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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Apctm1Mmt
targeted mutation 1, Makoto M Taketo
MGI:1857957
Summary 11 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Apctm1Mmt/Apctm1Mmt involves: 129S2/SvPas * C57BL/6J MGI:2175906
ht2
Apctm1Mmt/Apc+ involves: 129S2/SvPas * C57BL/6J MGI:2175907
cn3
Tle5tm1.1Mmt/Tle5tm1.1Mmt
Apctm1Mmt/Apc+
Tg(Vil1-cre/ERT2)23Syr/0
involves: 129S2/SvPas * C57BL/6 * DBA * SJL MGI:4888016
cx4
Cdx2tm1Mmt/Cdx2+
Apctm1Mmt/Apc+
B6.129-Cdx2tm1Mmt Apctm1Mmt MGI:3715020
cx5
Apctm1Mmt/Apc+
Mmp7tm1Lmm/Mmp7tm1Lmm
Smad4tm1Mmt/Smad4+
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ MGI:4365607
cx6
Apctm1Mmt/Apc+
Smad2tm2Kato/Smad2+
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J MGI:3790616
cx7
Apctm1Mmt/Apc+
Smad2tm1Kato/Smad2+
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J MGI:3790617
cx8
Apctm1Mmt/Apc+
Ptgs2tm1Jed/Ptgs2+
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3603949
cx9
Apctm1Mmt/Apc+
Ptgs2tm1Jed/Ptgs2tm1Jed
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J MGI:3603950
cx10
Apctm1Mmt/Apc+
Smad4tm1Mmt/Smad4+
involves: 129S2/SvPas * C57BL/6 MGI:2182802
cx11
Apctm1Mmt/Apc+
Nkd1tm1Tko/Nkd1tm1Tko
involves: 129X1/SvJ MGI:3531415


Genotype
MGI:2175906
hm1
Allelic
Composition
Apctm1Mmt/Apctm1Mmt
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most homozygous embryos die in utero prior to day 8 of gestation




Genotype
MGI:2175907
ht2
Allelic
Composition
Apctm1Mmt/Apc+
Genetic
Background
involves: 129S2/SvPas * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Nascent intestinal polyps in Apctm1Mmt/Apc+ mice

neoplasm
• intestinal polyps are polyploid, papillary, or sessile adenoma; every polyp consists of a microadenoma covered with a normal layer of villous epithelium (J:25200)
• increase in incidence follows loss of normal Apc allele in nascent polyps (J:25200)
• numerous intestinal tumors develop in homozygotes (J:79668)
• most tumors are small; one animal developed a tumor >6 mm in diameter (J:79668)

digestive/alimentary system
• multiple polyps develop soon after birth; all heterozygotes develop polyps by 7 weeks of age and numbers increase with age
• polyps are found from duodenum to rectum, mainly in small intestine
• intestinal polyps are polyploid, papillary, or sessile adenoma; every polyp consists of a microadenoma covered with a normal layer of villous epithelium (J:25200)
• increase in incidence follows loss of normal Apc allele in nascent polyps (J:25200)
• numerous intestinal tumors develop in homozygotes (J:79668)
• most tumors are small; one animal developed a tumor >6 mm in diameter (J:79668)

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




Genotype
MGI:4888016
cn3
Allelic
Composition
Tle5tm1.1Mmt/Tle5tm1.1Mmt
Apctm1Mmt/Apc+
Tg(Vil1-cre/ERT2)23Syr/0
Genetic
Background
involves: 129S2/SvPas * C57BL/6 * DBA * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
Tg(Vil1-cre/ERT2)23Syr mutation (1 available)
Tle5tm1.1Mmt mutation (0 available); any Tle5 mutation (19 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• adenocarcinomas by histopathological definition
• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apctm1Mmt adenomas, without a very malignant appearance
• adenocarcinomas by histopathological definition
• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apctm1Mmt adenomas, without a very malignant appearance
• treated with 4-hydroxytamoxifen to activate Cre recombinase at 3 weeks of age
• tumor invasion and intravasation into the smooth muscle layer of the small intestine and colon at 17 weeks of age
• in polyps larger than 2 mm in diameter, about half of them is found invading into the submucosa or beyond
• often seen inside vessels that are distended, reminiscent of tumor embolism

digestive/alimentary system
• adenocarcinomas by histopathological definition
• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apctm1Mmt adenomas, without a very malignant appearance
• adenocarcinomas by histopathological definition
• the extent of cellular atypia and epithelial architecture are rather similar to those in the Apctm1Mmt adenomas, without a very malignant appearance




