Mrl
Genetic
Background
involves: 129P2/OlaHsd * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Msh2tm1Mak mutation (0 available); any Msh2 mutation (62 available)
Nos2tm1Mrl mutation (4 available); any Nos2 mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mutants exhibit similar polyp formation in the small intestine and colon as mice heterozygous for ApcMin and homozygous for Msh2tm1Mak




Genotype
MGI:3582674
cx42
Allelic
Composition
ApcMin/Apc+
Blmtm1Grdn/Blm+
Genetic
Background
involves: 129P2/OlaHsd * 129S/SvEv * Black Swiss * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Blmtm1Grdn mutation (0 available); any Blm mutation (52 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 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
• developed low- and high-grade adenomas in the small intestine, whereas only low-grade adenomas were seen in heterozygous Apc mutant mice

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

Mouse Models of Human Disease
OMIM ID Ref(s)
Bloom Syndrome; BLM 210900 J:79058




Genotype
MGI:4429611
cx43
Allelic
Composition
ApcMin/Apc+
Msh2tm1Htr/Msh2tm1Htr
Genetic
Background
involves: 129P2/OlaHsd * BALB/c * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Msh2tm1Htr mutation (0 available); any Msh2 mutation (62 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice have an 8-fold increase in intestinal tumor load compared with ApcMin heterozygotes

mortality/aging
• survival is reduced 4-fold compared with ApcMin heterozygotes
• all mice die within 5 months

tumorigenesis
• mice have an 8-fold increase in intestinal tumor load compared with ApcMin heterozygotes




Genotype
MGI:5693797
cx44
Allelic
Composition
ApcMin/Apc+
Ccdc80tm1.1Ftk/Ccdc80tm1.1Ftk
Genetic
Background
involves: 129P2/OlaHsd * BALB/cJ * C57BL/6 * C57BL/6J * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Ccdc80tm1.1Ftk mutation (0 available); any Ccdc80 mutation (14 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival is 94 days compared to 142 days in control ApcMin heterozygotes

tumorigenesis
• mice develop tumors in the small intestine with no difference in number, distribution, size and histology from tumors in single ApcMin heterozygotes
• mean number of colonic tumors is 11.9 compared to 3.1 in control ApcMin 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 ApcMin heterozygotes, with 29% of tumors being adenocarcinoma
• no metastases to lymph nodes, liver or lungs are seen
• 35% of colon tumors are adenocarcinomas
• 97% of carcinomas are located in the distal colon
• 65% of colon tumors are adenomas

digestive/alimentary system
• vast majority of polyps localize to the small intestine
• mice develop tumors in the small intestine with no difference in number, distribution, size and histology from tumors in single ApcMin heterozygotes
• mean number of colonic tumors is 11.9 compared to 3.1 in control ApcMin 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 ApcMin heterozygotes, with 29% of tumors being adenocarcinoma
• no metastases to lymph nodes, liver or lungs are seen
• 35% of colon tumors are adenocarcinomas
• 97% of carcinomas are located in the distal colon

Mouse Models of Human Disease
OMIM ID Ref(s)
Colorectal Cancer; CRC 114500 J:216704




Genotype
MGI:4359622
cx45
Allelic
Composition
ApcMin/Apc+
Mom5129P2/?
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Mom5129P2 mutation (0 available); any Mom5 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• significantly reduced incidence of intestinal adenoma (around 20-25)




Genotype
MGI:3834880
cx46
Allelic
Composition
ApcMin/Apc+
Foxl1tm1Khk/Foxl1tm1Khk
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Foxl1tm1Khk mutation (0 available); any Foxl1 mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• mutants do not show increased tumor multiplicity up to 90 days in the small intestine compared to heterozygous ApcMin mice
• 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
• mice develop a 7.7-fold higher number of colonic polyps compared to heterozygous ApcMin mice with wild-type Foxl1
• mice develop an average of 5.5 polyps in the stomach by 3 months of age, compared to no polyps in heterozygous ApcMin 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
• 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 ApcMin 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 ApcMin mice




Genotype
MGI:3613447
cx47
Allelic
Composition
ApcMin/Apc+
Zbtb33tm1.1Bird/Y
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Zbtb33tm1.1Bird mutation (0 available); any Zbtb33 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice exhibit a similar number of intestinal tumors as compared to ApcMin mice

mortality/aging
• life span of these animals is an average of 317 days; this is improved over ApcMin mice alone at an average of 217 days

tumorigenesis
• mice exhibit a similar number of intestinal tumors as compared to ApcMin mice
• tumors in doubly heterozygous mice significantly smaller at 180 days of age




