Mouse Genome Informatics
hm1
    ApcMin/ApcMin
involves: AKR/J * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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
• 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


Mouse Genome Informatics
hm2
    ApcMin/ApcMin
involves: C57BL/6 * POMOD
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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
• embryos are small and embedded in maternal tissue

mortality/aging


Mouse Genome Informatics
hm3
    ApcMin/ApcMin
involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
cellular
• cultured adenomatous tissue form highly clonogenic spheroids


Mouse Genome Informatics
hm4
    ApcMin/ApcMin
involves: C57BL/6J * CAST/EiJ
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
ht5
    ApcMin/Apc+
(AKR/J x C57BL/6J)F1
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
ht6
    ApcMin/Apc+
B6(AKR)-ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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
• females of this genotype have an increased susceptibility to developing mammary neoplasia

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


Mouse Genome Informatics
ht7
    ApcMin/Apc+
B6.Cg-Brca2tm1Mbn ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
growth/size
• 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) (J:67445)
• absent in 26% of ENU-treated females (J:67445)
• remaining follicles are degenerating in ENU-treated females (J:67445)
• arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice (J:67445)
• complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females (J:67445)
• observed in ENU-treated females displaying ovarian failure (atrophy); endometrium and myometrium appear immature (J:67445)
• reduced in thickness and lined with vacuolated cells indicative of anestrus in ENU-treated females (J:67445)

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

endocrine/exocrine glands
• females exhibit some adrenal hyperplasia, while none is observed in males (J:67445)
• in ENU treated mice, male mammary ducts are elongated and in most males have extended to the lymph node of the fourth mammary gland, whereas wild-type and Brca2-heterozygous males are born with a small mammary gland rudiment, which grows no further, and no nipple (J:67445)
• no differences are observed in branching of female mammary glands among genotypes or wild-type females (J:67445)
(J:67445)
• absent in 26% of ENU-treated females (J:67445)
• remaining follicles are degenerating in ENU-treated females (J:67445)
• arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice (J:67445)
• complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females (J:67445)

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 (J:67445)
• no differences are observed in branching of female mammary glands among genotypes or wild-type females (J:67445)
(J:67445)


Mouse Genome Informatics
ht8
    ApcMin/Apc+
C57BL/6J-ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype

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

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

homeostasis/metabolism
• females exhibit increased free fatty acid levels at 15 weeks of age (J:86036)
• females show increased triglyceride levels at 15 weeks of age (J:86036)
• 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
• regular chow-fed males stop gaining weight, lose more weight, and are smaller at 15 weeks than beef-fed males (J:85142)

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


Mouse Genome Informatics
ht9
    ApcMin/Apc+
involves: 129/Sv * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
ht10
    ApcMin/Apc+
involves: 129P2/OlaHsd * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• no gastric adenomas are observed (J:95893)
• at 30 days, no colonic adenomas are found and normal colonic architecture and cellular morphology is observed (J:95893)


Mouse Genome Informatics
ht11
    ApcMin/Apc+
involves: AKR/J * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• visible tumors of the large and small intestine
• either polyploid, papillary or sessile adenomas
• 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

digestive/alimentary system
• bloody feces

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

homeostasis/metabolism

mortality/aging

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


Mouse Genome Informatics
ht12
    ApcMin/Apc+
involves: C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• mice die at 169 days

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


Mouse Genome Informatics
ht13
    ApcMin/Apc+
involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• heterozygotes begin to die at 7 months of age

tumorigenesis
• small and large adenomas are seen throughout the intestine with more lesions found in the ileum compared to Apctm1Cip heterozygotes
• 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

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


Mouse Genome Informatics
ht14
    ApcMin/Apctm1.1Klne
B6.Cg-ApcMin/Apctm1.1Klne
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• increased compared with ApcMin heterozygotes
• however, the number of polyps in the colon is the same as in 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

cellular
• increased compared with ApcMin heterozygotes


Mouse Genome Informatics
ht15
    ApcMin/Apctm1Tno
involves: 129/Sv * 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cn16
    ApcMin/Apc+
Hsd11b2tm1.1Mzz/Hsd11b2tm1.1Mzz
Tg(Vil-cre)997Gum/0

involves: 129 * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• reduced proliferation and increased apoptosis compared with tumors from ApcMin heterozygotes
• fewer total intestinal adenoma at 20 weeks with prevented initiation of polyp formation compared with 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