Genotype
MGI:3715020
cx4
Allelic
Composition
Cdx2tm1Mmt/Cdx2+
Apctm1Mmt/Apc+
Genetic
Background
B6.129-Cdx2tm1Mmt Apctm1Mmt
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
Cdx2tm1Mmt mutation (0 available); any Cdx2 mutation (22 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• increased anaphase bridge index
• accelerated transition from G1 to S phase
• increased DNA synthesis
• lower apoptotic rates
• increased in numbers relative to Apctm1Mmt
• mostly in the distal colon
• decreased anaphase bridge index
• decreased transition from G1 to S phase
• decreased DNA synthesis
• increased apoptotic rates
• significantly reduced number of polyps relative to Apctm1Mmt

cellular
• increased anaphase bridge index in the large intestine and decreased in the small intestine
• accelerated transition from G1 to S phase in the large intestine and decreased in the small intestine
• increased DNA synthesis in the large intestine and decreased in the small intestine
• lower apoptotic rates in the large intestine
• in the small intestine




Genotype
MGI:4365607
cx5
Allelic
Composition
Apctm1Mmt/Apc+
Mmp7tm1Lmm/Mmp7tm1Lmm
Smad4tm1Mmt/Smad4+
Genetic
Background
involves: 129S1/Sv * 129S2/SvPas * 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
Mmp7tm1Lmm mutation (1 available); any Mmp7 mutation (21 available)
Smad4tm1Mmt mutation (0 available); any Smad4 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice exhibit a decrease in tumors size compared to in Apctm1Mmt Smad4tm1Mmt homozygotes
• the ratio of small tumors is increased compared to in Apctm1Mmt Smad4tm1Mmt homozygotes
• however, mice exhibit the same tumor invasion depth and number of fibroblasts in tumor stroma as in Apctm1Mmt Smad4tm1Mmt homozygotes
• mice develop 50% fewer tumors than in Apctm1Mmt Smad4tm1Mmt homozygotes




Genotype
MGI:3790616
cx6
Allelic
Composition
Apctm1Mmt/Apc+
Smad2tm2Kato/Smad2+
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
Smad2tm2Kato mutation (0 available); any Smad2 mutation (50 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• a small number of mice die suddenly, before thirty weeks of age, as result of lethal intestinal obstruction by large tumorous polyps

neoplasm
• numerous intestinal tumors develop in homozygotes: compound mutants have more intestinal tumors >4 mm in diameter than Apctm1Mmt heterozygotes
• frequently one or two tumors >6 mm in diameter develop
• 10-15% of intestinal polyps exhibit stromal and vascular invasion
• tubular adenomas vary in size and shape, and solid colonies of poorly differentiated carcinoma cells are sometimes observed
• nuclei display more hyperchromaticity than those in tumors in Apc single heterozygotes; nuclear atypia in tumors is enhanced indicating increased malignancy

digestive/alimentary system
• numerous intestinal tumors develop in homozygotes: compound mutants have more intestinal tumors >4 mm in diameter than Apctm1Mmt heterozygotes
• frequently one or two tumors >6 mm in diameter develop
• 10-15% of intestinal polyps exhibit stromal and vascular invasion
• tubular adenomas vary in size and shape, and solid colonies of poorly differentiated carcinoma cells are sometimes observed
• nuclei display more hyperchromaticity than those in tumors in Apc single heterozygotes; nuclear atypia in tumors is enhanced indicating increased malignancy