Genotype
MGI:3579838
cx48
Allelic
Composition
ApcMin/Apc+
Mbd2tm1Bh/Mbd2tm1Bh
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Mbd2tm1Bh mutation (0 available); any Mbd2 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• homozygotes survive significantly longer than mice only heterozygous for ApcMin

tumorigenesis
• tumors present are smaller in size
• 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:3579839
cx49
Allelic
Composition
ApcMin/Apc+
Mbd2tm1Bh/Mbd2+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Mbd2tm1Bh mutation (0 available); any Mbd2 mutation (7 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• although survival is reduced, they live longer than mice only heterozygous for ApcMin

tumorigenesis
• tumor repression specific to the small intestine




Genotype
MGI:5426846
cx50
Allelic
Composition
ApcMin/Apc+
Phgdhtm1.1Shfu/Phgdh+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Phgdhtm1.1Shfu mutation (1 available); any Phgdh mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• mice exhibit the same tumorigenesis as ApcMin heterozygotes




Genotype
MGI:4366247
cx51
Allelic
Composition
ApcMin/Apc+
Ptgs1tm1Unc/Ptgs1tm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Ptgs1tm1Unc mutation (1 available); any Ptgs1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice live 12 months or longer unlike ApcMin heterozygotes that die after 7 to 8 months

tumorigenesis
• mice form 77% fewer, smaller intestinal tumors than in ApcMin heterozygotes

homeostasis/metabolism
• prostaglandin levels in normal intestinal tissue is lower than in ApcMin heterozygotes
• intestinal tumor tissue fails to exhibit an increase in prostaglandin levels unlike in ApcMin heterozygotes

digestive/alimentary system




Genotype
MGI:4946621
cx52
Allelic
Composition
ApcMin/Apc+
Cd44tm1Mak/Cd44tm1Mak
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Cd44tm1Mak mutation (1 available); any Cd44 mutation (40 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 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 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
• 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 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:3719427
cx53
Allelic
Composition
ApcMin/Apc+
Mbd4tm1Bird/Mbd4tm1Bird
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Mbd4tm1Bird mutation (0 available); any Mbd4 mutation (10 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice had a greater intestinal adenoma burden at death with a median of 28 tumors compared to Mbd4tm1Bird ApcMin heterozygotes (median of 14 tumors at time of death)

mortality/aging
• mice exhibit reduced survival

tumorigenesis
• mice had a greater intestinal adenoma burden at death with a median of 28 tumors compared to Mbd4tm1Bird ApcMin heterozygotes (median of 14 tumors at time of death)

homeostasis/metabolism
• repair of C to T transitions is reduced to 88% efficiency from 96% in Mbd4tm1Bird ApcMin heterozygotes

cellular
• repair of C to T transitions is reduced to 88% efficiency from 96% in Mbd4tm1Bird ApcMin heterozygotes




Genotype
MGI:5319648
cx54
Allelic
Composition
ApcMin/Apc+
Tcf7tm1Cle/Tcf7tm1Cle
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Tcf7tm1Cle mutation (0 available); any Tcf7 mutation (8 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• adenoacanthomas in the mammary glands of all female mice by 8 weeks of age
• also in older male mice

digestive/alimentary system
• adenomatous polyps form throughout the intestine
• large in size but showing no signs of tumor progression
• 60% of mice with adenomas and adenoacanthomas of the salivary glands at 6 months of age

endocrine/exocrine glands
• 60% of mice with adenomas and adenoacanthomas of the salivary glands at 6 months of age
• adenoacanthomas in the mammary glands of all female mice by 8 weeks of age
• also in older male mice

tumorigenesis
• adenomatous polyps form throughout the intestine
• large in size but showing no signs of tumor progression
• 60% of mice with adenomas and adenoacanthomas of the salivary glands at 6 months of age
• adenoacanthomas in the mammary glands of all female mice by 8 weeks of age
• also in older male mice




Genotype
MGI:3700062
cx55
Allelic
Composition
ApcMin/Apc+
Ptgdstm1Ohy/Ptgdstm1Ohy
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Ptgdstm1Ohy mutation (0 available); any Ptgds mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice with Ptgds deficiency do not show altered adenoma profile compared to Apc heterozygous Ptgds-wild-type mice

