Analysis Tools|
Allele Symbol Allele Name Allele ID |
Tg(Fabp1-cre)1Jig transgene insertion 1, Jeffrey I Gordon MGI:2447212 |
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| Summary |
20 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• large, prominent goblet cells develop in the colon
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• mice develop widespread hyperplasia throughout the colonic epithelium
• colonic epithelium has a larger transit amplifying cell zone than wild-type; cells in the colonic epithelium have a higher mitotic index than in wild-type
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• hyperplasia is typified by extreme lengthening of the crypts
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• hyperplasia is typified by extreme lengthening of the crypts
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• large, prominent goblet cells develop in the colon
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• animals have greatly reduced life-span compared to mutants expressing wild-type Kras
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• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio
• mice have more tumors than mutants expressing wild-type Kras
• terminally differentiated cells are absent from tumors
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• adenocarcinomas show uniform high-grade dysplasia, including large, fused glands with serrated borders, pseudostratified epithelium, loss of apical-basal polarity, and high nucleus to cytoplasm ratio
• mice have more tumors than mutants expressing wild-type Kras
• terminally differentiated cells are absent from tumors
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mutants exhibit increased susceptibility to N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced bladder cancer, with 50% developing transitional cell carcinomas (TCC) and 25% developing carcinoma in situ (CIS) and dysplasia compared to 8% of wild-type mice developing TCC and 8% developing CIS and dysplasia at 16 weeks after BBN administration
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• mutants develop spontaneous superficial papillary transitional cell carcinomas, with an incidence of 10% in 40-80 week old mutants
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• mutants develop spontaneous superficial papillary transitional cell carcinomas, with an incidence of 10% in 40-80 week old mutants
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• two mutants exhibit hydronephrosis due to presence of large cancers in the bladder or renal pelvis
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• thickening of the urothelial layer by 8 weeks of age due to increases in cell number and cell size
• urothelial hyperplasia is due to increased proliferation of bladder epithelial cells
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• absolute numbers of bladder epithelial cells are increased 1.6-fold over wild-type levels at 8 weeks of age and 2.6-fold at 48 weeks of age
• size of individual bladder epithelial cells is greater than control cells; increase in size is not due to polyploidy as both diploid and tetraploid cell fractions are increased
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• mutants exhibit increased susceptibility to N-butyl-N-(4-hydroxybutyl) nitrosamine (BBN)-induced bladder cancer, with 50% developing transitional cell carcinomas (TCC) and 25% developing carcinoma in situ (CIS) and dysplasia compared to 8% of wild-type mice developing TCC and 8% developing CIS and dysplasia at 16 weeks after BBN administration
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| urinary bladder cancer | DOID:11054 |
OMIM:109800 |
J:113388 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• significantly increased tumor load in the intestine of males but not females compared to heterozygous Apctm1Ecrm
• tumors in both the ilium and colon but smaller in size than in heterozygous Apctm1Ecrm
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• significantly increased tumor load in the intestine of males but not females compared to heterozygous Apctm1Ecrm
• tumors in both the ilium and colon but smaller in size than in heterozygous Apctm1Ecrm
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• focal, pedunculated adencarcinomas develop in the colon; lesions are typically heterogeneous showing both low grade and malignant epithelium
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• focal, pedunculated adencarcinomas develop in the colon; lesions are typically heterogeneous showing both low grade and malignant epithelium
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice succumb to intestinal tumors later than Apctm1.1Ecrm
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• mice develop intestinal tumors unlike wild-type mice with later premature death and fewer tumors than Apctm1.1Ecrm heterozygotes
• intestinal tumors develop predominantly in the large intestine that are larger than in Apctm1.1Ecrm heterozygotes
• large intestine tumors are pedunculated (polypoid) or sessile
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• intestinal tumors develop predominantly in the large intestine
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• intestinal tumors develop predominantly in the large intestine
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• intestinal tumors develop predominantly in the large intestine
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• low and high grade
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• mice develop intestinal tumors unlike wild-type mice with later premature death and fewer tumors than Apctm1.1Ecrm heterozygotes
• intestinal tumors develop predominantly in the large intestine that are larger than in Apctm1.1Ecrm heterozygotes
• large intestine tumors are pedunculated (polypoid) or sessile
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• intestinal tumors develop predominantly in the large intestine
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• intestinal tumors develop predominantly in the large intestine
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• intestinal tumors develop predominantly in the large intestine
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• low and high grade
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| colorectal cancer | DOID:9256 |
OMIM:114500 |
J:159883 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• hypoxia fails to induce an increase in colonic epithelial cell resistance unlike in similarly treated wild-type cells
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• TNBS-treated mice exhibit more severe colitis, slower weight gain during recovery, decreased colon length, and increased mortality compared with similarly treated wild-type mice
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• TNBS-treated mice exhibit more severe colitis, slower weight gain during recovery, decreased colon length, and increased mortality compared with similarly treated wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• bladder urothelium exhibits increased cell proliferation
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice show moderate colon epithelium crypt hyperplasia that is intermediate between wild-type mice and conditional Krastm4Tyj mice
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• colons show an intermediate hyperproliferative phenotype compared to wild-type mice or conditional Krastm4Tyj mice
• Paneth cells are intact in colons
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• mice show moderate colon epithelium crypt hyperplasia that is intermediate between wild-type mice and conditional Krastm4Tyj mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia
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• mice show slightly longer survival than conditional mice carrying the Krastm4Tyj allele
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• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| colorectal cancer | DOID:9256 |
OMIM:114500 |
J:276349 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exposed to hypoxic conditions exhibit reduced impairment in intestinal barrier function compared with similarly treated wild-type mice