Genotype
MGI:3790617
cx7
Allelic
Composition
Apctm1Mmt/Apc+
Smad2tm1Kato/Smad2+
Genetic
Background
involves: 129S2/SvPas * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
Smad2tm1Kato mutation (0 available); any Smad2 mutation (50 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• a small number of mice die suddenly, before thirty weeks of age, as result of lethal intestinal obstruction by large tumorous polyps

neoplasm
• numerous intestinal tumors develop in homozygotes: compound mutants have more intestinal tumors >4 mm in diameter than Apctm1Mmt heterozygotes
• frequently one or two tumors >6 mm in diameter develop
• 10-15% of intestinal polyps exhibit stromal and vascular invasion
• tubular adenomas vary in size and shape, and solid colonies of poorly differentiated carcinoma cells are sometimes observed
• nuclei display more hyperchromaticity than those in tumors in Apc single heterozygotes; nuclear atypia in tumors is enhanced indicating increased malignancy

digestive/alimentary system
• numerous intestinal tumors develop in homozygotes: compound mutants have more intestinal tumors >4 mm in diameter than Apctm1Mmt heterozygotes
• frequently one or two tumors >6 mm in diameter develop
• 10-15% of intestinal polyps exhibit stromal and vascular invasion
• tubular adenomas vary in size and shape, and solid colonies of poorly differentiated carcinoma cells are sometimes observed
• nuclei display more hyperchromaticity than those in tumors in Apc single heterozygotes; nuclear atypia in tumors is enhanced indicating increased malignancy




Genotype
MGI:3603949
cx8
Allelic
Composition
Apctm1Mmt/Apc+
Ptgs2tm1Jed/Ptgs2+
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (72 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• at 10 weeks, double heterozygotes develop only ~34% of the polyp number detected in the intestinal tracts of mice heterozygous for Apctm1Mmt alone
• at 10 weeks, double heterozygotes exhibit only 1.5 1.9 colonic polyps versus 6.8 7.2 detected in mice heterozygous for Apctm1Mmt alone




Genotype
MGI:3603950
cx9
Allelic
Composition
Apctm1Mmt/Apc+
Ptgs2tm1Jed/Ptgs2tm1Jed
Genetic
Background
involves: 129S2/SvPas * 129S7/SvEvBrd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
Ptgs2tm1Jed mutation (1 available); any Ptgs2 mutation (72 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• at 10 weeks, these mutants develop only ~14% of the polyp number detected in the intestinal tracts of mice heterozygous for Apctm1Mmt alone
• the size of intestinal polyps is significantly smaller (<1.0 mm) than that observed in mice heterozygous for Apctm1Mmt alone, with no polyps larger than 2.0 mm in diameter
• histologically, well-developed polyps are not covered with the normal intestinal epithelium and appear flatter than polyps found in Apctm1Mmt heterozygous controls
• notably, no colonic polyps are observed




Genotype
MGI:2182802
cx10
Allelic
Composition
Apctm1Mmt/Apc+
Smad4tm1Mmt/Smad4+
Genetic
Background
involves: 129S2/SvPas * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
Smad4tm1Mmt mutation (0 available); any Smad4 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• most mutants become moribund before 14-20 weeks and often die of intussusception of the small intestine

neoplasm
• polyps in small and large intestine develop into malignant adenocarcinomas, beginning at about 14 weeks
• adenocarcinomas found in ampullary region of the pancreatic duct, incomplete penetrance

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

endocrine/exocrine glands
• adenocarcinomas found in ampullary region of the pancreatic duct, incomplete penetrance

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

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

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




Genotype
MGI:3531415
cx11
Allelic
Composition
Apctm1Mmt/Apc+
Nkd1tm1Tko/Nkd1tm1Tko
Genetic
Background
involves: 129X1/SvJ
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Mmt mutation (0 available); any Apc mutation (154 available)
Nkd1tm1Tko mutation (0 available); any Nkd1 mutation (17 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• the number and size distribution of small intestinal polyps is not different from mice heterozygous for Apctm1Mmt alone





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last database update
03/12/2024
MGI 6.23
The Jackson Laboratory