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




Genotype
MGI:4366248
cx56
Allelic
Composition
ApcMin/Apc+
Ptgs1tm1Unc/Ptgs1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Ptgs1tm1Unc mutation (1 available); any Ptgs1 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive 10 months unlike ApcMin heterozygotes that die after 7 to 8 months

tumorigenesis
• mice form 43% fewer tumors than in ApcMin heterozygotes

digestive/alimentary system




Genotype
MGI:3610196
cx57
Allelic
Composition
ApcMin/Apc+
Hptm1Skl/Hptm1Skl
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Hptm1Skl mutation (0 available); any Hp mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• intestinal tumor burden at 60-65 days of age increased by 2-3 fold

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




Genotype
MGI:5636659
cx58
Allelic
Composition
ApcMin/Apc+
Msh2tm1Mak/Msh2tm1Mak
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Msh2tm1Mak mutation (0 available); any Msh2 mutation (62 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice become moribound and die from anemia and intestinal obstruction at a mean age of 82 days

tumorigenesis
• mice exhibit accelerated intestinal tumorigenesis compared to single ApcMin 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 ApcMin heterozygotes

digestive/alimentary system
• mice exhibit accelerated intestinal tumorigenesis compared to single ApcMin 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 ApcMin heterozygotes
• due to tumors

hematopoietic system
• 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
OMIM ID Ref(s)
Colorectal Cancer; CRC 114500 J:75393 , J:200824




Genotype
MGI:4366246
cx59
Allelic
Composition
ApcMin/Apc+
Ptgs2tm1Unc/Ptgs2tm1Unc
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Ptgs2tm1Unc mutation (1 available); any Ptgs2 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice survive 1 year unlike ApcMin heterozygotes that die after 7 to 8 months

tumorigenesis
• mice form 84% fewer, smaller intestinal tumors compared with ApcMin heterozygotes

homeostasis/metabolism
• intestinal tumor tissue fails to exhibit an increase in prostaglandin levels unlike in ApcMin heterozygotes

digestive/alimentary system




Genotype
MGI:5448541
cx60
Allelic
Composition
ApcMin/Apc+
Trp53tm1Mlh/Trp53tm1Mlh
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SWR
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Trp53tm1Mlh mutation (0 available); any Trp53 mutation (147 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 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
• 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
• 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
• 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
cx61
Allelic
Composition
ApcMin/Apc+
Dnd1Ter/Dnd1+
Genetic
Background
involves: 129P3/J * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Dnd1Ter mutation (1 available); any Dnd1 mutation (9 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• 1.5X increase in intestinal tumor rate relative to Apc single heterozygotes
• significantly elevated polyp mass

tumorigenesis
• 1.5X increase in intestinal tumor rate relative to Apc single heterozygotes
• significantly elevated polyp mass




Genotype
MGI:3722288
cx62
Allelic
Composition
ApcMin/ApcMin
Rr27tm1Rohl/Rr27+
Genetic
Background
involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Rr27tm1Rohl mutation (0 available); any Rr27 mutation (2 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mice develop twice as many intestinal and colonic adenomas as in ApcMin homozygotes
• mice develop twice as many colonic adenomas as in ApcMin homozygotes

digestive/alimentary system
• mice have longer crypts than wild-type mice
• mice develop twice as many intestinal and colonic adenomas as in ApcMin homozygotes

endocrine/exocrine glands
• mice have longer crypts than wild-type mice




Genotype
MGI:3831111
cx63
Allelic
Composition
ApcMin/Apc+
Tgfbr1tm1Bopa/Tgfbr1+
Genetic
Background
involves: 129S1/SvImJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Tgfbr1tm1Bopa mutation (0 available); any Tgfbr1 mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop twice as many intestinal tumors as in ApcMin heterozygotes
• mice develop small and predominantly scattered tumors in the small intestine as well as colonic tumors
• 3 mice develop large, polyploidy and ulcerated colonic tumors

tumorigenesis
• mice develop twice as many intestinal tumors as in ApcMin heterozygotes
• mice develop small and predominantly scattered tumors in the small intestine as well as colonic tumors
• 3 mice develop large, polyploidy and ulcerated colonic tumors

cellular
• 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
N
• despite disruptions in cell proliferation, hematopoiesis is normal




