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Allele Symbol Allele Name Allele ID |
Trp53tm3Tyj targeted mutation 3, Tyler Jacks MGI:3039265 |
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| Summary |
14 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• ovarian surface epithelium cells transfected with a cre-expressing adenovirus exhibit very limited proliferation potential and undergo senescence sooner than control cells that become immortalized
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• ovarian surface epithelium cells transfected with a cre-expressing adenovirus exhibit reduced invasion compared with similarly treated cells from Trp53tm1Brn/Trp53tm3Tyj mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• skin tumors develop between 200 and 300 days
• whether spontaneous or induced, mice develop epithelial, proliferative lesions forming a continuum from nonneoplastic squamous keratosis and acanthosis to squamous cell papillomas, actinic keratosis and keratoacanthoma with increasing degrees of atypia and dysplasia, carcinoma in situ, up to invasive squamous cell carcinoma
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• developed in one mouse
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• fewer CASP3+ cells area found following UVB treatment when compared to wild-type mice
• the reduction in apoptotic cells is slightly greater in homozygotes than in heterozygotes
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• skin tumors develop between 200 and 300 days
• whether spontaneous or induced, mice develop epithelial, proliferative lesions forming a continuum from nonneoplastic squamous keratosis and acanthosis to squamous cell papillomas, actinic keratosis and keratoacanthoma with increasing degrees of atypia and dysplasia, carcinoma in situ, up to invasive squamous cell carcinoma
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• about 18% of assessable tumor cases develop an acinar-cell carcinoma component of pancreatic tumors
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• high penetrance (29 of 30 mutants) of pancreatic ductal adenocarcinomas
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• average survival time is 84 days, with a range of 48-110 days
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• about 18% of assessable tumor cases develop an acinar-cell carcinoma component of pancreatic tumors
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• high penetrance (29 of 30 mutants) of pancreatic ductal adenocarcinomas
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic carcinoma | DOID:4905 |
OMIM:260350 |
J:166678 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• pancreatic insufficiency is occasionally observed in mutants
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• pancreatic insufficiency is occasionally observed in mutants
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• premature death before 600 days of age due to lymphoid malignancies and sarcomas
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• mutants develop lymphoid malignancies
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 308 days compared with 380 days in Trp53tm3Tyj Waptm1(cre)Arge double heterozygotes
• however, latency is similar to in Brca1tm2.1Cxd/Brca1tm2.1Cxd Trp53tm3Tyj/Trp53+ Waptm1(cre)Arge/Wap+
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• compared with Brca1tm2.1Cxd/Brca1tm2.1Cxd Trp53tm3Tyj/Trp53tm3Tyj Waptm1(cre)Arge/Waptm1(cre)Arge
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 308 days compared with 380 days in Trp53tm3Tyj Waptm1(cre)Arge double heterozygotes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• following cre-adenovirus treatment, all mice develop primary lung tumors that are shifted towards more lower grade tumor types
• following cre-adenovirus treatment, tumors occupy 36% of lung space
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• following cre-adenovirus treatment, all mice develop primary lung tumors that are shifted towards more lower grade tumor types
• following cre-adenovirus treatment, tumors occupy 36% of lung space
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• seen in older males
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• tumor formation is more prevalent and starts earlier in males compared to females
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• preneoplastic nodules are first detected at about 160 days of age in males
• liver nodules in quadruple transgenic mice are larger and more numerous compared to triple transgenic mice that are wild-type at the Trp53 locus
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• seen in older males
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• tumor formation is more prevalent and starts earlier in males compared to females
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 24 of 30 mutants develop pancreatic ductal adenocarcinomas
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• average survival time is 168 days, with a range of 60-254 days
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• 24 of 30 mutants develop pancreatic ductal adenocarcinomas
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 7 of 8 mice develop one or more tumors of the mammary gland after the first pregnancy
• mean latency time for spontaneous mammary tumor development is 19.7 +/- 8.6 weeks
• mammary tumors of both untreated and DMBA-treated mice are heterogeneous, including frequent adenocarcinomas, solid carcinomas, papillary carcinomas, and adenosquamous carcinomas, carcinosarcomas and sarcomas
• 67% of mammary tumors from untreated and DMBA-treated mice are estrogen receptor alpha-positive
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• 40% of females exposed to DMBA for 6 weeks develop mammary tumors, with a mean latency time of 8.5 +/- 4.7 weeks
• females exposed to DMBA also develop lymphomas, ovary, lung, stomach, uterus and skin tumors
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• some mice develop an additional lymphoma
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• some mice develop an additional sarcoma in the abdomen
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• some mice develop an additional tumor of the lung
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• premature death, with only 2 of 11 mice surviving past 78 weeks
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• 7 of 8 mice develop one or more tumors of the mammary gland after the first pregnancy
• mean latency time for spontaneous mammary tumor development is 19.7 +/- 8.6 weeks
• mammary tumors of both untreated and DMBA-treated mice are heterogeneous, including frequent adenocarcinomas, solid carcinomas, papillary carcinomas, and adenosquamous carcinomas, carcinosarcomas and sarcomas
• 67% of mammary tumors from untreated and DMBA-treated mice are estrogen receptor alpha-positive
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• 40% of females exposed to DMBA for 6 weeks develop mammary tumors, with a mean latency time of 8.5 +/- 4.7 weeks
• females exposed to DMBA also develop lymphomas, ovary, lung, stomach, uterus and skin tumors
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• 7 of 8 mice develop one or more tumors of the mammary gland after the first pregnancy
• mean latency time for spontaneous mammary tumor development is 19.7 +/- 8.6 weeks
• mammary tumors of both untreated and DMBA-treated mice are heterogeneous, including frequent adenocarcinomas, solid carcinomas, papillary carcinomas, and adenosquamous carcinomas, carcinosarcomas and sarcomas
• 67% of mammary tumors from untreated and DMBA-treated mice are estrogen receptor alpha-positive
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• some mice develop an additional tumor of the lung
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| breast cancer | DOID:1612 |
OMIM:114480 |
J:101617 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• skin tumors develop between 500 and 600 days
• UVB exposure results in 6.5+/-1.4 tumors at day 100 compared to 0.6+/-0.2 in wild-type mice
• whether spontaneous or induced, mice develop epithelial, proliferative lesions forming a continuum from nonneoplastic squamous keratosis and acanthosis to squamous cell papillomas, actinic keratosis and keratoacanthoma with increasing degrees of atypia and dysplasia, carcinoma in situ, up to invasive squamous cell carcinoma
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• one mouse developed a hemangiosarcoma in the intestine
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• developed in one mouse
|
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• fewer CASP3+ cells area found following UVB treatment when compared to wild-type mice
• the reduction in apoptotic cells is slightly greater in homozygotes than in heterozygotes
|
|
• skin tumors develop between 500 and 600 days
• UVB exposure results in 6.5+/-1.4 tumors at day 100 compared to 0.6+/-0.2 in wild-type mice
• whether spontaneous or induced, mice develop epithelial, proliferative lesions forming a continuum from nonneoplastic squamous keratosis and acanthosis to squamous cell papillomas, actinic keratosis and keratoacanthoma with increasing degrees of atypia and dysplasia, carcinoma in situ, up to invasive squamous cell carcinoma
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 26 of 30 mutants develop pancreatic ductal adenocarcinomas
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• average survival time is 143 days, with a range of 91-191 days
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• 26 of 30 mutants develop pancreatic ductal adenocarcinomas
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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 04/23/2024 MGI 6.23 |
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