Min (multiple intestinal neoplasia) is a mutant allele of the murine A
pe (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 i
s 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 sh
ow 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 ma
nner by treatment with ethylnitrosourea (ENU). Min mice provide a good
animal model for studying the role of Ape and interacting genes in th
e initiation and progression of intestinal and mammary tumorigenesis.