|
Allele Symbol Allele Name Allele ID |
Trp53tm1Brn targeted mutation 1, Anton Berns MGI:1931011 |
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| Summary |
227 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in 6 of 7 mice treated with a cre-expressing adenovirus
(J:86077)
• in 6 of 7 mice following treatment with cre-expressing adenovirus
(J:157319)
|
| N |
• ovarian surface epithelium (OSE) cells do not show any enhancement of proliferation after adenoviral cre treatment
|
|
• ovarian surface epithelium cells transfected with a cre-expressing adenovirus exhibit increased cell motility and invasion compared with cells transfected with a lacZ-expressing adenovirus
|
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• after adenoviral cre infection, OSE cells in culture show significantly higher sensitivity to cisplatin treatment compared to control cells (31% remain ater 48 hours compared to 40% of control cells remaining)
|
|
• ovarian surface epithelium cells transfected with a cre-expressing adenovirus exhibit increased cell motility compared with cells transfected with a lacZ-expressing adenovirus
|
| N |
• mice do not develop mesothelioma following injection of adenovirus expressing Cre into the bladder or intraperitoneally at 2-3 months of age
|
|
• in 6 of 7 mice treated with a cre-expressing adenovirus
(J:86077)
• in 6 of 7 mice following treatment with cre-expressing adenovirus
(J:157319)
|
|
• ovarian surface epithelium cells with a cre-expressing adenovirus exhibit enhanced wound closure compared with cells transfected with a lacZ-expressing adenovirus
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
 |
• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa develop bursal cysts 6 months after injection
• however, mice injected with an adenovirus expressing cre recombinase into the oviduct exhibit no change in phenotype 3 months after injection
|
|
|
• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa develop bursal cysts 6 months after injection
• however, mice injected with an adenovirus expressing cre recombinase into the oviduct exhibit no change in phenotype 3 months after injection
|
|
|
• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa exhibit ovary degeneration 6 months after injection
|
|
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• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa develop bursal cysts 6 months after injection
• however, mice injected with an adenovirus expressing cre recombinase into the oviduct exhibit no change in phenotype 3 months after injection
|
|
|
• 2 of 7 mice injected with an adenovirus expressing cre recombinase into the bursa exhibit ovary degeneration 6 months after injection
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in all mice treated with a cre-expressing adenovirus
(J:86077)
• in 6 of 7 mice following treatment with cre-expressing adenovirus
(J:157319)
|
|
• in all mice treated with a cre-expressing adenovirus
(J:86077)
• in 6 of 7 mice following treatment with cre-expressing adenovirus
(J:157319)
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• ovarian surface epithelium cells transfected with a cre-expressing adenovirus exhibit increased invasion compared with control cells that is not as severe as in similarly treated cells from Trp53tm1Brn homozygotes
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• median survival is 38.4 weeks
|
|
• 4-8 week old mice only show areas of well differentiated follicular carcinomas but go on to develop well-differentiated follicular carcinomas by 8-10 months of age exhibiting spindle cell morphology, giant, osteoclast-like, multinucleated cells and areas of osseous metaplasia resembling human thyroid anaplastic carcinomas
• anaplastic thyroid carcinomas undergo dedifferentiation, genomic instability and epithelial-to-mesenchymal transition and exhibit a shift from an oxidative to a glycolytic pathway
|
|
• aggressive tumors invade locally into the muscle and trachea and metastasize to the lungs in 28% of mice, or less often, to the liver
|
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• all 8-10 month old mice exhibit enlarged thyroid gland causing severe tracheal compression
|
|
• 4-8 week old mice only show areas of well differentiated follicular carcinomas but go on to develop well-differentiated follicular carcinomas by 8-10 months of age exhibiting spindle cell morphology, giant, osteoclast-like, multinucleated cells and areas of osseous metaplasia resembling human thyroid anaplastic carcinomas
• anaplastic thyroid carcinomas undergo dedifferentiation, genomic instability and epithelial-to-mesenchymal transition and exhibit a shift from an oxidative to a glycolytic pathway
|
|
• reduction in TSH serum levels
• however, T4 levels are normal
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| thyroid gland carcinoma | DOID:3963 | J:211100 | ||
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• as in Rb1tm2Brn/Rb1tm2Brn Trp53tm1Brn/Trp53tm1Brn Tg(Gfap-cre)2Brn mice
|
|
• as in Rb1tm2Brn/Rb1tm2Brn Trp53tm1Brn/Trp53tm1Brn Tg(Gfap-cre)2Brn mice
|
|
• large cell carcinoma
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• spontaneous development of malignant melanoma by 200 days of age in all mice treated with tamoxifen