Mouse Genome Informatics
cn17
    ApcMin/Apc+
Dnmt3btm1Jae/Dnmt3btm1Jae
Tg(Fabp1-cre)1Jig/0

involves: 129 * C57BL/6 * C57BL/6J * FVB/N
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cn18
    ApcMin/Apc+
Ptentm1Hwu/Ptentm1Hwu
Tg(Vil-cre)997Gum/0

involves: 129S4/SvJae * BALB/c * C57BL/6J * SJL
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cn19
    ApcMin/Apc+
Col1a1tm1(CAG-Sirt1)Dsin/Col1a1+
Tg(Vil-cre)997Gum/0

involves: 129S4/SvJae * C57BL/6 * C57BL/6J * SJL
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
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
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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 (J:193873)

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 (J:193873)


Mouse Genome Informatics
cn21
    ApcMin/Apc+
Erbb3tm1.1Dwt/Erbb3tm2.1Dwt
Tg(Vil-cre)997Gum/0

involves: 129S6/SvEvTac * C57BL/6 * C57BL/6J * SJL
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
N
• unlike ApcMin heterozygotes, mice do not develop colonic polyps (J:152703)
• 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


Mouse Genome Informatics
cn22
    ApcMin/Apc+
Gt(ROSA)26Sortm2(Rnf187)Jhai/Gt(ROSA)26Sor+
Tg(Vil-cre)20Syr/0

involves: 129S6/SvEvTac * C57BL/6 * DBA/2
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• intestinal tumors exhibit increased cell proliferation and size compared to in ApcMin/Apc+ Tg(Vil-cre)20Syr
• intestinal tumors are increased in number compared to in ApcMin/Apc+ Tg(Vil-cre)20Syr


Mouse Genome Informatics
cn23
    ApcMin/Apc+
Gpa33tm1(GNAS)Wtsi/Gpa33+
Hprttm1(CMV-cre)Brd/?

involves: 129S7/SvEvBrd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• compared with ApcMin heterozygotes


Mouse Genome Informatics
cn24
    ApcMin/Apc+
Tcf7l2tm1(EGFP/cre)Mrc/Tcf7l2tm2.1Mrc

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• mice do not exhibit develop intestinal adenomas (J:170088)


Mouse Genome Informatics
cn25
    ApcMin/Apc+
Igf2bp1tm1Vssp/Igf2bp1tm1Vssp
Tg(Vil-cre)997Gum/0

involves: C57BL/6J * SJL
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice develop reduced number of intestinal tumors compared with Apcmin heterozygotes at 90 days


Mouse Genome Informatics
cx26
    ApcMin/Apc+
Pla2g2aMom1-s/Pla2g2a+

(AKR/J x C57BL/6J-ApcMin)F1
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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 Pla2g2a from AKR/J produced by backcrossing the F1 to AKR/J produced offspring with a lower mean tumor incidence of 1.7 +/- 1.7
• mice heterozygous for Pla2g2a from C57BL/6J and AKR/J produced by backcrossing the F1 to C57BL/6J show a mean tumor incidence significantly lower than seen in mice having a C57BL/6J background but significantly higher than mice homozygous for Pla2g2a from AKR/J
• inbred srains MA/MyJ and CAST/Ei also carry the tumor suppressing allele Pla2g2a s
• inbred strains AKR/J, MA/MyJ, and CAST/Ei are homozygous for the tumor suppressing allele Pla2g2a


Mouse Genome Informatics
cx27
    ApcMin/Apc+
Brca2tm1Mbn/Brca2+

B6.Cg-Brca2tm1Mbn ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
growth/size
N
• body weight of mice at time of sacrifice does not differ significantly from Apc-heterozygous, Brca2-heterozygous, or wild-type animals (J:67445)

reproductive system
N
• only observed in 1/8 ENU-treated males, similar to wild-type males (1/9) (J:67445)
• absent in 22% of ENU-treated females (J:67445)
• remaining follicles are degenerating in ENU-treated females (J:67445)
• arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice (J:67445)
• complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females (J:67445)
• observed in ENU-treated females displaying ovarian failure (atrophy); endometrium and myometrium appear immature (J:67445)
• reduced in thickness and lined with vacuolated cells indicative of anestrus in ENU-treated females (J:67445)

