Analysis Tools
normal phenotype
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• mice exhibit normal development and lifespan
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Allele Symbol Allele Name Allele ID |
Brca2tm1Brn targeted mutation 1, Anton Berns MGI:2156556 |
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| Summary |
19 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exhibit normal development and lifespan
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 100% of mice develop medulloblastoma beginning at 5 weeks
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• 100% of mice develop medulloblastoma beginning at 5 weeks
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 100% of mice develop medulloblastoma beginning at 10 weeks
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• 100% of mice develop medulloblastoma beginning at 10 weeks
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• cells treated with PARP-inhibition exhibit increased chromosomal damage compared with cells from Brca2tm1Brn/Brca2tm1Brn Cd19tm1(cre)Cgn/Cd19tm1(cre)Cgn mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• cells treated with PARP-inhibition exhibit increased chromosomal damage compared with untreated cells
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 87% of mice develop medulloblastoma beginning at 13 weeks
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• 87% of mice develop medulloblastoma beginning at 13 weeks
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| medulloblastoma | DOID:0050902 |
OMIM:155255 |
J:144617 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• tumors exhibit a loss of heterozygosity at the Trp53 gene
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• 72% of mice develop medulloblastoma beginning at 21 weeks
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• 72% of mice develop medulloblastoma beginning at 21 weeks
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| medulloblastoma | DOID:0050902 |
OMIM:155255 |
J:144617 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 68% of mice injected with a cre-expressing adenovirus under the bursa develop serous epithelial ovarian cancer pathology
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• 68% of mice injected with a cre-expressing adenovirus under the bursa develop serous epithelial ovarian cancer pathology
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• 68% of mice injected with a cre-expressing adenovirus under the bursa develop serous epithelial ovarian cancer pathology
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| ovarian cancer | DOID:2394 |
OMIM:167000 OMIM:607893 |
J:189304 | |
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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; spectrum of anomalies are seen from isolated paucity of the islets of Langerhans to complete fibro-inflammatory or cystic degeneration of both the endocrine and exocrine pancreas
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• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls
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• pancreatic insufficiency; spectrum of anomalies are seen from isolated paucity of the islets of Langerhans to complete fibro-inflammatory or cystic degeneration of both the endocrine and exocrine pancreas
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• mutants not succumbing to pancreatic insufficiency later develop pancreatic ductal adenocarcinomas with a moderate latency and incomplete penetrance (6 of 32 mutants)
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• mutants exhibit shortened pancreatic ductal adenocarcinoma-free survival
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• mutants not succumbing to pancreatic insufficiency later develop pancreatic ductal adenocarcinomas with a moderate latency and incomplete penetrance (6 of 32 mutants)
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• pancreata from 6 day old mutants exhibits an increase in apoptotic cells compared to controls
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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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• small fraction of mutants develop pancreatic insufficiency
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• small fraction of mutants develop pancreatic insufficiency
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• premature death in the small fraction of mutants with pancreatic insufficiency
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
High-grade prostate intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Tg(Pbsn-cre)4Prb/0 Trp53tm1Brn/Trp53tm1Brn and prostate hyperplasia and intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Trp53tm1Brn/Trp53+ Tg(Pbsn-cre)4Prb/0 mice
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• focal low grade PIN are seen at 10 - 14 months of age
• by 15 - 20 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• levels of cell proliferation are 9 fold higher in PIN lesions
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• focal hyperplasia is seen beginning at 10 -14 months of age
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• focal low grade PIN are seen at 10 - 14 months of age
• by 15 - 20 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• levels of cell proliferation are 9 fold higher in PIN lesions
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• areas of hyperplasia are positive for markers of DNA damage
• 4 fold increase in apoptotic cells in PIN foci
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• focal hyperplasia is seen beginning at 10 -14 months of age
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• focal low grade PIN are seen at 10 - 14 months of age
• by 15 - 20 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• levels of cell proliferation are 9 fold higher in PIN lesions
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• areas of hyperplasia are positive for markers of DNA damage
• 4 fold increase in apoptotic cells in PIN foci
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Prostate hyperplasia and low-grade prostate intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Tg(Pbsn-cre)4Prb/0 mice
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• focal low grade PIN are seen in the lumen at 15 - 20 months of age
• low grade PIN lesions form characteristic tufting and cribiform patterns
• hyperplasia and low grade PIN are seen all 4 lobes
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• focal hyperplasia containing atypical cells is seen beginning at 10 -14 months of age