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• TNBS-treated mice do not exhibit weight loss, as severe reduction in colon length, as much mortality, or an increase in intestinal permeability unlike similarly treated wild-type mice
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• TNBS-treated mice do not exhibit weight loss, as severe reduction in colon length, as much mortality, or an increase in intestinal permeability unlike similarly treated wild-type mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice show colon epithelium crypt hyperplasia that is greater than seen in conditional Krastm1.1Khai mice
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• Paneth cells are absent in colons
• mice treated with trametinib show restoration of Paneth cell differentiation in colons
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• colons show a greater hyperproliferative phenotype than in conditional Krastm1.1Khai mice
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• mice show colon epithelium crypt hyperplasia that is greater than seen in conditional Krastm1.1Khai mice
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• Paneth cells are absent in colons
• mice treated with trametinib show restoration of Paneth cell differentiation in colons
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia
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• mice show 100% lethality before 150 days of age
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• mice develop colonic tumors, characterized as adenomas with low-grade dysplasia
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| colorectal cancer | DOID:9256 |
OMIM:114500 |
J:276349 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• only 45% of males survive to 13.5 months of age, compared to 75% of females surviving to this age
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• hyperplasia in the anterior prostate is observed at 8 days of age
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• within the first year of life, 97% of males develop tumors of the anterior prostate
• prostate tumors are carcinomas
• in males over one year of age, the tumor takes over the entire prostate and seminal vesicle
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• hyperplasia in the urinary tract
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• urothelial carcinoma of the kidney
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• urothelial carcinoma of the bladder
• 22% of mutants exhibit bladder cancer by 13.5 months of age
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• males exhibit hydronephrosis of the kidney
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• epithelial hypertrophy and nuclear atypia are evident in bladders at birth
• 100% penetrance of hypertrophy and hyperplasia in the bladder by 6 weeks of age
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• 1/3 of male deaths are due to inability to urinate due to urinary tract blockage
• females do not lose the ability to urinate
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• hyperplasia in the anterior prostate is observed at 8 days of age
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• within the first year of life, 97% of males develop tumors of the anterior prostate
• prostate tumors are carcinomas
• in males over one year of age, the tumor takes over the entire prostate and seminal vesicle
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• within the first year of life, 97% of males develop tumors of the anterior prostate
• prostate tumors are carcinomas
• in males over one year of age, the tumor takes over the entire prostate and seminal vesicle
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• metastasis of the bladder and urothelial carcinomas is observed
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• urothelial carcinoma of the bladder, ureter, and kidney
• squamous cell carcinoma of the vagina and rectum
• carcinomas of the prostate, seminal vesicles and urethra
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• urothelial carcinoma of the kidney
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• 41% of females develop vaginal squamous cell carcinoma
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• urothelial carcinoma of the bladder
• 22% of mutants exhibit bladder cancer by 13.5 months of age
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• diffuse hyperplasia and dysplasia of the colonic crypts is seen by 4 weeks of age
• increased proliferation of the hyperplastic and dysplastic colonic epithelium is seen in mutants
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• no developmental or physiological defects are detected in the distal small intestine, cecum, colon, or bladder
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• unlike mice with complete recombination of the floxed allele in the entire intestinal epithelium, mice with a mosaic pattern of recombination show no increase in mortality up to at least 1 year of age
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• the small intestine contains patches of abnormal crypts with a recombined allele mixed with areas of normal crypts with an unrecombined allele
• crypts with the recombined allele completely lack goblet, Paneth, and enteroendocrine cells instead containing only absorptive enterocytes
• a significant increase in BrdU+ cells and mitotic figures is seen in crypts with a recombined allele
• crypts with a recombined allele are smaller than neighboring crypts in which recombination did not occur
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• the adaptive response following resection of the middle 50% of the small bowel is blunted with a smaller increase in crypt depth compared to control mice
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• the small intestine contains patches of abnormal crypts with a recombined allele mixed with areas of normal crypts with an unrecombined allele
• crypts with the recombined allele completely lack goblet, Paneth, and enteroendocrine cells instead containing only absorptive enterocytes
• a significant increase in BrdU+ cells and mitotic figures is seen in crypts with a recombined allele
• crypts with a recombined allele are smaller than neighboring crypts in which recombination did not occur
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• disruption of the mucosal architecture with prominent villous distortion characterized by widening and decreased number of villi
• increase in numbers of activated CD4+ cells within their intestinal mucosa
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• prominent villous distortion characterized by widening and decreased number of villi
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• low-grade inflammatory cell infiltration with both active and chronic components is seen in the colon
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• chronic small intestinal inflammation
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• mice exhibit severe inflammatory changes in the ilea, including dense infiltration of the lamina propria by acute (polymorphonuclear), but mainly chronic (lymphocytes, macrophages), inflammatory cells
• however, no inflammation is seen in other parts of the small intestine, including the jejunum , and mice do not develop inflammatory arthritis
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• low-grade inflammatory cell infiltration with both active and chronic components is seen in the colon
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• chronic small intestinal inflammation
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• mice exhibit severe inflammatory changes in the ilea, including dense infiltration of the lamina propria by acute (polymorphonuclear), but mainly chronic (lymphocytes, macrophages), inflammatory cells
• however, no inflammation is seen in other parts of the small intestine, including the jejunum , and mice do not develop inflammatory arthritis
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| inflammatory bowel disease | DOID:0050589 |
OMIM:PS266600 |
J:204557 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• expression of mutant Nras appears to have no effect on the histology of the colonic epithelium
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Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 11/19/2024 MGI 6.24 |
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