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Publication : ApcMin: a mouse model for intestinal and mammary tumorigenesis.

First Author  Moser AR Year  1995
Journal  Eur J Cancer Volume  31A
Issue  7-8 Pages  1061-4
PubMed ID  7576992 Mgi Jnum  J:28572
Mgi Id  MGI:76095 Doi  10.1016/0959-8049(95)00181-h
Citation  Moser AR, et al. (1995) ApcMin: a mouse model for intestinal and mammary tumorigenesis. Eur J Cancer 31A(7-8):1061-4
abstractText  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.
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