Genotype
MGI:4365606
cx64
Allelic
Composition
ApcMin/Apc+
Il6tm1Kopf/Il6tm1Kopf
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Il6tm1Kopf mutation (7 available); any Il6 mutation (15 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
muscle
N
• no gastrocnemius muscle wasting

adipose tissue
N
• normal epididymal fat pads

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




Genotype
MGI:5298869
cx65
Allelic
Composition
ApcMin/Apc+
Esr2tm1Mma/Esr2tm1Mma
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Esr2tm1Mma mutation (0 available); any Esr2 mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased proliferation of cells in the colon
• fewer mature goblet cells in the colon with prevalent pregoblet cells
• mice develop increased tumors in the large intestine, including the cecum and one third of the colons, compared with Apcmin heterozygotes
• mice develop sessile and pedunculated forms of colonic adenomas unlike Apcmin heterozygotes
• while tumor progression is stimulated to a greater extent than in Apcmin heterozygotes, tumor initiation is the same
• mononuclear cell infiltrates in the colon

tumorigenesis
• mice develop increased tumors in the large intestine, including the cecum and one third of the colons, compared with Apcmin heterozygotes
• mice develop sessile and pedunculated forms of colonic adenomas unlike Apcmin heterozygotes
• while tumor progression is stimulated to a greater extent than in Apcmin heterozygotes, tumor initiation is the same

immune system
• mononuclear cell infiltrates in the colon

cellular
• increased proliferation of cells in the colon

endocrine/exocrine glands
• fewer mature goblet cells in the colon with prevalent pregoblet cells




Genotype
MGI:4820588
cx66
Allelic
Composition
ApcMin/Apc+
Pms2tm1Lisk/Pms2tm1Lisk
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Pms2tm1Lisk mutation (1 available); any Pms2 mutation (23 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die earlier than Apcmin heterozygotes

tumorigenesis
• mice develop 2.3 times more adenomatous polyps in the intestine compared with Apcmin heterozygotes
• however, no evidence of adenocarcinoma is observed
• tumors exhibit microsatellite instability

digestive/alimentary system
• mice develop 2.3 times more adenomatous polyps in the intestine compared with Apcmin heterozygotes
• mice develop 2.3 times more adenomatous polyps in the intestine compared with Apcmin heterozygotes
• however, no evidence of adenocarcinoma is observed
• tumors exhibit microsatellite instability




Genotype
MGI:5298870
cx67
Allelic
Composition
ApcMin/Apc+
Esr1tm1.1Mma/Esr1tm1.1Mma
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging




Genotype
MGI:4357790
cx68
Allelic
Composition
ApcMin/Apc+
Hdac2Gt(W035F03)Joe/Hdac2Gt(W035F03)Joe
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Hdac2Gt(W035F03)Joe mutation (0 available); any Hdac2 mutation (18 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• intestinal adenocarcinoma occurs in these mice though not to the extent as in ApcMin controls

tumorigenesis
• intestinal adenocarcinoma occurs in these mice though not to the extent as in ApcMin controls
• mice develop fewer intestinal tumors than ApcMin 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 ApcMin controls




Genotype
MGI:5298871
cx69
Allelic
Composition
ApcMin/Apc+
Esr1tm1.1Mma/Esr1+
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Esr1tm1.1Mma mutation (0 available); any Esr1 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apcmin heterozygotes
• mice develop sessile and pedunculated forms of colonic adenomas unlike Apcmin heterozygotes
• while tumor progression is stimulated to a greater extent than in Apcmin heterozygotes, tumor initiation is the same
• all mice develop invasive carcinomas in the intestine and colon unlike Apcmin heterozygotes

digestive/alimentary system
• increased proliferation of cells in the colon
• some mice exhibit abnormal submucosal with thickening of the muscularis mucosae and enrichment of stromal components compared with Apcmin heterozygotes
• some mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice
• fewer mature goblet cells in the colon with prevalent pregoblet cells
• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apcmin heterozygotes
• mice develop sessile and pedunculated forms of colonic adenomas unlike Apcmin heterozygotes
• while tumor progression is stimulated to a greater extent than in Apcmin heterozygotes, tumor initiation is the same

endocrine/exocrine glands
• some mice exhibit reduced crypt length and distortion of surface epithelial cells in the colon compared with control mice
• fewer mature goblet cells in the colon with prevalent pregoblet cells

