作者: Joerg Heyer , Kan Yang , Martin Lipkin , Winfried Edelmann , Raju Kucherlapati
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摘要: Colorectal cancer (CRC) is one of the most common cancers in Western world. Much has been learned about colorectal from human inherited syndromes, such as familial adenomatous polyposis (FAP) and hereditary non-polyposis (HNPCC). Mouse models for CRC were generated by introducing mutations into mouse genes, whose counterparts implicated onset progression CRC. Central among these are mice carrying Adenomatous coli (Apc) gene. Although Apc share some phenotypes homozygous embryonic lethality tumor predisposition, severity predisposition variable. Mice with mismatch repair Msh2 Mlh1, exhibit a defect predisposed to developing gastrointestinal cancer, lymphomas tumors other organ systems. mutation Pms2 gene tumors. Msh6 have base show phenotype. Msh5 defects meiosis suggesting unique roles genes gametogenesis.