ApcMin: A mouse model for intestinal and mammary tumorigenesis

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

Research output: Contribution to journalArticlepeer-review

185 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)1061-1064
Number of pages4
JournalEuropean Journal of Cancer
Volume31
Issue number7-8
DOIs
StatePublished - 1995
Externally publishedYes

Keywords

  • Apc (adenomatous polyposis coli)
  • Min (multiple intestinal neoplasia)
  • animal model
  • intestinal adenomas
  • mammary tumours
  • mouse

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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