• tumors of tamoxifen-treated mice are relatively small, with regular ovoid shape and high levels of Ki-67 staining
• naevi are not seen above dermal malignant melanomas in tamoxifen treated mice, although small nests of melanocytes in a subepidermal location are occasionally seen
• early lesions of tamoxifen treated mice do not show evidence of tumor derivation from the upper dermis and appear to be derived from follicular or other deep dermal precursors
• majority of tumors of tamoxifen treated mice are located on the back
|
|
• all mice treated with tamoxifen develop malignant melanoma before 150 days of age after a single neonatal UVB dose
• tamoxifen-treated mice show a diminished response of melanocyte emigration from the upper regions of hair follicles to the epidermal basal layer 3-5 days after neonatal UV radiation compared to controls
|
|
• spontaneous development of malignant melanoma by 200 days of age in all mice treated with tamoxifen
• tumors of tamoxifen-treated mice are relatively small, with regular ovoid shape and high levels of Ki-67 staining
• naevi are not seen above dermal malignant melanomas in tamoxifen treated mice, although small nests of melanocytes in a subepidermal location are occasionally seen
• early lesions of tamoxifen treated mice do not show evidence of tumor derivation from the upper dermis and appear to be derived from follicular or other deep dermal precursors
• majority of tumors of tamoxifen treated mice are located on the back
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 4 of 40 mice develop lung metastasis
|
|
• 15 of 17 mice develop mammary neoplasms
• mammary tumor cells exhibit increased genomic instability compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice
|
|
• 15 of 17 mice develop mammary neoplasms
• mammary tumor cells exhibit increased genomic instability compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice
|
|
• 15 of 17 mice develop mammary neoplasms
• mammary tumor cells exhibit increased genomic instability compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice
|
|
• cell proliferation in mammary carcinomas is increased compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice
|
|
• 10 of 43 neoplasms are well-differentiated carcinomas
• while one tumor is an adenosquamous carcinoma the remaining tumors are poorly differentiated carcinomas with spindle or polygonal, frequently pleomorphic cells
|
|
• 1 adenosquamous carcinoma
|
|
• 4 of 40 mice develop lung metastasis
|
|
• mammary tumor cells exhibit increased genomic instability compared to in Trp53tm1Brn/Trp53tm1Brn Tg(MMTV-cre)105Ayn mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 3 of 27 mice develop lung metastasis
|
|
• by 700 days, 8 of 16 mice develop mammary neoplasms
• however, mice do not exhibit lymphomas or other non-mammary neoplasms
|
|
• by 700 days, 8 of 16 mice develop mammary neoplasms
• however, mice do not exhibit lymphomas or other non-mammary neoplasms
|
|
• by 700 days, 8 of 16 mice develop mammary neoplasms
• however, mice do not exhibit lymphomas or other non-mammary neoplasms
|
|
• 8 of 27 neoplasms are well-differentiated carcinomas
• while one tumor is an adenosquamous carcinoma the remaining tumors are poorly differentiated carcinomas with spindle or polygonal, frequently pleomorphic cells
|
|
• 1 adenosquamous carcinoma
|
|
• 3 of 27 mice develop lung metastasis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• pancreatic tumors and liver metastasis express high levels of glucagon and mice exhibit increased circulating glucagon levels indicating that tumors are glucagonoma
|
|
• mice develop pancreatic neuroendocrine tumors that are classified as metastatic islet cell carcinoma; tumors are nodular and highly vascularized
• marker analysis indicates that both the primary pancreatic tumor and the liver metastases are pancreatic neuroendocrine in origin
|
|
• metastasis to the liver and lymph node is seen; liver metastases are nodular and highly vascularized
• liver also contains many separate metastatic foci
|
|
• mice develop subcutaneous tumors infrequently at around 3-4 months of age; these tumors have a solid growth pattern and are consistent with high-grade vascular sarcoma
|
|
• pancreatic tumors and liver metastasis express high levels of glucagon and mice exhibit increased circulating glucagon levels indicating that tumors are glucagonoma
|
|
• mice develop pancreatic neuroendocrine tumors that are classified as metastatic islet cell carcinoma; tumors are nodular and highly vascularized
• marker analysis indicates that both the primary pancreatic tumor and the liver metastases are pancreatic neuroendocrine in origin
|
|
• primary mortality is from metastatic pancreatic neuroendocrine disease with lethal onset beginning at around 22 weeks of age
• in rare instances, mice develop subcutaneous tumors and need to be euthanized at around 12-16 weeks of age and in even more rare cases, mice die as early as 8 weeks of age of unknown causes; these cases constitute about 12% of mice
|
|
• mice show increased circulating glucagon levels at 4, 5 and 6 months but not at 2 months of age
|
|
• 32% reduction in body weight of sick mutants
