Analysis Tools|
Allele Symbol Allele Name Allele ID |
Cdh1tm2Kem targeted mutation 2, Rolf Kemler MGI:2389020 |
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| Summary |
10 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.2 months of age and no distant metastases are seen
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• mice develop intestinal adenocarcinomas with a median tumor-free survival of 5.2 months of age and no distant metastases are seen
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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
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• 33% of mice show lung metastasis
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• 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
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• 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
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• most common cause of death is duodenal obstruction, followed by gastric outlet obstruction
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• 36% of mice develop duodenal adenocarcinomas
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• 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
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• 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
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• 24% of mice develop forestomach squamous cell carcinomas
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• 36% of mice develop duodenal adenocarcinomas
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• 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
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| stomach cancer | DOID:10534 |
OMIM:613659 |
J:212549 | |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice develop gastric adenocarcinomas with a median tumor-free survival of 9.4 months but do not develop distant metastases
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• mice develop gastric adenocarcinomas with a median tumor-free survival of 9.4 months but do not develop distant metastases
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• on day 16 of pregnancy, mammary glands of pregnant mice show only occasional and small units of secretion compared to wild-type mice; this becomes more striking by day 18 and at parturition
• mammary gland is disorganized, with poorly developed, condensed alveoli at parturition
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• at day 2 of lactation, majority of lobulo-alveolar structures have collapsed, leaving clusters of epithelial cords with small lumina and extensive tissue remodeling
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• on day 16 of pregnancy, mammary glands of pregnant mice show only occasional and small units of secretion compared to wild-type mice; this becomes more striking by day 18 and at parturition
• mammary gland is disorganized, with poorly developed, condensed alveoli at parturition
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• expression of B-casein and whey acidic protein (WAP) re drastically reduced in mammary glands during lactation, indicating that gland is inefficient at producing milk proteins
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• mutant mice cannot nurse their offspring due to mammary gland defects; 80% of offspring die within 24 hours and all die within 2-3 days of birth
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• at day 2 of lactation, majority of lobulo-alveolar structures have collapsed, leaving clusters of epithelial cords with small lumina and extensive tissue remodeling
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• on day 16 of pregnancy, mammary glands of pregnant mice show only occasional and small units of secretion compared to wild-type mice; this becomes more striking by day 18 and at parturition
• mammary gland is disorganized, with poorly developed, condensed alveoli at parturition
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• expression of B-casein and whey acidic protein (WAP) re drastically reduced in mammary glands during lactation, indicating that gland is inefficient at producing milk proteins
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• mutant mice cannot nurse their offspring due to mammary gland defects; 80% of offspring die within 24 hours and all die within 2-3 days of birth
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice die within 1 to 2 hours of birth
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• mice are small at birth
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• unlike in wild-type mice, dye is readily absorbed through the paws, facial skin, ear buds and lower belly
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• mice exhibit focal gaps in the epithelial sheets of the epidermis due to degeneration of cells
• however, desmosomes are still present in normal numbers
• intercellular junctions are perturbed unlike in wild-type epidermis
• adherence and tight junction components fail to localize to cell borders unlike in wild-type epidermis
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• the typically columnar orientation of cells within the basal layer and flattened squamous morphology of the suprabasal cells are lost
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• cells in the spinous layer fail to flatten as in wild-type mice
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• the typically columnar orientation of cells within the basal layer and flattened squamous morphology of the suprabasal cells are lost
• unlike in wild-type mice, cells within condensed nuclei indicating apoptosis are found in the suprabasal layer
• suprabasal keratin intermediate filament organization is perturbed compared to in wild-type mice
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• around the mouth, umbilicus and tail
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• ventrally
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• skin is inflexible
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• mice exhibit increased apoptosis in the epidermis compared to wild-type mice
• however, cell proliferation in the epidermis is normal, and no inflammatory response is observed
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• unlike in wild-type mice, dye is readily absorbed through the paws, facial skin, ear buds and lower belly
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• in 7 day and 1, but not 3, month old mice
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• 2-fold increase in blood vessel density in insulin-positive areas
• however, beta cell organization is normal
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• at 3 months
• 2.5-fold at 3 to 4 months
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• glucose-stimulated at 4, but not 1, months
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• glucose-stimulated at 4, but not 1, months
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• at 3 to 4 months
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• 2-fold increase in blood vessel density in insulin-positive areas
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| N |
• mice exhibit normal body weight
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• in 7 day and 1, but not 3, month old 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 12/17/2024 MGI 6.24 |
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