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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Apctm1Rak
targeted mutation 1, Raju Kucherlapati
MGI:1857951
Summary 17 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Apctm1Rak/Apctm1Rak involves: 129P2/OlaHsd * C57BL/6 MGI:2175908
ht2
Apctm1Rak/Apc+ B6.129P2-Apctm1Rak MGI:3766127
ht3
Apctm1Rak/Apc+ (C57BL/6J x 129P2/OlaHsd)F1 MGI:4360687
ht4
Apctm1Rak/Apc+ involves: 129P2/OlaHsd * C57BL/6 MGI:2175909
ht5
Apctm1Rak/Apc+ involves: 129P2/OlaHsd * C57BL/6J MGI:3830621
cx6
Apctm1Rak/Apc+
Smad4E6sad/Smad4+
B6.129P2-Apctm1Rak +/+ Smad4E6sad MGI:3766126
cx7
Apctm1Rak/Apc+
Smad4E6sad/Smad4+
B6.129P2-Apctm1Rak Smad4E6sad/+ + MGI:3766123
cx8
Apctm1Rak/Apc+
Msh2tm1Rak/Msh2tm1Rak
involves: 129P2/OlaHsd MGI:4355516
cx9
Apctm1Rak/Apc+
Pms2tm1.1Sks/Pms2tm1.1Sks
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J MGI:6764552
cx10
Apctm1Rak/Apc+
Mlh1tm1Rak/Mlh1tm1Rak
involves: 129P2/OlaHsd * C57BL/6 MGI:4412021
cx11
Apctm1Rak/Apc+
Hmmrtm1Baa/Hmmrtm1Baa
involves: 129P2/OlaHsd * C57BL/6 MGI:2682909
cx12
Apctm1Rak/Apc+
Mlh1tm1Rak/Mlh1+
involves: 129P2/OlaHsd * C57BL/6 MGI:4412022
cx13
Apctm1Rak/Apc+
Dcctm1.1Mehl/Dcctm1.1Mehl
involves: 129P2/OlaHsd * C57BL/6 MGI:5312326
cx14
Apctm1Rak/Apc+
Ctnnb1tm1.2Wvv/Ctnnb1+
involves: 129P2/OlaHsd * C57BL/6J MGI:5430610
cx15
Apctm1Rak/Apc+
Cdh1tm1Cbm/Cdh1+
involves: 129P2/OlaHsd * C57BL/6J MGI:3830619
cx16
Apctm1Rak/Apc+
Mbd4tm1Wed/Mbd4tm1Wed
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * SJL MGI:3719440
cx17
Fen1tm1Rak/Fen1+
Apctm1Rak/Apc+
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * SJL/J MGI:3843881


Genotype
MGI:2175908
hm1
Allelic
Composition
Apctm1Rak/Apctm1Rak
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• probably after implantation but before E11 or E12




Genotype
MGI:3766127
ht2
Allelic
Composition
Apctm1Rak/Apc+
Genetic
Background
B6.129P2-Apctm1Rak
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• 50% of mice have died by 13 months of age due to intestinal tumors, with the remaining mice dying by 18 months of age

digestive/alimentary system
• 100% incidence of low to high dysplastic polyps in 6-18 months of age
• 19% incidence of low to high dysplastic polyps in 6-18 months of age
• 25% incidence of polyps in the gastric mucosa of mice 6-18 months of age
• 88% incidence of polyps in the periampullar region




Genotype
MGI:4360687
ht3
Allelic
Composition
Apctm1Rak/Apc+
Genetic
Background
(C57BL/6J x 129P2/OlaHsd)F1
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mice die prior to 16 weeks

neoplasm
• mice develop multiple gastro-intestinal tumors
• mice develop pyloric tumors
• mice develop desmoid with increased mutliplicity in males

integument
• with increased multiplicity in males

growth/size/body
• with increased multiplicity in males

digestive/alimentary system
• mice develop multiple gastro-intestinal tumors
• mice develop pyloric tumors