• hyperplasia and low grade PIN are seen all 4 lobes
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• focal low grade PIN are seen in the lumen at 15 - 20 months of age
• low grade PIN lesions form characteristic tufting and cribiform patterns
• hyperplasia and low grade PIN are seen all 4 lobes
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• areas of hyperplasia are positive for markers of DNA damage
• 3 fold increase in apoptotic cells in areas of hyperplasia and low grade PIN
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• focal hyperplasia containing atypical cells is seen beginning at 10 -14 months of age
• hyperplasia and low grade PIN are seen all 4 lobes
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• focal low grade PIN are seen in the lumen at 15 - 20 months of age
• low grade PIN lesions form characteristic tufting and cribiform patterns
• hyperplasia and low grade PIN are seen all 4 lobes
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• areas of hyperplasia are positive for markers of DNA damage
• 3 fold increase in apoptotic cells in areas of hyperplasia and low grade PIN
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
High-grade prostate intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Tg(Pbsn-cre)4Prb/0 Trp53tm1Brn/Trp53tm1Brn and prostate hyperplasia and intraepithelial neoplasia in Brca2tm1Brn/Brca2tm1Brn Trp53tm1Brn/Trp53+ Tg(Pbsn-cre)4Prb/0 mice
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• by 10 - 14 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• frequently multiple ducts of each lobe have high grade PIN, which are present in proximal and distal regions of the prostate and consist of many atypical cells filling
the lumen
• high grade PIN lesions are predominantly seen in the anterior and dorsal prostate
• levels of cell proliferation are 30 fold higher in PIN lesions
• high grade PIN lesions frequently contain large groups of basal cells some of which are rounder in shape and positioned near the lumen
• high grade lesions continue to proliferate post castration
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• focal hyperplasia is seen beginning as early as 6 months of age
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• by 10 - 14 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• frequently multiple ducts of each lobe have high grade PIN, which are present in proximal and distal regions of the prostate and consist of many atypical cells filling
the lumen
• high grade PIN lesions are predominantly seen in the anterior and dorsal prostate
• levels of cell proliferation are 30 fold higher in PIN lesions
• high grade PIN lesions frequently contain large groups of basal cells some of which are rounder in shape and positioned near the lumen
• high grade lesions continue to proliferate post castration
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• areas of hyperplasia are positive for markers of DNA damage
• 20 fold increase in apoptotic cells in areas of high grade PIN
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• focal hyperplasia is seen beginning as early as 6 months of age
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• by 10 - 14 months of age both focal low grade and high grade PIN are seen
• the incidence of high grade PIN is increased in mutant mice homozygous for the Trp53 allele relative to mice heterozygous for the Trp53 allele
• frequently multiple ducts of each lobe have high grade PIN, which are present in proximal and distal regions of the prostate and consist of many atypical cells filling
the lumen
• high grade PIN lesions are predominantly seen in the anterior and dorsal prostate
• levels of cell proliferation are 30 fold higher in PIN lesions
• high grade PIN lesions frequently contain large groups of basal cells some of which are rounder in shape and positioned near the lumen
• high grade lesions continue to proliferate post castration
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• areas of hyperplasia are positive for markers of DNA damage
• 20 fold increase in apoptotic cells in areas of high grade PIN
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| prostate cancer | DOID:10283 |
OMIM:176807 OMIM:300147 OMIM:300704 OMIM:601518 OMIM:602759 OMIM:608656 OMIM:608658 OMIM:609299 OMIM:609558 OMIM:610321 OMIM:610997 OMIM:611100 OMIM:611868 OMIM:611928 OMIM:611955 OMIM:611958 OMIM:611959 |
J:161511 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• compared to germ line deletions of this gene, mice exhibit no increase in apoptosis during neural development
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop tumors with a short median latency period of 298 days
• tumors exhibit expansive growth pattern, a high nuclear grade, and a high mitotic index
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• in 55% of mice
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• mice develop skin carcinomas
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• in 55% of mice
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• mice develop skin carcinomas
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• in 55% of mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop tumors with a short median latency period of 181 days
• tumors exhibit expansive growth pattern, a high nuclear grade, and a high mitotic index
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• in 72% of mice
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• mice develop skin carcinomas
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• in 72% of mice
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• mice develop skin carcinomas
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• in 72% of mice
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| breast cancer | DOID:1612 |
OMIM:114480 |
J:73028 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop tumors with a short median latency period of 360 days
• tumors exhibit expansive growth pattern, a high nuclear grade, and a high mitotic index
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• in 31% of mice
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• mice develop skin carcinomas
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• in 31% of mice
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• mice develop skin carcinomas
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• in 31% of mice
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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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