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

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 (J:67445)
• no differences are observed in branching of female mammary glands among genotypes or wild-type females (J:67445)
(J:67445)
• absent in 22% of ENU-treated females (J:67445)
• remaining follicles are degenerating in ENU-treated females (J:67445)
• arrested follicular development is 6-fold more prevalent compared to ENU-treated Brca2-deficient mice (J:67445)
• complete loss of follicles (ovarian atrophy) is observed in about 25% of ENU-treated mutants, whereas almost no incidence is observed in ENU-treated wild-type or Brca2-mutant females (J:67445)

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 (J:67445)
• no differences are observed in branching of female mammary glands among genotypes or wild-type females (J:67445)
(J:67445)

Mouse Models of Human Disease
OMIM IDRef(s)
Breast Cancer 114480 J:67445


Mouse Genome Informatics
cx28
    ApcMin/Apc+
Gt(ROSA)26Sor/Gt(ROSA)26Sor+

B6.Cg-Gt(ROSA)26Sor ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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 mammary or intestinal tumors than mice carrying either ApcMin alone or C57BL/6 controls
• 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

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


Mouse Genome Informatics
cx29
    ApcMin/Apc+
Mir10atm1.1Ahl/Mir10atm1.1Ahl

B6.Cg-Mir10atm1.1Ahl Apcmin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• twice as many tumors in the small intestine as in Apcmin heterozygotes (J:205135)
• however, tumor multiplicity in male mice is the same as in Apcmin heterozygotes (J:205135)
• in the small intestine of female and male mice with increased frequency with of high-grade dysplasia and higher incidence of tubule-villous adenomas (more evident in female mice than male mice)
• however, tumor size is the same as in Apcmin heterozygotes


Mouse Genome Informatics
cx30
    ApcMin/Apc+
MthfsGt(RRK291)Byg/Mthfs+

B6.Cg-MthfsGt(RRK291)Byg ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• small intestine and colon tumor incidence is similar to mice heterozygous for ApcMin alone (J:185874)


Mouse Genome Informatics
cx31
    ApcMin/Apc+
Nos2tm1Lau/Nos2tm1Lau

B6.Cg-Nos2tm1Lau ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• polyp size reduced
• 29% of tumor incidence observed in controls
• multiplicity of tumors reduced to about 9% of control level


Mouse Genome Informatics
cx32
    ApcMin/Apc+
Nos2tm1Lau/Nos2+

B6.Cg-Nos2tm1Lau ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• polyp size reduced
• 68% of tumor incidence observed in controls
• multiplicity of tumors reduced to about 33% of control level


Mouse Genome Informatics
cx33
    ApcMin/Apc+
Pla2g4atm1Jvb/Pla2g4atm1Jvb

B6.Cg-Pla2g4atm1Jvb ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cx34
    ApcMin/Apc+
Rab25tm1Jrgo/Rab25tm1Jrgo

B6.Cg-Rab25tm1Jrgo ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype

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

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

digestive/alimentary system
• 2-fold increase in colonic polyp number compared with heterozygous Apcmin mice
• increased polyp size
• more widely distributed polyps in the colon

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


Mouse Genome Informatics
cx35
    ApcMin/Apc+
Rab25tm1Jrgo/Rab25+

B6.Cg-Rab25tm1Jrgo ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• 2-fold increase in tumor number in the middle and distal intestines compared with heterozygous Apcmin mice


Mouse Genome Informatics
cx36
    ApcMin/Apc+
Shmt1Gt(AD0236)Wtsi/Shmt1Gt(AD0236)Wtsi

B6.Cg-Shmt1Gt(AD0236)Wtsi ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• mice exhibit the same tumorigenesis as ApcMin heterozygotes (J:183477)


Mouse Genome Informatics
cx37
    ApcMin/Apc+
Tgfbr1tm1Bopa/Tgfbr1+

B6.Cg-Tgfbr1tm1Bopa ApcMin
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
cx38
    ApcMin/Apc+
Hpgdstm1Urad/Hpgds+

involves: 129 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
cx39
    ApcMin/Apc+
Hpgdstm1Urad/Hpgdstm1Urad

involves: 129 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
cx40
    ApcMin/Apctm1Tno
Ctnnb1tm4.1Wbm/Ctnnb1+

involves: 129/Sv * 129P2/OlaHsd * 129S4/SvJae * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
nervous system
N
• normal head morphology (J:156864)

craniofacial
N
• normal head morphology (J:156864)