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| adenoma | DOID:657 | J:216559 | ||
| pancreatic carcinoma | DOID:4905 |
OMIM:260350 |
J:216559 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice survive to around 13.9 weeks
• treatment of mice with RANK-Fc prolongs survival to around 17.8 weeks
|
|
• mice develop osteosarcoma within 10.3 weeks of age
• tumors are marked by high TNFSF11 (RANKL)/low TNFRSF11A (RANK) levels
• treatment of mice with RANK-Fc for 52 weeks beginning at 12.6 weeks of age keeps mice tumor-free until 64.6 weeks of age
|
|
• mice develop osteosarcoma within 10.3 weeks of age
• tumors are marked by high TNFSF11 (RANKL)/low TNFRSF11A (RANK) levels
• treatment of mice with RANK-Fc for 52 weeks beginning at 12.6 weeks of age keeps mice tumor-free until 64.6 weeks of age
|
|
• in a scratch wound healing assay, tumor cells show greater migration than tumor cells from conditional Rb1tm2Brn heterozygous Trp53tm1Brn homozygous double mutants
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| osteosarcoma | DOID:3347 |
OMIM:259500 |
J:234128 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice do not live longer than 11 weeks
• treatment of mice with RANK-Fc prolongs survival to around to around 13.3 weeks
|
|
• mice develop osteosarcoma within 6.3 weeks of age
• tumors are marked by high (TNFSF11) RANKL/low (TNFRSF11A) RANK levels
• treatment of mice with RANK-Fc starting at 2.4 weeks of age suppresses tumor growth
• mice develop tumors 4.3 weeks after the discontinuation of RANK-Fc treatment and large numbers of osteoclasts are seen lining the boundary of tumor cells and adjacent osteopetrotic bone
|
|
• mice develop osteosarcoma within 6.3 weeks of age
• tumors are marked by high (TNFSF11) RANKL/low (TNFRSF11A) RANK levels
• treatment of mice with RANK-Fc starting at 2.4 weeks of age suppresses tumor growth
• mice develop tumors 4.3 weeks after the discontinuation of RANK-Fc treatment and large numbers of osteoclasts are seen lining the boundary of tumor cells and adjacent osteopetrotic bone
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| osteosarcoma | DOID:3347 |
OMIM:259500 |
J:234128 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• all mice develop thyroid tumors
|
|
• death within 3 months of tamoxifen treatment
|
|
• small cell lung tumors 2.5 months after tamoxifen treatment
|
|
• increased proliferation of pulmonary neuroendocrine cells
|
|
• all mice develop thyroid tumors
|
|
• increased invasiveness at 2.5 months after tamoxifen treatment
|
|
• small cell lung tumors 2.5 months after tamoxifen treatment
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor
|
|
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor
|
|
• mice injected with an adenovirus expressing cre (adeno-cre) into the lateral ventricle predominantly develop poorly differentiated, well-circumscribed neoplasms with similarity to supratentorial primitive neuroectodermal tumors (sPNET)
• expression profiles of tumors resemble human atypical teratoid/rhabdoid tumor
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• low penetrance (8.33%) of osteosarcomas with a long latency of 338 days of age on average
|
|
• low penetrance (8.33%) of osteosarcomas with a long latency of 338 days of age on average
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• complete penetrance of osteosarcomas with an average latency of 292 days
|
|
• mice die from around 250 to 375 days of age
|
|
• tumors show metastasis, most frequently to the lung and then the liver
|
|
• complete penetrance of osteosarcomas with an average latency of 292 days
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice exhibit a shortened overall survival, with a median lifespan of 184 days versus 239 days in control littermates that are wild-type for Dlg2
|
|
• tumor cells are more proliferative than those in control littermates that are wild-type for Dlg2, as indicated by Ki-67 staining
|
|
• mice show accelerated osteosarcoma development with anatomical distribution and histological features similar to those in control littermates that are wild-type for Dlg2
• osteoblastic tumors are aggressive in nature, as indicated by abundant osteoid deposition at the invasive front of thoracic vertebra osteosarcomas
• plump tumorous osteoblasts and massive osteoid deposition are seen in tumors that develop at different sites
|
|
• at 22 weeks of age, mice show accelerated tumor onset with visible signs of osteosarcomas on the tibia and ribs, unlike control littermates that are wild-type for Dlg2
|
|
• mice show accelerated osteosarcoma development with anatomical distribution and histological features similar to those in control littermates that are wild-type for Dlg2
• osteoblastic tumors are aggressive in nature, as indicated by abundant osteoid deposition at the invasive front of thoracic vertebra osteosarcomas
• plump tumorous osteoblasts and massive osteoid deposition are seen in tumors that develop at different sites
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice survive up to 38.1 weeks of age
|
|
• mice develop osteosarcoma by 20 weeks of age
|
|
• mice develop osteosarcoma by 20 weeks of age
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice survive up to 55.4 weeks of age
|