cellular
• increased proliferation of cells in the colon




Genotype
MGI:5298868
cx70
Allelic
Composition
ApcMin/Apc+
Esr2tm1Mma/Esr2+
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Esr2tm1Mma mutation (0 available); any Esr2 mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apcmin heterozygotes
• mice develop sessile and pedunculated forms of colonic adenomas unlike Apcmin heterozygotes
• while tumor progression is stimulated to a greater extent than in Apcmin heterozygotes, tumor initiation is the same

digestive/alimentary system
• increased proliferation of cells in the colon in ovariectomized
• mice develop increased tumors in the small and large intestines, including the cecum and one third of the colons, compared with Apcmin heterozygotes
• mice develop sessile and pedunculated forms of colonic adenomas unlike Apcmin heterozygotes
• while tumor progression is stimulated to a greater extent than in Apcmin heterozygotes, tumor initiation is the same

cellular
• increased proliferation of cells in the colon in ovariectomized




Genotype
MGI:5313421
cx71
Allelic
Composition
ApcMin/Apc+
Col1a1tm11(tetO-Dnmt3b_i6)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Col1a1tm11(tetO-Dnmt3b_i6)Jae mutation (0 available); any Col1a1 mutation (88 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (12 available); any Gt(ROSA)26Sor mutation (317 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes




Genotype
MGI:5313423
cx72
Allelic
Composition
ApcMin/Apc+
Col1a1tm12(tetO-Dnmt3a_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Col1a1tm12(tetO-Dnmt3a_i1)Jae mutation (0 available); any Col1a1 mutation (88 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (12 available); any Gt(ROSA)26Sor mutation (317 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes




Genotype
MGI:4430577
cx73
Allelic
Composition
ApcMin/Apc+
Col1a1tm1(CAG-Sirt1)Dsin/Col1a1+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Col1a1tm1(CAG-Sirt1)Dsin mutation (1 available); any Col1a1 mutation (88 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice develop intestinal tumors in the duodenum and ileum

tumorigenesis
• mice develop intestinal tumors in the duodenum and ileum

growth/size/body
• at 16 weeks

hematopoietic system
• at 16 weeks




Genotype
MGI:3839104
cx74
Allelic
Composition
ApcMin/Apc+
Ptprhtm1.1Mato/Ptprhtm1.1Mato
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Ptprhtm1.1Mato mutation (1 available); any Ptprh mutation (25 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mice develop fewer small intestinal macroadenomas compared to ApcMin heterozygotes
• however, proliferation and apoptosis within the tumor mass is the same as in ApcMin heterozygotes




Genotype
MGI:5313420
cx75
Allelic
Composition
ApcMin/Apc+
Col1a1tm10(tetO-Dnmt3b_i3)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Col1a1tm10(tetO-Dnmt3b_i3)Jae mutation (0 available); any Col1a1 mutation (88 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (12 available); any Gt(ROSA)26Sor mutation (317 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes




Genotype
MGI:5313419
cx76
Allelic
Composition
ApcMin/Apc+
Col1a1tm9(tetO-Dnmt3b_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+
Genetic
Background
involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Col1a1tm9(tetO-Dnmt3b_i1)Jae mutation (1 available); any Col1a1 mutation (88 available)
Gt(ROSA)26Sortm1(rtTA*M2)Jae mutation (12 available); any Gt(ROSA)26Sor mutation (317 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apcmin heterozygotes

tumorigenesis
• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apcmin heterozygotes
• doxycycline-treated mice develop more macro- and microadenomas in the small intestinal and, to a lesser extent colon, compared with Apcmin heterozygotes
• doxycycline-treated mice exhibit increased size of microadenomas compared with Apcmin heterozygotes

cellular
• 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




Genotype
MGI:3848453
cx77
Allelic
Composition
ApcMin/Apc+
Dnmt1tm1Jae/Dnmt1tm1Pwl
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Dnmt1tm1Jae mutation (2 available); any Dnmt1 mutation (70 available)
Dnmt1tm1Pwl mutation (0 available); any Dnmt1 mutation (70 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
N
• no intestinal polyps are observed unlike in ApcMin heterozygotes




Genotype
MGI:3848450
cx78
Allelic
Composition
ApcMin/Apc+
Dnmt1tm1Pwl/Dnmt1+
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Dnmt1tm1Pwl mutation (0 available); any Dnmt1 mutation (70 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice exhibit fewer intestinal polyps compared with ApcMin heterozygotes
• polyps are smaller than in ApcMin heterozygotes




