APC(MIN) - A MOUSE MODEL FOR INTESTINAL AND MAMMARY TUMORIGENESIS

被引:242
作者
MOSER, AR
LUONGO, C
GOULD, KA
MCNELEY, MK
SHOEMAKER, AR
DOVE, WF
机构
[1] UNIV WISCONSIN,MCARDLE LAB,MADISON,WI 53706
[2] UNIV WISCONSIN,GENET LAB,MADISON,WI 53706
关键词
MIN (MULTIPLE INTESTINAL NEOPLASIA); APC (ADENOMATOUS POLYPOSIS COLI); MOUSE; INTESTINAL ADENOMAS; MAMMARY TUMORS; ANIMAL MODEL;
D O I
10.1016/0959-8049(95)00181-H
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Min (multiple intestinal neoplasia) is a mutant allele of the murine Ape (adenomatous polyposis coli) locus, encoding a nonsense mutation at codon 850. Like humans with germline mutations in APC, Min/+ mice are predisposed to intestinal adenoma formation. The number of adenomas is influenced by modifier loci carried by different inbred strains. One modifier locus, Mom-1 (modifier of Min-1), maps to distal chromosome 4. Intestinal tumours from both B6 (C57BL/6J) and hybrid Min/+ mice show extensive loss of the wild-type allele at Ape. B6 Min/+ female mice are predisposed to spontaneous mammary tumours. The incidence of both intestinal and mammary tumours can be increased in an age-specific manner by treatment with ethylnitrosourea (ENU). Min mice provide a good animal model for studying the role of Ape and interacting genes in the initiation and progression of intestinal and mammary tumorigenesis.
引用
收藏
页码:1061 / 1064
页数:4
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