|
• mice develop osteosarcoma by 35 weeks of age
• tumors are marked by low TNFSF11 (RANKL)/high TNFRSF11A (RANK) levels
|
|
• mice develop osteosarcoma by 35 weeks of age
• tumors are marked by low TNFSF11 (RANKL)/high TNFRSF11A (RANK) levels
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• large cell carcinoma
|
|
• choroid plexus papilloma
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• all mice develop thyroid tumors
|
|
• death within 6-7 months of tamoxifen treatment
|
|
• small cell lung tumors 5-6 months after tamoxifen treatment in 4 of 32 mice examined, all with pulmonary neuroendocrine cells hyperplasia as well
|
|
• pulmonary neuroendocrine cells hyperplasia 5-6 months after tamoxifen treatment in 16 of 32 mice examined
• increased proliferation of pulmonary neuroendocrine cells
|
|
• all mice develop thyroid tumors
|
|
• small cell lung tumors 5-6 months after tamoxifen treatment in 4 of 32 mice examined, all with pulmonary neuroendocrine cells hyperplasia as well
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• tumor-free survival is 146.5 days
|
|
• 52.4% incidence
|
|
• 52.4% incidence
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• impaired survival is seen beginning around 2 months of age
• death appears to result from excessive bleeding due to invasion of uterine blood vessels by tumor cells
|
|
|
• hyperplasia progresses to carcinoma by 3 weeks of age
|
|
|
• by P10, luminal and glandular epithelial hyperplasia are seen
|
|
|
• enlarged relative to conditional mutants that are wild type for Trp53
|
|
|
• hyperplasia progresses to carcinoma by 3 weeks of age
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| endometrial cancer | DOID:1380 |
OMIM:608089 |
J:139053 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants develop pancreatic tumors with an average latency of 21.8 weeks
|
|
• 100% of tumors are well differentiated ductal adenocarcinomas
|
|
• mutants develop pancreatic tumors with an average latency of 21.8 weeks
|
|
• 100% of tumors are well differentiated ductal adenocarcinomas
|
|
• 33% of tumors exhibit metastasis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants develop pancreatic tumors with an average latency of 13.1 weeks
• 25% of tumors exhibit sarcomatoid carcinoma histology
|
|
• 75% of tumors exhibit well differentiated ductal adenocarcinoma histology
|
|
• mutants develop pancreatic tumors with an average latency of 13.1 weeks
• 25% of tumors exhibit sarcomatoid carcinoma histology
|
|
• 75% of tumors exhibit well differentiated ductal adenocarcinoma histology
|
|
• 25% of tumors exhibit metastasis
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic ductal adenocarcinoma | DOID:3498 | J:108298 | ||
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants develop pancreatic tumors with an average latency of 14.7 weeks
• 19% of tumors exhibit sarcomatoid differentiation
|
|
• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology
|
|
• mutants develop pancreatic tumors with an average latency of 14.7 weeks
• 19% of tumors exhibit sarcomatoid differentiation
|
|
• 81% of tumors exhibit well differentiated ductal adenocarcinoma histology
|
|
• 25% of tumors exhibit metastasis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants develop pancreatic tumors with an average latency of 7.2 weeks
• 60% of tumors exhibit anaplastic carcinoma histology
|
|
• 40% of tumors exhibit well differentiated ductal adenocarcinoma histology
|
|
• mutants develop pancreatic tumors with an average latency of 7.2 weeks
• 60% of tumors exhibit anaplastic carcinoma histology
|
|
• 40% of tumors exhibit well differentiated ductal adenocarcinoma histology
|
|
• 20% of tumors exhibit metastasis
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic ductal adenocarcinoma | DOID:3498 | J:108298 | ||
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants develop pancreatic tumors with an average latency of 6.5 weeks
• 20% of tumors exhibit anaplastic carcinoma histology
|
|
• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology
|
|
• mutants develop pancreatic tumors with an average latency of 6.5 weeks
• 20% of tumors exhibit anaplastic carcinoma histology
|
|
• 80% of tumors exhibit well differentiated ductal adenocarcinoma histology
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic ductal adenocarcinoma | DOID:3498 | J:108298 | ||
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mutants develop pancreatic tumors with an average latency of 6.2 weeks
|
|
• mutants exhibit rapid pancreatic ductal adenocaracinoma progression, developing lethal tumors by 8 weeks of age
• 100% of tumors are well differentiated ductal adenocarcinomas
|
|
• mutants develop pancreatic tumors with an average latency of 6.2 weeks
|
|
• mutants exhibit rapid pancreatic ductal adenocaracinoma progression, developing lethal tumors by 8 weeks of age
• 100% of tumors are well differentiated ductal adenocarcinomas
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic ductal adenocarcinoma | DOID:3498 | J:108298 | ||
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• decreased tumor free survival time
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• tumor free survival time is increased compared to mutant mice wild-type for Sox2