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


Mouse Genome Informatics
cx41
    ApcMin/ApcMin
Ctnnb1tm4.1Wbm/Ctnnb1+

involves: 129/Sv * 129P2/OlaHsd * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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)


Mouse Genome Informatics
cx42
    ApcMin/Apc+
Ppardtm1Jps/Ppardtm1Jps

involves: 129/Sv * AKR/J * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cx43
    ApcMin/Apc+
Il22tm1Flv/Il22tm1Flv

involves: 129/Sv * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• decrease in tumor numbers in the small intestine and colon compared to mice heterozygous for ApcMin alone


Mouse Genome Informatics
cx44
    ApcMin/Apc+
Blmtm1Grdn/Blm+

involves: 129P2/OlaHsd * 129S/SvEv * Black Swiss * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• all colonic adenomas displayed high-grade dysplasia
• 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

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


Mouse Genome Informatics
cx45
    ApcMin/Apc+
Msh2tm1Htr/Msh2tm1Htr

involves: 129P2/OlaHsd * BALB/c * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
cx46
    ApcMin/Apc+
Foxl1tm1Khk/Foxl1tm1Khk

involves: 129P2/OlaHsd * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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 (J:95893)
• adenomatous polyps contain a large number of proliferating epithelial cells
• no evidence of invasion or metastases are observed in any tumors in the colon

digestive/alimentary system
• 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


Mouse Genome Informatics
cx47
    ApcMin/Apc+
Mom5129P2/?

involves: 129P2/OlaHsd * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• significantly reduced incidence of intestinal adenoma (around 20-25)


Mouse Genome Informatics
cx48
    ApcMin/Apc+
Mbd2tm1Bh/Mbd2tm1Bh

involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
N
• homozygotes survive significantly longer than mice only heterozygous for ApcMin (J:83087)

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


Mouse Genome Informatics
cx49
    ApcMin/Apc+
Mbd2tm1Bh/Mbd2+

involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cx50
    ApcMin/Apc+
Zbtb33tm1.1Bird/Y

involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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 (J:104155)

tumorigenesis
• tumors in doubly heterozygous mice significantly smaller at 180 days of age (J:104155)
• mice exhibit a similar number of intestinal tumors as compared to ApcMin mice (J:104155)


Mouse Genome Informatics
cx51
    ApcMin/Apc+
Phgdhtm1.1Shfu/Phgdh+

involves: 129P2/OlaHsd * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• mice exhibit the same tumorigenesis as ApcMin heterozygotes (J:183477)


Mouse Genome Informatics
cx52
    ApcMin/Apc+
Trp53tm1Mlh/Trp53tm1Mlh

involves: 129P2/OlaHsd * C57BL/6 * SWR
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• 22% of mice with abnormalities of the endocrine 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

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


Mouse Genome Informatics
cx53
    ApcMin/Apc+
Hptm1Skl/Hptm1Skl

involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• intestinal tumor burden at 60-65 days of age increased by 2-3 fold


Mouse Genome Informatics
cx54
    ApcMin/Apc+
Ptgdstm1Ohy/Ptgdstm1Ohy

involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice with Ptgds deficiency do not show altered adenoma profile compared to Apc heterozygous Ptgds-wild-type mice


Mouse Genome Informatics
cx55
    ApcMin/Apc+
Mbd4tm1Bird/Mbd4tm1Bird

involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
cx56
    ApcMin/Apc+
Ptgs2tm1Unc/Ptgs2tm1Unc

involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cx57
    ApcMin/Apc+
Ptgs1tm1Unc/Ptgs1tm1Unc

involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
N
• mice live 12 months or longer unlike ApcMin heterozygotes that die after 7 to 8 months (J:64401)

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


Mouse Genome Informatics
cx58
    ApcMin/Apc+
Ptgs1tm1Unc/Ptgs1+

involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cx59
    ApcMin/Apc+
Cd44tm1Mak/Cd44tm1Mak

involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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

