Dietary modulation of carcinoma development in a mouse model for human familial adenomatous polyposis.
Dietary modulation of carcinoma development in a mouse model for human familial adenomatous polyposis.
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发表时间：
1998-12
期刊：
影响因子：
11.2
通讯作者：
Kang Yang;W. Edelmann;K. Fan;K. Lau;D. Leung;H. Newmark;R. Kucherlapati;M. Lipkin
中科院分区：
文献类型：
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作者：
Kang Yang;W. Edelmann;K. Fan;K. Lau;D. Leung;H. Newmark;R. Kucherlapati;M. Lipkin
家族性腺瘤性息肉病（FAP）是由大肠腺瘤性息肉病（APC）基因的显性突变引起的。患有FAP的个体逐渐发展为结肠和直肠的腺瘤和癌。我们通过遗传修饰Apc基因开发了这种疾病的小鼠模型。产生的小鼠Apc 1638在结肠和胃肠道的其余部分中逐渐发展肿瘤。在这项研究中，当Apc 1638小鼠喂食西式饮食时，它们的癌症终点发生率和侵袭性肿瘤数量增加。因此，这些发现证明了饮食调节具有靶向突变的小鼠的癌症发病率，为研究癌症中的基因-环境相互作用提供了模型。
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.