Spontaneous intestinal carcinomas and skin neoplasms in Msh2-deficient mice.

作者：Armin H. Reitmair, Mark S. Redston, Jian Cai, Tony Chih-Yuan Chuang, Matthew Bjerknes, Hazel Cheng, Kazy Hay, Steven Gallinger, Bharati V. Bapat, Tak W. Mak · 发表于：PubMed · 年份：1996 · 被引用次数：166 · 研究领域：Genetic factors in colorectal cancer、Cancer Genomics and Diagnostics、Colorectal Cancer Treatments and Studies

Hereditary nonpolyposis colorectal cancer is associated with defects in DNA mismatch repair. Here, we characterize tumor susceptibility of the recently described Msh2-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 syndrome. Msh2-/- mice implicate a direct role for mismatch repair in several neoplasms with striking phenotypic similarities to humans.