Genotype
MGI:2175909
ht4
Allelic
Composition
Apctm1Rak/Apc+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Neoplastic lesions in an Apctm1Rak/Apc+ mouse

mortality/aging
• began dying around 32 weeks of age
• 70% were dead before 1 year of age

neoplasm
• found in the colon and in the duodenum and jejunum of the small intestine
• moderately to highly differentiated with infiltration into the muscularis mucosa, submucosa, or inner layer of the muscularis
• intestinal tumors were polypoid hyperplastic lesions
• benign villous or tubulovillous adenomas
• focal lesions of the glandular epithelium of the liver seen at 1 year of age

cardiovascular system
• rectal bleeding in older mice

digestive/alimentary system
• rectal bleeding in older mice
• found in the colon and in the duodenum and jejunum of the small intestine
• moderately to highly differentiated with infiltration into the muscularis mucosa, submucosa, or inner layer of the muscularis
• intestinal tumors were polypoid hyperplastic lesions
• benign villous or tubulovillous adenomas

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

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




Genotype
MGI:3830621
ht5
Allelic
Composition
Apctm1Rak/Apc+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop an average of 1.24 tumors per animal in the small intestine unlike wild-type mice
• mice develop fewer tumors than in Apctm1Rak Cdh1tm1Cbm heterozygotes
• tumors are invasive although no metastasis is detected
• mice develop fewer gastric tumors than in Apctm1Rak Cdh1tm1Cbm heterozygotes
• unlike wild-type mice, gastric tumors develop

digestive/alimentary system
• mice develop an average of 1.24 tumors per animal in the small intestine unlike wild-type mice
• mice develop fewer tumors than in Apctm1Rak Cdh1tm1Cbm heterozygotes
• tumors are invasive although no metastasis is detected
• mice develop fewer gastric tumors than in Apctm1Rak Cdh1tm1Cbm heterozygotes
• unlike wild-type mice, gastric tumors develop




Genotype
MGI:3766126
cx6
Allelic
Composition
Apctm1Rak/Apc+
Smad4E6sad/Smad4+
Genetic
Background
B6.129P2-Apctm1Rak +/+ Smad4E6sad
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Smad4E6sad mutation (0 available); any Smad4 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• Background Sensitivity: all mice have died by 8 months of age due to complications arising from intestinal tumors

digestive/alimentary system
• Background Sensitivity: in 100% of mice by 7 months of age
• Background Sensitivity: in two of seven mice, adenocarcinomas with invasion of the muscolaris mucosa are observed
• Background Sensitivity: by 7 months of age, mice present with an average of 20 tumors along the intestinal tract
• Background Sensitivity: tumors are mainly villous or tubulovillous adenomas with foci of severe dysplasia

neoplasm
• Background Sensitivity: in two of seven mice, adenocarcinomas with invasion of the muscolaris mucosa are observed
• Background Sensitivity: by 7 months of age, mice present with an average of 20 tumors along the intestinal tract
• Background Sensitivity: tumors are mainly villous or tubulovillous adenomas with foci of severe dysplasia




Genotype
MGI:3766123
cx7
Allelic
Composition
Apctm1Rak/Apc+
Smad4E6sad/Smad4+
Genetic
Background
B6.129P2-Apctm1Rak Smad4E6sad/+ +
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Smad4E6sad mutation (0 available); any Smad4 mutation (43 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• Background Sensitivity: all mice have died by 3 months of age due to complications arising from intestinal tumors

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

digestive/alimentary system
• Background Sensitivity: an average of 60 tumors per mouse by 6 weeks of age
• Background Sensitivity: polyps are either sessile or villous with mild to severe dysplasia
• Background Sensitivity: found in 25% of 3-6 week old mice
• Background Sensitivity: numerous microadenomas in the upper gastrointestinal tract are present upon microscopic inspection

hematopoietic system
• Background Sensitivity: found in moribund mice
• Background Sensitivity: moribund mice have frank anemia

