Spontaneous Intestinal Carcinomas and Skin Neoplasms in /Vfs7?2-deficient Mice1
نویسندگان
چکیده
Hereditary nonpolyposis colorectal cancer is associated with defects in DNA mismatch repair. Here, we characterize tumor susceptibility of the recently described AfsA2-deficient mouse model. Within the first year of observation, all homozygous mice succumbed to disease, with lymphomas observed in at least 80% of the cases. The majority (70%) of animals 6 months or older developed intestinal neoplasms associated with APC inactivation. Microsatellite instability was more common in carcinomas than in adenomas, but uncommon in normal tissues. Some animals (7%) developed a variety of skin neoplasms analogous to the Muir-Torre syn drome. Msh2~'~ mice implicate a direct role for mismatch repair in several neoplasms with striking phenotypic similarities to humans.
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Enhanced Intestinal Adenomatous Polyp Formation in Pms2 ' ;Min Mice1
Analysis of two human familial cancer syndromes, hereditary nonpol yposis colorectal cancer and familial adenomatous polyposis, indicates that mutations in either one of four DNA mismatch repair gene homo logues or the adenomatous polyposis coli (APC) gene, respectively, are important for the development of colorectal cancer. To further investigate the role of DNA mismatch repair in intestinal ...
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