Moser A R, Luongo C, Gould K A, McNeley M K, Shoemaker A R, Dove W F
McArdle Laboratory, University of Wisconsin, Madison 53706, USA.
Eur J Cancer. 1995 Jul-Aug;31A(7-8):1061-4. doi: 10.1016/0959-8049(95)00181-h.
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.
Min（多发性肠道肿瘤）是小鼠Apc（腺瘤性息肉病 coli）基因座的一个突变等位基因，在第850密码子处编码一个无义突变。与APC发生种系突变的人类一样，Min/+小鼠易患肠道腺瘤。腺瘤的数量受不同近交系携带的修饰基因座影响。一个修饰基因座Mom-1（Min-1的修饰基因）定位于4号染色体远端。来自B6（C57BL/6J）和杂交Min/+小鼠的肠道肿瘤在Apc处均显示野生型等位基因广泛缺失。B6 Min/+雌性小鼠易患自发性乳腺肿瘤。通过用乙基亚硝基脲（ENU）处理，肠道和乳腺肿瘤的发病率均可按年龄特异性方式增加。Min小鼠为研究Apc及相互作用基因在肠道和乳腺肿瘤发生起始和进展中的作用提供了一个良好的动物模型。