|
|
• compared to mutant mice wild-type for Sox2
• tumors are uniformly Sox2 positive
|
|
• compared to mutant mice wild-type for Sox2
• tumors are uniformly Sox2 positive
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• tumor free survival time is increased compared to mutant mice wild-type for Sox2
|
|
• compared to mutant mice wild-type for Sox2
• tumors are uniformly Sox2 positive
|
|
• compared to mutant mice wild-type for Sox2
• tumors are uniformly Sox2 positive
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• after 2 weeks of tamoxifen treatment
|
|
• widespread high-grade dysplasia and numerous intramucosal carcinomas invading the lamina propria in most of the small-bowel crypts and villi within 2 weeks of tamoxifen treatment
|
|
• increased proliferation after tamoxifen treatment throughout the crypt-villus axis
|
|
• in the gut of tamoxifen treated mice but no more so than in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Tg(Vil-cre/ERT2)23Syr mice
|
|
• increased proliferation after tamoxifen treatment throughout the crypt-villus axis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• within 6 months, 7 of 9 tamoxifen-treated mice develop invasive carcinomas that permeates the bowel muscular wall into the subserosal fat with some involvement of the serosal surface (stage T4)
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.2 months of age and no distant metastases are seen
|
|
• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.2 months of age and no distant metastases are seen
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
 |
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• tumors are more aggressive than in mutant mice wild-type for Smad4
|
|
|
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• tumors are more aggressive than in mutant mice wild-type for Smad4
|
|
• survival time is shorter than in mutant mice wild-type for Smad4
• median survival time of 17.05 weeks
|
|
|
• all develop rapidly progressive, locally invasive prostate adenocarcinomas
• tumors are more aggressive than in mutant mice wild-type for Smad4
|
|
• bone metastases are seen in some (3 of 24) mice unlike in mutant mice wild-type for Smad4
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice develop mammary gland carcinoma with a median tumor-free survival of 10.4 months of age
• tumors are invasive ductal carcinomas with a squamous component, however lobular carcinomas are not seen
|
|
• mice develop mammary gland carcinoma with a median tumor-free survival of 10.4 months of age
• tumors are invasive ductal carcinomas with a squamous component, however lobular carcinomas are not seen
|
|
• mice develop mammary gland carcinoma with a median tumor-free survival of 10.4 months of age
• tumors are invasive ductal carcinomas with a squamous component, however lobular carcinomas are not seen
|
|
• 33% of mice show lung metastasis
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice develop gastric adenocarcinomas with a median tumor-free survival of 9.4 months but do not develop distant metastases
|
|
• mice develop gastric adenocarcinomas with a median tumor-free survival of 9.4 months but do not develop distant metastases
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 36% of mice develop duodenal adenocarcinomas
|
|
• 84% of mice develop spontaneous tumors in the glandular stomach with a median tumor-free survival of 8 months
• gastric tumors resemble diffuse-type gastric adenocarcinomas, are E-cadherin-negative, and are invasive into the muscle layers and regional lymph nodes
• intramucosal adenocarcinomas with signet ring cell feature is seen in 2 of 4 mice at 6 months of age
• gastric premalignant lesions such as atrophic gastritis, metaplasia or dysplasia are not seen at 4 and 5 months of age
|
|
• most common cause of death is duodenal obstruction, followed by gastric outlet obstruction
|
|
• 36% of mice develop duodenal adenocarcinomas
|
|
• 84% of mice develop spontaneous tumors in the glandular stomach with a median tumor-free survival of 8 months
• gastric tumors resemble diffuse-type gastric adenocarcinomas, are E-cadherin-negative, and are invasive into the muscle layers and regional lymph nodes
• intramucosal adenocarcinomas with signet ring cell feature is seen in 2 of 4 mice at 6 months of age
• gastric premalignant lesions such as atrophic gastritis, metaplasia or dysplasia are not seen at 4 and 5 months of age
|
|
• 3 of 21 mice with gastric adenocarcinomas develop lung metastases
• metastatic lesions have similar cytologic features to primary gastric tumors
• 8% of mice exhibit adenocarcinomas in the pancreas, most likely due to invasion of the primary duodenal or gastric adenocarcinomas
|
|
• 24% of mice develop forestomach squamous cell carcinomas
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| stomach cancer | DOID:10534 |
OMIM:613659 |
J:212549 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• tumor-free survival is 398 days compared to 146.5 days in mutant mice wild-type for Nell1
|
|
• 85.2% decrease in the proliferative-index in tumors compared to tumors in mutant mice wild-type for Nell1
|
|
• 66.1% decrease in tumor-associated vasculature compared to mutant mice wild-type for Nell1
