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ApcMin: a mouse model for intestinal and mammary tumorigenesis.

作者信息

Moser A R, Luongo C, Gould K A, McNeley M K, Shoemaker A R, Dove W F

机构信息

McArdle Laboratory, University of Wisconsin, Madison 53706, USA.

出版信息

Eur J Cancer. 1995 Jul-Aug;31A(7-8):1061-4. doi: 10.1016/0959-8049(95)00181-h.

Abstract

Min (multiple intestinal neoplasia) is a mutant allele of the murine Apc (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 Apc. 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 Apc and interacting genes in the initiation and progression of intestinal and mammary tumorigenesis.

摘要

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