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


Mouse Genome Informatics
cx60
    ApcMin/Apc+
Tcf7tm1Cle/Tcf7tm1Cle

involves: 129P2/OlaHsd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
cx61
    ApcMin/ApcMin
Rr27tm1Rohl/H19+

involves: 129S1/Sv * 129X1/SvJ * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice develop twice as many colonic adenomas as in ApcMin homozygotes
• mice develop twice as many intestinal and colonic adenomas as in ApcMin homozygotes

digestive/alimentary system
• mice have longer crypts than wild-type mice

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


Mouse Genome Informatics
cx62
    ApcMin/Apc+
Tgfbr1tm1Bopa/Tgfbr1+

involves: 129S1/SvImJ * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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 (J:143706)


Mouse Genome Informatics
cx63
    ApcMin/Apc+
Il6tm1Kopf/Il6tm1Kopf

involves: 129S2/SvPas * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
muscle
N
• no gastrocnemius muscle wasting (J:130429)

adipose tissue
N
• normal epididymal fat pads (J:130429)

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


Mouse Genome Informatics
cx64
    ApcMin/Apc+
Hdac2Gt(W035F03)Joe/Hdac2Gt(W035F03)Joe

involves: 129S2/SvPas * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
cx65
    ApcMin/Apc+
Pms2tm1Lisk/Pms2tm1Lisk

involves: 129S2/SvPas * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cx66
    ApcMin/Apc+
Esr2tm1Mma/Esr2+

involves: 129S2/SvPas * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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

cellular
• increased proliferation of cells in the colon in ovariectomized


Mouse Genome Informatics
cx67
    ApcMin/Apc+
Esr2tm1Mma/Esr2tm1Mma

involves: 129S2/SvPas * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• increased proliferation of cells in the colon
• fewer mature goblet cells in the colon with prevalent pregoblet cells
• 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


Mouse Genome Informatics
cx68
    ApcMin/Apc+
Esr1tm1.1Mma/Esr1tm1.1Mma

involves: 129S2/SvPas * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• no mice are produced


Mouse Genome Informatics
cx69
    ApcMin/Apc+
Esr1tm1.1Mma/Esr1+

involves: 129S2/SvPas * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• all mice develop invasive carcinomas in the intestine and colon unlike Apcmin heterozygotes
• 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
• 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 prevelant pregoblet cells

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

cellular
• increased proliferation of cells in the colon


Mouse Genome Informatics
cx70
    ApcMin/Apc+
Ptprhtm1.1Mato/Ptprhtm1.1Mato

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cx71
    ApcMin/Apc+
Col1a1tm1(CAG-Sirt1)Dsin/Col1a1+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice develop intestinal tumors in the duodenum and ileum

growth/size
• at 16 weeks

hematopoietic system
• at 16 weeks


Mouse Genome Informatics
cx72
    ApcMin/Apc+
Col1a1tm9(tetO-Dnmt3b_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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 exhibit increased size of microadenomas 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

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


Mouse Genome Informatics
cx73
    ApcMin/Apc+
Col1a1tm10(tetO-Dnmt3b_i3)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes (J:127808)


Mouse Genome Informatics
cx74
    ApcMin/Apc+
Col1a1tm11(tetO-Dnmt3b_i6)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes (J:127808)


Mouse Genome Informatics
cx75
    ApcMin/Apc+
Col1a1tm12(tetO-Dnmt3a_i1)Jae/Col1a1+
Gt(ROSA)26Sortm1(rtTA*M2)Jae/Gt(ROSA)26Sor+

involves: 129S4/SvJae * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• doxycycline-treated mice develop intestinal adenomas at the same rate as in Apcmin heterozygotes (J:127808)


Mouse Genome Informatics
cx76
    ApcMin/Apc+
Dnmt1tm1Pwl/Dnmt1+

involves: 129S4/SvJae * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• mice exhibit fewer intestinal polyps compared with ApcMin heterozygotes
• polyps are smaller than in ApcMin heterozygotes


Mouse Genome Informatics
cx77
    ApcMin/Apc+
Dnmt1tm1Jae/Dnmt1+

involves: 129S4/SvJae * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• mice exhibit fewer intestinal polyps compared with ApcMin heterozygotes
• polyps are smaller than in ApcMin heterozygotes