|
|
• 15.8% incidence compared to 52.4% incidence in mutant mice wild-type for Nell1
|
|
• 15.8% incidence compared to 52.4% incidence in mutant mice wild-type for Nell1
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 100% of mice induced with tamoxifen at P0 and P1 develop medulloblastoma with a median onset of morbidity of 63 days of age
• medullablastomas of tamoxifen treated mice show extensive and abnormal vascularization and highly differentiated tumor cells surrounding a perivascular tumor stem cell niche that is not seen in single Trp53 conditional mutants
• blood clots are often seen in the lumen of abnormal blood vessels
• medulloblastoma initiates from a perivascular tumor stem cell niche
• medulloblastomas of tamoxifen treated mice acquire somatic inactivation of Ptch1 and show expression signatures of sonic hedgehog subgroup medulloblastoma
|
|
• 18 of 26 mice treated with tamoxifen at P0 and P1 develop gliomas in the forebrain and brain stem
|
|
• 100% of mice induced with tamoxifen at P0 and P1 develop medulloblastoma with a median onset of morbidity of 63 days of age
• medullablastomas of tamoxifen treated mice show extensive and abnormal vascularization and highly differentiated tumor cells surrounding a perivascular tumor stem cell niche that is not seen in single Trp53 conditional mutants
• blood clots are often seen in the lumen of abnormal blood vessels
• medulloblastoma initiates from a perivascular tumor stem cell niche
• medulloblastomas of tamoxifen treated mice acquire somatic inactivation of Ptch1 and show expression signatures of sonic hedgehog subgroup medulloblastoma
|
|
• 18 of 26 mice treated with tamoxifen at P0 and P1 develop gliomas in the forebrain and brain stem
|
|
• cerebellum at P21 of mice treated with tamoxifen at birth shows disrupted lamination and abundant Ki67+ proliferative cells throughout the cerebellum , which are concentrated around blood vessels either under the pial surface or in the parenchyma
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| medulloblastoma | DOID:0050902 |
OMIM:155255 |
J:237990 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 53% of mice induced with tamoxifen at P0 and P1 develop non-CNS tumors or other type of brain tumors
|
|
• 53% of mice induced with tamoxifen at P0 and P1 develop non-CNS tumors or other type of brain tumors
|
|
• 47% of mice induced with tamoxifen at P0 and P1 develop medulloblastoma with a median onset of morbidity of 135 days
|
|
• 53% of mice induced with tamoxifen at P0 and P1 develop non-CNS tumors or other type of brain tumors
|
|
• 47% of mice induced with tamoxifen at P0 and P1 develop medulloblastoma with a median onset of morbidity of 135 days
|
|
|
| ♀ | 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 cells from Trp53tm1Brn homozygotes transfected with a lacZ-expressing adenoviru
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 92% of mice have mammary tumors
• many mice have tumors in more than one gland
• mammary tumors are either spindle/epithelial-mesenchymal transition or poorly differentiated adenocarcinoma
|
|
• 92% of mice have mammary tumors
• many mice have tumors in more than one gland
• mammary tumors are either spindle/epithelial-mesenchymal transition or poorly differentiated adenocarcinoma
|
|
• 92% of mice have mammary tumors
• many mice have tumors in more than one gland
• mammary tumors are either spindle/epithelial-mesenchymal transition or poorly differentiated adenocarcinoma
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• in some mice treated with a cre-expressing adenovirus
|
|
• small in some mice treated with a cre-expressing adenovirus
|
|
• some mice treated with a cre-expressing adenovirus exhibit metastasis in the mediastinum, ovary and adrenal gland
|
|
• in some mice treated with a cre-expressing adenovirus
|
|
• small in some mice treated with a cre-expressing adenovirus
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• mice treated with cre-expressing adenovirus median tumor-free survival is 475 days
|
|
• in some mice treated with a cre-expressing adenovirus
(J:86077)
• in some mice following treatment with cre-expressing adenovirus
(J:157319)
|
|
• large in 5 of 13 mice treated with a cre-expressing adenovirus
(J:86077)
• in some mice following treatment with cre-expressing adenovirus
(J:157319)
|
|
• medullary thyroid carcinomas in 2 of 13 mice treated with a cre-expressing adenovirus
(J:86077)
• following treatment with cre-expressing adenovirus, 2 of 13 mice exhibit medullary thyroid carcinoma unlike wild-type mice
(J:157319)
|
|
• medullary thyroid carcinomas in 2 of 13 mice treated with a cre-expressing adenovirus
(J:86077)
• following treatment with cre-expressing adenovirus, 2 of 13 mice exhibit medullary thyroid carcinoma unlike wild-type mice
(J:157319)
|
|
• mice treated with cre-expressing adenovirus median tumor-free survival is 475 days
|
|
• in some mice treated with a cre-expressing adenovirus
(J:86077)
• in some mice following treatment with cre-expressing adenovirus
(J:157319)
|
|
• large in 5 of 13 mice treated with a cre-expressing adenovirus
(J:86077)
• in some mice following treatment with cre-expressing adenovirus
(J:157319)
