Tumorigenesis in Mlh1 and Mlh1/Apc1638N mutant mice.
作者： Raju Kucherlapati , Mari Kuraguchi , Winfried Edelmann , Marie Lia , Kunhua Fan
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摘要: MutL homologue 1 (MLH1) is a member of the family proteins required for DNA mismatch repair. Germ-line mutations in MLH1 lead to cancer susceptibility syndrome hereditary nonpolyposis colorectal (HNPCC). We generated mice carrying null mutation Mlh1 gene. showed that heterozygous and homozygous gene are predisposed developing tumors gastrointestinal (GI) tract, lymphomas, number other tumor types. also examined role adenomatous polyposis coli (Apc) GI mutant by different methods express little or no protein. When an Apc was bred into mice, incidence increased 40–100-fold. The wild-type allele these found contain mutations. Together, results show we have developed two mouse models human HNPCC mechanisms development tract involve loss function manner very similar seen HNPCC.
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