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PMID:9453487
| Citation |
Smits, R, van der Houven van Oordt, W, Luz, A, Zurcher, C, Jagmohan-Changur, S, Breukel, C, Khan, PM and Fodde, R (1998) Apc1638N: a mouse model for familial adenomatous polyposis-associated desmoid tumors and cutaneous cysts. Gastroenterology 114:275-83 |
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| Abstract |
Germline mutations in the adenomatous polyposis coli (APC) gene are responsible for familial adenomatous polyposis (FAP), an autosomal dominant predisposition to the formation of multiple colorectal adenomas. Moreover, patients with FAP are at high risk of developing several extracolonic manifestations, including desmoids, cutaneous cysts, and tumors of the upper gastrointestinal tract. Although by definition desmoids are nonmalignant, because of their aggressive invasion of local structures, they represent one of the major causes of morbidity and mortality among patients with FAP. |
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| Keywords |
Adenomatous Polyposis Coli/complications; Adenomatous Polyposis Coli/genetics; Age of Onset; Animals; Cysts/etiology; Cysts/pathology; Disease Models, Animal; Female; Fibromatosis, Aggressive/etiology; Fibromatosis, Aggressive/pathology; Genes, APC/genetics; Genes, p53/genetics; Loss of Heterozygosity; Male; Mice; Mice, Inbred A; Mice, Inbred C3H; Mice, Inbred C57BL; Mutation/physiology; Neoplasms, Multiple Primary/complications; Phenotype; Sex Distribution; Skin Diseases/etiology; Skin Diseases/pathology |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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See also
References
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