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
• after a single ovarian intrabursal injection of an adenovirus expressing Cre, mutant females develop epithelial ovarian cancer similar in progression of disease in women, with ovarian neoplasms spreading, forming ascites and metastasizing to the contralateral ovary, the lung and the liver
• 39% are well-differentiated serous epithelial neoplasms of the ovary and 45% are poorly differentiated CK8-positive neoplasms of the ovary
|
|
|
• the ovarian cancer found after a single ovarian intrabursal injection of an adenovirus expressing Cre is characterisitic of serous adenocarcinoma
|
|
• medullary thyroid carcinomas in some mice treated with a cre-expressing adenovirus
(J:86077)
• following treatment with cre-expressing adenovirus, 6 of 33 mice develop medullary thyroid carcinoma unlike wild-type mice
(J:157319)
|
|
• 97% of mice succumb to ovarian tumors at a median age of 227 days after after a single ovarian intrabusal injection of an adenovirus expressing Cre
|
|
|
• after a single ovarian intrabursal injection of an adenovirus expressing Cre, mutant females develop epithelial ovarian cancer similar in progression of disease in women, with ovarian neoplasms spreading, forming ascites and metastasizing to the contralateral ovary, the lung and the liver
• 39% are well-differentiated serous epithelial neoplasms of the ovary and 45% are poorly differentiated CK8-positive neoplasms of the ovary
|
|
|
• the ovarian cancer found after a single ovarian intrabursal injection of an adenovirus expressing Cre is characterisitic of serous adenocarcinoma
|
|
• medullary thyroid carcinomas in some mice treated with a cre-expressing adenovirus
(J:86077)
• following treatment with cre-expressing adenovirus, 6 of 33 mice develop medullary thyroid carcinoma unlike wild-type mice
(J:157319)
|
|
• various metastases in some mice treated with a cre-expressing adenovirus
|
|
• 15% of tumors that form in females after a single ovarian intrabursal injection of an adenovirus expressing Cre metastasized to the opposite ovary, 18% of tumors metastasized to the lung, and 6% of tumors metastasized to the liver
|
|
• mice treated with cre-expressing adenovirus median tumor-free survival is 210 days
|
|
• bronchioalveolar carcinomas in some mice treated with a cre-expressing adenovirus
|
|
• mice treated with a cre-expressing adenovirus exhibit multiple dysplastic foci of clustering small cells in the bronchial and bronchiolar mucosa
(J:86077)
• mice treated with cre-expressing adenovirus exhibit dysplastic foci of clustering small cells in the bronchial and bronchiolar mucosa unlike in wild-type mice
(J:157319)
|
|
|
• after a single ovarian intrabursal injection of an adenovirus expressing Cre, mutant females develop epithelial ovarian cancer similar in progression of disease in women, with ovarian neoplasms spreading, forming ascites and metastasizing to the contralateral ovary, the lung and the liver
• 39% are well-differentiated serous epithelial neoplasms of the ovary and 45% are poorly differentiated CK8-positive neoplasms of the ovary
|
|
|
• the ovarian cancer found after a single ovarian intrabursal injection of an adenovirus expressing Cre is characterisitic of serous adenocarcinoma
|
|
• mice treated with cre-expressing adenovirus median tumor-free survival is 210 days
|
|
• bronchioalveolar carcinomas in some mice treated with a cre-expressing adenovirus
|
|
• mice treated with a cre-expressing adenovirus exhibit multiple dysplastic foci of clustering small cells in the bronchial and bronchiolar mucosa
(J:86077)
• mice treated with cre-expressing adenovirus exhibit dysplastic foci of clustering small cells in the bronchial and bronchiolar mucosa unlike in wild-type mice
(J:157319)
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| lung small cell carcinoma | DOID:5409 |
OMIM:182280 |
J:86077 , J:157319 | |
| ovarian cancer | DOID:2394 |
OMIM:167000 OMIM:607893 |
J:84345 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• after adenoviral cre treatment, double mutant OSE cells show significantly enhanced proliferation compared to control cells
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 8 weeks after adenoCre treatment, lungs show rapid cancer progression with increased proliferation compared to Trp53-sufficient mice
• tumors show nodules composed of central papillary structures with solid peripheral areas
• all double mutants show increased proliferation, and cells show altered nuclear morphology, while Trp53 conditional single mutants have normal lung phenotypes
|
|
• 2/5 mice are found to have prominent adenocarcinomas, composed of glandular structures lined by atypical cells with enlarged nuclei, hyperchromasia, contour irregularities, and prominent nucleoli
• large areas of necrosis are present in adenocarcinomas, with evidence of lymphatic and vascular invasion
|
|
• 8 weeks after adenoCre treatment, lungs show rapid cancer progression with increased proliferation compared to Trp53-sufficient mice
• tumors show nodules composed of central papillary structures with solid peripheral areas
• all double mutants show increased proliferation, and cells show altered nuclear morphology, while Trp53 conditional single mutants have normal lung phenotypes
