mortality/aging
• probably after implantation but before E11 or E12
|
Allele Symbol Allele Name Allele ID |
Apctm1Rak targeted mutation 1, Raju Kucherlapati MGI:1857951 |
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Summary |
17 genotypes
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• probably after implantation but before E11 or E12
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 50% of mice have died by 13 months of age due to intestinal tumors, with the remaining mice dying by 18 months of age
|
• 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
|
• 88% incidence of polyps in the periampullar region
• 25% incidence of polyps in the gastric mucosa of mice 6-18 months of age
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• mice die prior to 16 weeks
|
• mice develop multiple gastro-intestinal tumors
|
• mice develop pyloric tumors
|
• mice develop desmoid with increased mutliplicity in males
|
• with increased multiplicity in males
|
• with increased multiplicity in males
|
• mice develop multiple gastro-intestinal tumors
|
• mice develop pyloric tumors
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• began dying around 32 weeks of age
• 70% were dead before 1 year of age
|
• 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
|
• rectal bleeding in older mice
|
• 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
|
• 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 |
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 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
|
• 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
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• Background Sensitivity: all mice have died by 8 months of age due to complications arising from intestinal tumors
|
• 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
|
• 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
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• Background Sensitivity: all mice have died by 3 months of age due to complications arising from intestinal tumors
|
• Background Sensitivity: numerous microadenomas in the upper gastrointestinal tract are present upon microscopic inspection
|
• Background Sensitivity: numerous microadenomas in the upper gastrointestinal tract are present upon microscopic inspection
|
• 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: found in moribund mice
|
• Background Sensitivity: found in moribund mice
|
• Background Sensitivity: found in moribund mice
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• mortality at 2-3 months of age
|
• average of 81 tumors/mouse
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• mice exhibit increased intestinal polyp formation with microsatellite instability compared with Apctm1Rak heterozygotes
• however, morphology of polyps is the same as in Apctm1Rak heterozygotes
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• all mice die by 4 months of age
|
• 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)
|
• 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
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
Lynch syndrome | DOID:3883 |
OMIM:PS120435 |
J:53451 |
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• decreased number of aggressive fibromatosis tumors formed relative to Apctm1Rak heterozygotes
• the number of gastrointestinal polyps was not altered relative to Apctm1Rak heterozygotes
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• all mice die by 14 months of age
|
• 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
|
• 77% of mice develop gastrointestinal tract tumors
• mice exhibit a 7-fold increase in gastrointestinal tumors compared to Mlh1tm1Rak heterozygotes
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 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
|
• all mice have tumors whereas 21.4% of heterozygous Apctm1Rak controls are tumor free
• tumor apoptosis rate in adenomas is reduced
|
• 100% have adenocarcenomas
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• anterior truncation
|
• severe reduction in the telencephalic region of the brain
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 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
|
• 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
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• 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
|
• mice tumors have more CG to TA transition mutations in the Apc gene than in Apctm1Rak heterozygotes
|
• 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
|
|
|
♀ | phenotype observed in females |
♂ | phenotype observed in males |
N | normal phenotype |
• median survival of 9 months as compared to 13 months for Apctm1Rak single heterozygotes
|
• 100% develop gastrointestinal tumors by 1 year of age
|
• incidence of malignant tumors is higher than in Apctm1Rak single heterozygotes
|
• extensive microsatellite instability in tumor DNA
|
• 100% develop gastrointestinal tumors by 1 year of age
|
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
||
Citing These Resources Funding Information Warranty Disclaimer, Privacy Notice, Licensing, & Copyright Send questions and comments to User Support. |
last database update 12/10/2024 MGI 6.24 |
|
|