Genotype
MGI:3848451
cx79
Allelic
Composition
ApcMin/Apc+
Dnmt1tm1Jae/Dnmt1+
Genetic
Background
involves: 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Dnmt1tm1Jae mutation (2 available); any Dnmt1 mutation (70 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice exhibit fewer intestinal polyps compared with ApcMin heterozygotes
• polyps are smaller than in ApcMin heterozygotes




Genotype
MGI:2653701
cx80
Allelic
Composition
ApcMin/ApcMin
Asphtm1Jed/Asphtm1Jed
Genetic
Background
involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6J * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Asphtm1Jed mutation (0 available); any Asph mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• approximately 2-fold increase in small intestinal tumor number and increase in tumor size compared to single homozygous ApcMin mice

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

tumorigenesis
• approximately 2-fold increase in small intestinal tumor number and increase in tumor size compared to single homozygous ApcMin mice




Genotype
MGI:5451046
cx81
Allelic
Composition
ApcMin/Apc+
Dp(17Nfkbil1-Olfr91)1Cogr/0
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Dp(17Nfkbil1-Olfr91)1Cogr mutation (1 available); any Dp(17Nfkbil1-Olfr91)1Cogr mutation (1 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
N
• mice exhibit the same tumor-free survival as ApcMin heterozygotes




Genotype
MGI:3512138
cx82
Allelic
Composition
ApcMin/Apc+
Eregtm1Dwt/Eregtm1Dwt
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Eregtm1Dwt mutation (1 available); any Ereg mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• the number, average size, and location of intestinal polyps is similar to ApcMin heterozygotes

tumorigenesis
• the number, average size, and location of intestinal polyps is similar to ApcMin heterozygotes




Genotype
MGI:5446699
cx83
Allelic
Composition
ApcMin/Apc+
Il22ra2tm2Vlcg/Il22ra2tm2Vlcg
Genetic
Background
involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Il22ra2tm2Vlcg mutation (0 available); any Il22ra2 mutation (11 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• in the colon but not the small intestine compared to compared to mice heterozygous for ApcMin alone

tumorigenesis
• in the colon but not the small intestine compared to compared to mice heterozygous for ApcMin alone
• in the colon but not the small intestine compared to compared to mice heterozygous for ApcMin alone




Genotype
MGI:3812011
cx84
Allelic
Composition
ApcMin/Apc+
Myctm1Jlc/Myc+
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Myctm1Jlc mutation (0 available); any Myc mutation (24 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
N
• mice exhibit a life span of 291 days compared to 169 days in ApcMin heterozygotes

digestive/alimentary system
• mice develop fewer and smaller polyps than in ApcMin heterozygotes
• cell proliferation in polyps is decreased compared to in ApcMin heterozygotes while levels of apoptosis are increased compared to in ApcMin heterozygotes and wild-type mice

hematopoietic system
N
• unlike in ApcMin heterozygotes, hematocrit levels and spleen size are normal
• expression of angiogenic factors is decreased compared to in ApcMin heterozygotes




Genotype
MGI:3575580
cx85
Allelic
Composition
ApcMin/Apc+
Recql4tm1Glu/Recql4tm1Glu
Genetic
Background
involves: 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Recql4tm1Glu mutation (0 available); any Recql4 mutation (12 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• the average maximal diameter of macroadenomas was larger than in double heterozygous controls
• 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
• mutants always developed tumors in the large intestine, a site that is inconsistently affected in double heterozygous controls

Mouse Models of Human Disease
OMIM ID Ref(s)
Rothmund-Thomson Syndrome; RTS 268400 J:97101




Genotype
MGI:4429574
cx86
Allelic
Composition
ApcMin/Apctm1Tno
Ctnnb1tm4.1Wbm/Ctnnb1+
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Apctm1Tno mutation (0 available); any Apc mutation (85 available)
Ctnnb1tm4.1Wbm mutation (0 available); any Ctnnb1 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
liver/biliary system
• hepatocellular carcinomas (HCC) in 47% of mutant mice (n=15), including 20% that showed intestinal comorbidity
• mice only have HCC (n=4) live longer than Apcmin/+ mice

nervous system
N
• normal head morphology

craniofacial
N
• normal head morphology

digestive/alimentary system
• reduced tumor multiplicity and incidence, leaving 6 of 15 mice (40%) free of polyps
• the remaining macroscopic lesions are of tubulo-villous structure
• similar size and latency to those observed in age-matched Apcmin/+ mice

tumorigenesis
• hepatocellular carcinomas (HCC) in 47% of mutant mice (n=15), including 20% that showed intestinal comorbidity
• mice only have HCC (n=4) live longer than Apcmin/+ mice