Mouse Genome Informatics
cx78
    ApcMin/Apc+
Dnmt1tm1Jae/Dnmt1tm1Pwl

involves: 129S4/SvJae * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
N
• no intestinal polyps are observed unlike in ApcMin heterozygotes (J:75230)


Mouse Genome Informatics
cx79
    ApcMin/ApcMin
Asphtm1Jed/Asphtm1Jed

involves: 129S6/SvEvTac * 129S7/SvEvBrd * C57BL/6J * C57BL/6NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
cx80
    ApcMin/Apc+
Eregtm1Dwt/Eregtm1Dwt

involves: 129S6/SvEvTac * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• the number, average size, and location of intestinal polyps is similar to ApcMin heterozygotes


Mouse Genome Informatics
cx81
    ApcMin/Apc+
Dp(17Nfkbil1-Olfr91)1Cogr/0

involves: 129S6/SvEvTac * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
N
• mice exhibit the same tumor-free survival as ApcMin heterozygotes (J:190754)


Mouse Genome Informatics
cx82
    ApcMin/Apc+
Il22ra2tm2Vlcg/Il22ra2tm2Vlcg

involves: 129S6/SvEvTac * C57BL/6J * C57BL/6NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
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


Mouse Genome Informatics
cx83
    ApcMin/Apc+
Myctm1Jlc/Myc+

involves: 129S7/SvEvBrd * C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
N
• mice exhibit a life span of 291 days compared to 169 days in ApcMin heterozygotes (J:134087)

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 (J:134087)
• expression of angiogenic factors is decreased compared to in ApcMin heterozygotes


Mouse Genome Informatics
cx84
    ApcMin/Apc+
Recql4tm1Glu/Recql4tm1Glu

involves: 129S7/SvEvBrd * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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 IDRef(s)
Rothmund-Thomson Syndrome; RTS 268400 J:97101


Mouse Genome Informatics
cx85
    ApcMin/ApcMin
Sat1tm1Alh/Y

involves: 129X1/SvJ * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• total tumor counts in small intestine were reduced by about 75% for both small and large tumors (J:99381)
• 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 (J:99381)


Mouse Genome Informatics
cx86
    ApcMin/Apc+
Mmom2129X1/SvJ/Mmom2C57BL/6J

involves: 129X1/SvJ * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females
• increased tumor latency


Mouse Genome Informatics
cx87
    ApcMin/Apc+
EgfrWa5/Egfr+

involves: BALB/cAnN * C3H/HeN * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
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


Mouse Genome Informatics
cx88
    ApcMin/Apc+
Pla2g2aMom1-r/?
PrkdcBALB/c/PrkdcBALB/c

involves: BALB/cByJ * C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice show 2-3 fold increase in adenoma incidence in the small intestine after X-irradiation


Mouse Genome Informatics
cx89
    ApcMin/Apc+
Tg(Rorc-EGFP)1Ebe/?

involves: C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
immune system
• in the mesenteric lymph node (MLN), the ratio of IL-17 producing cells to Foxp3-positive cells within the GFP-positive T cell population is significantly decreased compared to controls
• this observation is compared to an induced-colitis control where ratio of the two effector cell populations remain the same in the MLN despite inflammation occuring
• mesenteric lymph nodes are hyperplastic

digestive/alimentary system
• ileal polyps occur in these mice
• occur in these mice

hematopoietic system
• in the mesenteric lymph node (MLN), the ratio of IL-17 producing cells to Foxp3-positive cells within the GFP-positive T cell population is significantly decreased compared to controls
• this observation is compared to an induced-colitis control where ratio of the two effector cell populations remain the same in the MLN despite inflammation occuring


Mouse Genome Informatics
cx90
    ApcMin/Apc+
Mom5C57BL/6/Mom5C57BL/6

involves: C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• higher numbers of intestinal adenomas in homozygotes than in heterozygotes (around 50-55)


Mouse Genome Informatics
cx91
    ApcMin/Apc+
Rr21tm1Jta/Rr21+

involves: C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• similar frequency of intestinal polyps compared to mice heterozygous for ApcMin alone


Mouse Genome Informatics
cx92
    ApcMin/Apc+
Dclk1tm1.1(cre/ERT2)Seno/Dclk1tm1.1(cre/ERT2)Seno

involves: C57BL/6
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• Dclk1 mutant homozygotes develop polyps in similar numbers and with similar size distribution as Dclk1 wild-type, ApcMin/+ controls