immune system
• Background Sensitivity: found in moribund mice

growth/size/body
• Background Sensitivity: found in moribund mice




Genotype
MGI:4355516
cx8
Allelic
Composition
Apctm1Rak/Apc+
Msh2tm1Rak/Msh2tm1Rak
Genetic
Background
involves: 129P2/OlaHsd
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Msh2tm1Rak mutation (1 available); any Msh2 mutation (95 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• mortality at 2-3 months of age

neoplasm
• average of 81 tumors/mouse




Genotype
MGI:6764552
cx9
Allelic
Composition
Apctm1Rak/Apc+
Pms2tm1.1Sks/Pms2tm1.1Sks
Genetic
Background
involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Pms2tm1.1Sks mutation (0 available); any Pms2 mutation (50 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
digestive/alimentary system
• mice exhibit increased intestinal polyp formation with microsatellite instability compared with Apctm1Rak heterozygotes
• however, morphology of polyps is the same as in Apctm1Rak heterozygotes




Genotype
MGI:4412021
cx10
Allelic
Composition
Apctm1Rak/Apc+
Mlh1tm1Rak/Mlh1tm1Rak
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Mlh1tm1Rak mutation (1 available); any Mlh1 mutation (42 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die by 4 months of age

neoplasm
• all mice develop tumors at an average age of 3.3 months
• all mice develop gastrointestinal tract tumors and 9% develop non-gastrointestinal tract tumors
• all mice develop gastrointestinal tract tumors
• mice exhibit a 30-fold increase in gastrointestinal tumors compared to Mlh1tm1Rak homozygotes
• mice exhibit a 4- to 5-fold increase in stomach and colon tumors, and a 25- to 100-fold increase in duodenum, jejunum, and ileum compared to in homozygous mice
• one mouse develops skin carcinoma with lung metastasis
• 34% of mice develop microadenomas and 36% adenomas
• non-Hodgkin's lymphoma in two mice
• mice develop gastrointestinal adenocarcinomas, early invasive carcinomas (in 13% of mice), and carcinomas (in 17% of mice)

digestive/alimentary system
• all mice develop gastrointestinal tract tumors
• mice exhibit a 30-fold increase in gastrointestinal tumors compared to Mlh1tm1Rak homozygotes
• mice exhibit a 4- to 5-fold increase in stomach and colon tumors, and a 25- to 100-fold increase in duodenum, jejunum, and ileum compared to in homozygous mice
• at 2 to 4 weeks of age

integument
• one mouse develops skin carcinoma with lung metastasis

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




Genotype
MGI:2682909
cx11
Allelic
Composition
Apctm1Rak/Apc+
Hmmrtm1Baa/Hmmrtm1Baa
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Hmmrtm1Baa mutation (0 available); any Hmmr mutation (47 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• decreased number of aggressive fibromatosis tumors formed relative to Apctm1Rak heterozygotes
• the number of gastrointestinal polyps was not altered relative to Apctm1Rak heterozygotes




Genotype
MGI:4412022
cx12
Allelic
Composition
Apctm1Rak/Apc+
Mlh1tm1Rak/Mlh1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Mlh1tm1Rak mutation (1 available); any Mlh1 mutation (42 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• all mice die by 14 months of age

neoplasm
• 85% of mice develop tumors at an average age of 9.4 months
• 77% of mice develop gastrointestinal tract tumors and 23% of mice develop extra-gastrointestinal tract tumors
• 77% of mice develop gastrointestinal tract tumors
• mice exhibit a 7-fold increase in gastrointestinal tumors compared to Mlh1tm1Rak heterozygotes

digestive/alimentary system
• mice exhibit a 7-fold increase in gastrointestinal tumors compared to Mlh1tm1Rak heterozygotes
• 77% of mice develop gastrointestinal tract tumors