Genotype
MGI:4429575
cx87
Allelic
Composition
ApcMin/ApcMin
Ctnnb1tm4.1Wbm/Ctnnb1+
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Ctnnb1tm4.1Wbm mutation (0 available); any Ctnnb1 mutation (26 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• death immediately after gastrulation
• embryos only detected at embryonic day 4.5 (E4.5) and E5.5 but not at later stages (E6 and E7)




Genotype
MGI:3510235
cx88
Allelic
Composition
ApcMin/Apc+
Ppardtm1Jps/Ppardtm1Jps
Genetic
Background
involves: 129/Sv * AKR/J * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Ppardtm1Jps mutation (0 available); any Ppard mutation (52 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• colon cancer is more severe and mortality occurs earlier than in controls

digestive/alimentary system
• increased numbers of small intestine polyps as well in females
• colon cancer is more severe and mortality occurs earlier than in controls




Genotype
MGI:5446700
cx89
Allelic
Composition
ApcMin/Apc+
Il22tm1Flv/Il22tm1Flv
Genetic
Background
involves: 129/Sv * C57BL/6 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Il22tm1Flv mutation (0 available); any Il22 mutation (6 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• decrease in tumor numbers in the small intestine and colon compared to mice heterozygous for ApcMin alone

tumorigenesis
• decrease in tumor numbers in the small intestine and colon compared to mice heterozygous for ApcMin alone




Genotype
MGI:3709984
cx90
Allelic
Composition
ApcMin/ApcMin
Sat1tm1Alh/Y
Genetic
Background
involves: 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Sat1tm1Alh mutation (1 available); any Sat1 mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• total tumor counts in small intestine were reduced by about 75% for both small and large tumors
• however, there is no significant effect on colonic tumor number or size despite the fact that Sat1 over-expression increases tumor number about 6-fold




Genotype
MGI:3803126
cx91
Allelic
Composition
ApcMin/Apc+
Mmom2129X1/SvJ/Mmom2C57BL/6J
Genetic
Background
involves: 129X1/SvJ * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Mmom2129X1/SvJ mutation (0 available); any Mmom2 mutation (0 available)
Mmom2C57BL/6J mutation (0 available); any Mmom2 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
endocrine/exocrine glands
• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females
• increased tumor latency

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

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




Genotype
MGI:3623317
cx92
Allelic
Composition
ApcMin/Apc+
EgfrWa5/Egfr+
Genetic
Background
involves: BALB/cAnN * C3H/HeN * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
EgfrWa5 mutation (2 available); any Egfr mutation (33 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• 46% reduction in the number of macroscopic intestinal polyps in comparison to mice heterozygous only for ApcMin at 3 months of age
• no reduction in tumor size




Genotype
MGI:4461429
cx93
Allelic
Composition
ApcMin/Apc+
Pla2g2aMom1-r/?
PrkdcBALB/c/PrkdcBALB/c
Genetic
Background
involves: BALB/cByJ * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Pla2g2aMom1-r mutation (0 available); any Pla2g2a mutation (1 available)
PrkdcBALB/c mutation (0 available); any Prkdc mutation (188 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
tumorigenesis
• mice show 2-3 fold increase in adenoma incidence in the small intestine after X-irradiation




Genotype
MGI:5463417
cx94
Allelic
Composition
ApcMin/Apc+
Rr21tm1Jta/Rr21+
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Rr21tm1Jta mutation (0 available); any Rr21 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• similar frequency of intestinal polyps compared to mice heterozygous for ApcMin alone




Genotype
MGI:4359621
cx95
Allelic
Composition
ApcMin/Apc+
Mom5C57BL/6/Mom5C57BL/6
Genetic
Background
involves: C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
ApcMin mutation (8 available); any Apc mutation (85 available)
Mom5C57BL/6 mutation (0 available); any Mom5 mutation (0 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• higher numbers of intestinal adenomas in homozygotes than in heterozygotes (around 50-55)

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




Genotype
MGI:5475210
cx96