Mouse Genome Informatics
cx93
    ApcMin/Apc+
Mmp7tm1Lmm/Mmp7tm1Lmm

involves: C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• average diameter of tumors is 20% smaller
• although tumor incidence is increased relative to wild-type controls, incidence is reduced in comparison to animals heterozygous for Apc but Mmp7<+/+> by 58% (from 25.4 to 10.5 tumors/animal)


Mouse Genome Informatics
cx94
    ApcMin/Apc+
Slc5a8tm1.1Boet/Slc5a8tm1.1Boet

involves: C57BL/6 * C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice develop colon tumors at the same rate as ApcMin homozygotes


Mouse Genome Informatics
cx95
    ApcMin/Apc+
Rr21tm1.1Jta/Rr21tm1.1Jta

involves: C57BL/6 * FVB/N
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• decrease in the frequency of intestinal polyps compared to mice heterozygous for ApcMin alone


Mouse Genome Informatics
cx96
    ApcMin/Apc+
Dcctm1Wbg/Dcc+

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• heterozygosity for the Dcc allele did not affect the polyp initiation or average size or morphology of the adenomas that occur in the ApcMin heterozygous mice


Mouse Genome Informatics
cx97
    ApcMin/Apc+
Thbs1tm1Hyn/Thbs1tm1Hyn

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging

tumorigenesis
• intestinal carcinoma in situ

digestive/alimentary system
• intestinal dysplasia

growth/size

hematopoietic system

skeleton


Mouse Genome Informatics
cx98
    ApcMin/Apc+
Ccnd1tm1Dsn/Ccnd1tm1Dsn

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice heterozygous for "multiple intestinal neoplasia" (F2 Min) and homozygous null for Ccnd1tm1Dsn developed significantly fewer tumors (tumor range: 1-39) than mice doubly heterozygous for Min and Ccnd1tm1Dsn (tumor range: 3-129) or mice heterozygous for Min and wild-type for Ccnd1 (tumor range: 2-112)
• no difference in tumor size was observed between the various Ccnd1 genotypes in heterozygous F2 Min mice
• also, no association was found between tumor number and animal weight


Mouse Genome Informatics
cx99
    ApcMin/ApcMin
Ppardtm1.1Rev/Ppardtm1.1Rev

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• mice harbor conspicuous intestinal polyps; average number is similar to wild-type and heterozygous mice
• there is a decrease in large diameter polyps relative to controls, while small polyp number is similar between all groups
• mice harbor conspicuous colonic polyps

tumorigenesis
• polyps are low grade noninvasive tubular adenomas


Mouse Genome Informatics
cx100
    ApcMin/Apc+
Glp2rtm1Ddr/Glp2r+

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• size similar to situation in ApcMin heterozygous mice
• number similar to situation in ApcMin heterozygous mice

digestive/alimentary system
• villus height is similar to ApcMin heterozygotes
• crypt morphology is similar to ApcMin heterozygotes
• number similar to situation in ApcMin heterozygous mice

endocrine/exocrine glands
• crypt morphology is similar to ApcMin heterozygotes


Mouse Genome Informatics
cx101
    ApcMin/Apc+
Glp2rtm1Ddr/Glp2rtm1Ddr

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
digestive/alimentary system
• villus height is similar to ApcMin heterozygotes
• crypt morphology is similar to ApcMin heterozygotes
• number similar to situation in ApcMin heterozygous mice

endocrine/exocrine glands
• crypt morphology is similar to ApcMin heterozygotes

tumorigenesis
• size similar to situation in ApcMin heterozygous mice
• number similar to situation in ApcMin heterozygous mice


Mouse Genome Informatics
cx102
    ApcMin/Apc+
Tcf7l2tm1.1(EGFP/cre)Mrc/Tcf7l2+

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice develop colorectal tubular adenomas unlike Apcmin heterozygotes


Mouse Genome Informatics
cx103
    ApcMin/Apc+
Tcf7l2tm2.2Mrc/Tcf7l2+

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice develop colorectal tubular adenomas unlike Apcmin heterozygotes