Genotype
MGI:5312326
cx13
Allelic
Composition
Apctm1Rak/Apc+
Dcctm1.1Mehl/Dcctm1.1Mehl
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Dcctm1.1Mehl mutation (0 available); any Dcc mutation (76 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• all mice have tumors whereas 21.4% of heterozygous Apctm1Rak controls are tumor free
• tumor apoptosis rate in adenomas is reduced
• 100% have adenocarcenomas
• 45.5% of tumors involve serosal invasion compared to 8% in controls
• micrometastatic lesions are found in the liver when serosal invasion occurs

digestive/alimentary system
• all mice have tumors whereas 21.4% of heterozygous Apctm1Rak controls are tumor free
• tumor apoptosis rate in adenomas is reduced
• 100% have adenocarcenomas




Genotype
MGI:5430610
cx14
Allelic
Composition
Apctm1Rak/Apc+
Ctnnb1tm1.2Wvv/Ctnnb1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Ctnnb1tm1.2Wvv mutation (0 available); any Ctnnb1 mutation (49 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging

embryo
• anterior truncation

nervous system
• severe reduction in the telencephalic region of the brain




Genotype
MGI:3830619
cx15
Allelic
Composition
Apctm1Rak/Apc+
Cdh1tm1Cbm/Cdh1+
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Cdh1tm1Cbm mutation (0 available); any Cdh1 mutation (171 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
neoplasm
• mice develop an average of 11.3 tumors per animal in the small intestine unlike wild-type mice
• mice develop more tumors than in Apctm1Rak heterozygotes with tumor size the same as in Apctm1Rak heterozygotes
• tumors are invasive although no metastasis is detected
• 5-fold more mice develop gastric cancer compared to in Apctm1Rak heterozygotes

digestive/alimentary system
• mice develop an average of 11.3 tumors per animal in the small intestine unlike wild-type mice
• mice develop more tumors than in Apctm1Rak heterozygotes with tumor size the same as in Apctm1Rak heterozygotes
• tumors are invasive although no metastasis is detected
• 5-fold more mice develop gastric cancer compared to in Apctm1Rak heterozygotes




Genotype
MGI:3719440
cx16
Allelic
Composition
Apctm1Rak/Apc+
Mbd4tm1Wed/Mbd4tm1Wed
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Mbd4tm1Wed mutation (1 available); any Mbd4 mutation (31 available)
phenotype observed in females
phenotype observed in males
N normal phenotype

Microadenoma in Mbd4tm1Wed/Mbd4tm1Wed Apctm1Rak/Apc+ gastrointestinal tract

neoplasm
• the multiplicity of gastro-intestinal tumors is increased 2.4 times relative to Apctm1Rak heterozygotes
• mice have greater number of tumors in the jejunum and ileum than in Apctm1Rak heterozygotes
• mice have 10-fold increase in microadenomas compared to Apctm1Rak heterozygotes
• tumor progression is accelerated relative to Apctm1Rak heterozygotes

cellular
• mice tumors have more CG to TA transition mutations in the Apc gene than in Apctm1Rak heterozygotes

digestive/alimentary system
• the multiplicity of gastro-intestinal tumors is increased 2.4 times relative to Apctm1Rak heterozygotes
• mice have greater number of tumors in the jejunum and ileum than in Apctm1Rak heterozygotes
• mice have 10-fold increase in microadenomas compared to Apctm1Rak heterozygotes
• tumor progression is accelerated relative to Apctm1Rak heterozygotes




Genotype
MGI:3843881
cx17
Allelic
Composition
Fen1tm1Rak/Fen1+
Apctm1Rak/Apc+
Genetic
Background
involves: 129/Sv * 129P2/OlaHsd * C57BL/6 * SJL/J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Apctm1Rak mutation (1 available); any Apc mutation (154 available)
Fen1tm1Rak mutation (1 available); any Fen1 mutation (30 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
mortality/aging
• median survival of 9 months as compared to 13 months for Apctm1Rak single heterozygotes

neoplasm
• 100% develop gastrointestinal tumors by 1 year of age
• incidence of malignant tumors is higher than in Apctm1Rak single heterozygotes

cellular
• extensive microsatellite instability in tumor DNA

digestive/alimentary system
• 100% develop gastrointestinal tumors by 1 year of age





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last database update
03/19/2024
MGI 6.23
The Jackson Laboratory