Analysis Tools
normal phenotype
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• mice exhibit no abnormalities
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neoplasm
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Allele Symbol Allele Name Allele ID |
Apctm1Rsmi targeted mutation 1, Ron Smits MGI:3848479 |
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| Summary |
5 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• mice exhibit no abnormalities
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 62.5% of mice develop endometrioid tubal tumors in distal and fimbrial parts of the oviduct showing severe nuclear atypia, subnuclear vacuolization, abnormal proliferation, complete loss of normal oviduct architecture and compression of the lumen
• tumors resemble human endometrioid tubal cancer
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• 27.9% of mice develop endometrioid ovarian tumors which may originate form the endometrioid ovarian cysts, resembling human endometrioid ovarian cancer
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• 1 of 43 mice develop a granulosa cell tumor which is distinct from the endometrioid tubal cancer
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• 62.5% of mice develop endometrioid tubal tumors in distal and fimbrial parts of the oviduct showing severe nuclear atypia, subnuclear vacuolization, abnormal proliferation, complete loss of normal oviduct architecture and compression of the lumen
• tumors resemble human endometrioid tubal cancer
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• 27.9% of mice develop endometrioid ovarian tumors which may originate form the endometrioid ovarian cysts, resembling human endometrioid ovarian cancer
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• 1 of 43 mice develop a granulosa cell tumor which is distinct from the endometrioid tubal cancer
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• 9.4% of mice show extraovarian endometrioid lesions within the utero-ovarian ligament, next to the tubal and ovarian tumors
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• 16.3% of mice show ovarian endometrioid cysts, mostly in younger mice
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• 87.2% of mice exhibit tubular intraepithelial lesions in the epithelium of the distal oviduct and fimbriae
• lesions show loss of cilia, bulging of cells into the lumen, layering and suspicious stratification of cells, and rounding and hyperchromatization of the nucleus
• 20% of mice develop glandular transformation of the normal papillary architecture of the oviduct characterized by glandular growth, loss of cilia, and general loss of normal cellular morphology
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• presence of extraovarian endometrioid lesions coincide with lesions found in the oviduct and ovary
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• 16.3% of mice show ovarian endometrioid cysts, mostly in younger mice
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• 27.9% of mice develop endometrioid ovarian tumors which may originate form the endometrioid ovarian cysts, resembling human endometrioid ovarian cancer
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• 1 of 43 mice develop a granulosa cell tumor which is distinct from the endometrioid tubal cancer
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• 16.3% of mice show ovarian endometrioid cysts, mostly in younger mice
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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:210095 | |
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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 |
Skeletogenesis is severely impaired in Apctm1Rsmi/Apctm1Rsmi Tg(Col2a1-cre)1Rsjo/0 mice
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• most mice die by the first day after birth
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• no mice survive to one month of age
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• at E16.5, mineralization is observed in the hind skull unlike in wild-type mice
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• at E12.5
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• no chondrogenic and osteogenic differentiation occurs in the humerus
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• ribs are characterized by inadequate orientation, size, and shape unlike in wild-type mice
• proximal ribs are severely misshapen compared to in wild-type mice
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• at E16.5, ribs are thicker and shorter than normal
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• at E16.5, chondrocytes in the nasal septum and endochondral bone dedifferentiate unlike in wild-type mice
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• at E12.5, the axial skeleton contains patchy and irregular cartilaginous structures that do not organize in vertebrae unlike in wild-type mice
• no chondrogenic and osteogenic differentiation occurs in the humerus
• no cartilaginous primordial of the pelvic bone are observed unlike in wild-type mice
• based on marker expression, differentiation of skeletal precursors in long bones and vertebrae is inhibited while osteoblastogenesis in the proximal ribs is enhanced
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• osteoblastogenesis in the proximal ribs is enhanced
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• mice fail to develop a cartilaginous molds of both the mandibles and occipital bone unlike in wild-type mice
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• at E16.5, mineralization of proximal ribs is enhanced compared to in wild-type mice
• at E16.5, mineralization is observed in the hind skull unlike in wild-type mice
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• all endochondral bones are misshaped and lack structural integrity unlike in wild-type mice
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• forelimbs are severely truncated with distorted cartilage rudiments unlike in wild-type mice
• distal forelimb structures are agenetic and replaced with irregular cartilaginous structure
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• no chondrogenic and osteogenic differentiation occurs in the humerus
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• forelimbs are severely truncated
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• severely truncated and fail to form bone
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• hindlimbs are severely truncated
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• at E12.5, mice display limb outgrowth abnormalities
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• at E14.5 and E16.5, the abdominal cavity is open unlike in wild-type mice
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• at E14.5 and E16.5, the thoracic cavity is open unlike in wild-type mice
• the thoracic basket fails to form
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• at E14.5 and E16.5
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• at E14.5 and E16.5
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• at E14.5 and E16.5
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• at E16.5, mineralization is observed in the hind skull unlike in wild-type mice
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• at E12.5
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• at E14.5 and at E16.5, mice develop large skin blisters especially on dorso-lumbar regions unlike in wild-type mice
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• osteoblastogenesis in the proximal ribs is enhanced
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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 | |
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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