Mouse Genome Informatics
cx104
    ApcMin/Apc+
Cd44tm2Stpa/Cd44tm2Stpa

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• mice survive longer than ApcMin heterozygotes

tumorigenesis
• decreased adenoma and microadenoma compared with ApcMin heterozygotes without a change in intestinal crypt apoptosis and proliferation rates


Mouse Genome Informatics
cx105
    ApcMin/Apc+
Cd44tm1Stpa/Cd44tm2Stpa

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• mice develop the same number of intestinal adenoma and microadenoma as in ApcMin heterozygotes


Mouse Genome Informatics
cx106
    ApcMin/Apc+
Cd44tm1Mak/Cd44tm1Mak

involves: C57BL/6J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• mice survive longer than ApcMin heterozygotes

tumorigenesis
• decreased adenoma and microadenoma compared with ApcMin heterozygotes without a change in intestinal crypt apoptosis and proliferation rates

digestive/alimentary system
• compared with ApcMin heterozygotes

cellular
• compared with ApcMin heterozygotes


Mouse Genome Informatics
cx107
    ApcMin/Apc+
Cd44tm1Stpa/Cd44tm1Stpa

involves: C57BL/6J * C57BL/6JIco
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
mortality/aging
• as in ApcMin heterozygotes

tumorigenesis
• mice develop the same number of intestinal adenoma and microadenoma as in ApcMin heterozygotes


Mouse Genome Informatics
cx108
    ApcMin/Apc+
Atp5a1Mom2-C57BL/6J/Atp5a1Mom2-C57BL/6J

involves: C57BL/6J * DBA/2J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• resistance to intestinal polyps


Mouse Genome Informatics
cx109
    ApcMin/Apc+
Atp5a1Mom2-C57BL/6J/Atp5a1+

involves: C57BL/6J * DBA/2J
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• resistance to intestinal polyps


Mouse Genome Informatics
cx110
    ApcMin/Apc+
Tg(CAG-PGDS)S-55Hjl/0

involves: C57BL/6J * FVB/N
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• transgenic mice have 70-80% fewer adenomas than controls


Mouse Genome Informatics
cx111
    ApcMin/Apc+
Tg(Vil1-PPARGC1A)#Amos/0

involves: C57BL/6J * FVB/N
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• fewer intestinal tumors form
• average size of intestinal tumors is reduced
• higher apoptosis rates in intestinal tumors
• fewer intestinal tumors form than in controls
• tumors are smaller in size than in controls


Mouse Genome Informatics
cx112
    ApcMin/Apc+
Mmom1C57BL/6J/Mmom1FVB/NTac

involves: C57BL/6J * FVB/NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females


Mouse Genome Informatics
cx113
    ApcMin/Apc+
Mmom1C57BL/6J/Mmom1FVB/NTac
Mmom3C57BL/6J/Mmom3FVB/NTac

involves: C57BL/6J * FVB/NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• 50% decrease in mammary tumor number after ENU mutagenesis compared to C57BL/6J-homozygous females


Mouse Genome Informatics
cx114
    ApcMin/Apc+
Mmom2C57BL/6J/Mmom2FVB/NTac

involves: C57BL/6J * FVB/NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• 24% decrease in mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females
• increased tumor latency


Mouse Genome Informatics
cx115
    ApcMin/Apc+
Mmom2C57BL/6J/Mmom2FVB/NTac
Mmom3C57BL/6J/Mmom3FVB/NTac

involves: C57BL/6J * FVB/NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• decreased mammary tumor number after ENU treatment compared to C57BL/6J-homozygous females


Mouse Genome Informatics
cx116
    ApcMin/Apc+
Mmom2C57BL/6J/Mmom2FVB/NTac
Mmom4C57BL/6J/Mmom4FVB/NTac

involves: C57BL/6J * FVB/NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• increased tumor latency after ENU treatment compared to C57BL/6J-homozygous females


Mouse Genome Informatics
cx117
    ApcMin/Apc+
Mmom4C57BL/6J/Mmom4FVB/NTac

involves: C57BL/6J * FVB/NTac
Key:
phenotype observed in females WTSI Wellcome Trust Sanger Institute
phenotype observed in males EuPh Europhenome
N normal phenotype
tumorigenesis
• increased mammary tumor latency after ENU treatment compared to C57BL/6J-homozygous females