A targeted chain-termination mutation in the mouse Apc gene results in multiple intestinal tumors

摘要: Germ-line mutations in the human adenomatous polyposis coli (APC) gene result familial polyposis, an autosomal dominant disorder characterized by early onset of multiple polyps large bowel with a high likelihood developing colorectal carcinomas. To understand role APC intestinal tumor formation, we have introduced chain-termination mutation 15th exon mouse Apc and employed it to modify endogenous homologous recombination embryonic stem cells. Mice which are heterozygous for modification progressively develop tumors manner that is similar observed patients mice carry called neoplasia (Min). Our results indicate critical event initiation formation predisposition toward development spontaneous colonic mice.