Yang K, Edelmann W, Fan K, Lau K, Leung D, Newmark H, Kucherlapati R, Lipkin M
Strang Cancer Prevention Center and The New York Hospital-Cornell Medical Center, New York 10021, USA.
Cancer Res. 1998 Dec 15;58(24):5713-7.
Familial adenomatous polyposis (FAP) is caused by a dominant mutation in the adenomatous polyposis coli (APC) gene. Individuals with FAP progressively develop adenomas and carcinomas of the colon and rectum. We developed a mouse model for this disorder by genetically modifying the Apc gene. The resulting mice Apc1638 progressively develop neoplasms in the colon and remainder of the gastrointestinal tract. In this study when Apc1638 mice were fed a Western-style diet, they developed an increased incidence of the end point of carcinomas and number of invasive tumors. The findings therefore demonstrated dietary modulation of carcinoma incidence in mice with a targeted mutation providing a model for the study of gene-environment interactions in cancer.
家族性腺瘤性息肉病（FAP）由腺瘤性息肉病 coli（APC）基因的显性突变引起。患有 FAP 的个体逐渐发展为结肠和直肠的腺瘤和癌。我们通过对 Apc 基因进行基因改造，为这种疾病建立了一个小鼠模型。产生的 Apc1638 小鼠在结肠和胃肠道其余部分逐渐发展为肿瘤。在本研究中，当给 Apc1638 小鼠喂食西式饮食时，它们患癌终点的发生率和侵袭性肿瘤的数量增加。因此，这些发现证明了饮食对具有靶向突变的小鼠癌症发生率的调节作用，为研究癌症中的基因-环境相互作用提供了一个模型。