|
|
• 2/5 mice are found to have prominent adenocarcinomas, composed of glandular structures lined by atypical cells with enlarged nuclei, hyperchromasia, contour irregularities, and prominent nucleoli
• large areas of necrosis are present in adenocarcinomas, with evidence of lymphatic and vascular invasion
|
|
• 8 weeks after Cre treatment, some small airways display papillary hyperplasia, not seen in Braf-conditional mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• early B cell development is rescued in tamoxifen treated mice
|
|
• reduced LSK and lymphoid-primed multipotent progenitors in tamoxifen-treated mice
|
|
• tamoxifen-treated LSK cells exhibit a complete loss of lymphoid development
|
| N |
• early B cell development is rescued in tamoxifen treated mice
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 4/4 of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age
|
|
• 4/4 of mice receiving 4 Gy radiation at P5 develop cerebellar tumors by 5 months of age
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| medulloblastoma | DOID:0050902 |
OMIM:155255 |
J:102702 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
| N |
• unlike mice with conditional loss of Pten, endometrial morphology and histology appear normal through 5 months of age
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• increased proliferation in the entire bowel
• distal gut dysplasia appears later than in mice with Trp53tm2.1Tyj (containing the R172H missense mutation)
|
|
• jejunal and ileal organoids exhibit increased proliferation, decreased differentiation, and resemble highly dysplastic spheroids
|
|
• high-grade dysplasia in the entire bowel
|
|
• enlarged and dysplastic
|
|
• enlarged and dysplastic
|
|
• increased proliferation in the entire bowel
• distal gut dysplasia appears later than in mice with Trp53tm2.1Tyj (containing the R172H missense mutation)
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) at a median age of 7.9 weeks following doxycycline treatment at 3 weeks of age
|
|
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) at a median age of 7.9 weeks following doxycycline treatment at 3 weeks of age
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic carcinoma | DOID:4905 |
OMIM:260350 |
J:186194 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age
• tumors exhibit features of human PDAC, including glandular tumor structures, exuberant stroma, local invasion into surrounding structures such as the duodenum, and distant metastases to the liver and lung
• mice show rapid tumor regression staring 48 hours and peaking at 72 hours following doxycycline withdrawal, with a reduction in tumor mass of about 50% after 1 week of doxycycline withdrawal; tumor regression is accompanied by decreased tumor cell proliferation and increased apoptosis
• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro
|
|
• all mice succumb to pancreatic ductal adenocarcinoma (PDAC) between 11 and 25 weeks of age following doxycycline treatment at 3 weeks of age
• tumors exhibit features of human PDAC, including glandular tumor structures, exuberant stroma, local invasion into surrounding structures such as the duodenum, and distant metastases to the liver and lung
• mice show rapid tumor regression staring 48 hours and peaking at 72 hours following doxycycline withdrawal, with a reduction in tumor mass of about 50% after 1 week of doxycycline withdrawal; tumor regression is accompanied by decreased tumor cell proliferation and increased apoptosis
• withdrawal of doxycycline results in decreased glucose uptake and lactate production by cells in vitro
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| pancreatic carcinoma | DOID:4905 |
OMIM:260350 |
J:186194 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 2 in 5 mice develop an rhabdomyosarcoma by day 75 to 91
|
|
• 2 in 5 mice develop an rhabdomyosarcoma by day 75 to 91
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| alveolar rhabdomyosarcoma | DOID:4051 |
OMIM:268220 |
J:93444 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• 1 in 12 mice develop an rhabdomyosarcoma by day 202
|
|
• 1 in 12 mice develop an rhabdomyosarcoma by day 202
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| alveolar rhabdomyosarcoma | DOID:4051 |
OMIM:268220 |
J:93444 | |
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
|
• earlier tumor onset, from 32 to 65 days of age
• bortezomib treated mice have better survival
|
|
• earlier tumor onset, from 32 to 65 days of age
• bortezomib treated mice have better survival
|
|
|
| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
Skin hyperpigmentation in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Tg(KRT14-cre/ERT)20Efu/0 mice but not in Csnk1a1tm1.1Ybn/Csnk1a1tm1.1Ybn Trp53tm1Brn/Trp53tm1Brn Tg(KRT14-cre/ERT)20Efu/0 mice
|
• after tamoxifen i.p. treatment, the epidermis becomes dysplastic with no melanin deposition
|
|
• at day 28 after tamoxifen i.p. treatment, BrdU+ (proliferating) cells and beta-catenin nuclear staining are increased in the basal layer of the epidermis; however, most of the positive cells are multinucleated clumping cells indicating abnormal mitoses associated with epidermal dysplasia
|
Analysis Tools