Yanagawa Y, Sasazuki T
Dept. of Genetics, Kyushu University, Fukuoka.
Gan To Kagaku Ryoho. 1989 Sep;16(9):3093-8.
The inherited cancer disease familial polyposis coli (FPC) provides an excellent model not only for studying tumor progression in colorectal cancer but also for elucidating molecular mechanism of carcinogenesis in general. This paper reviews recent remarkable progress in the molecular mechanism of tumorigenesis in FPC. Included in this review is information on the localization of the FPC major gene and several types of genetic alterations during the development of tumors. One of these genetic alterations is activation of oncogenes such as mutated ras genes and another is inactivation of tumor suppression genes such as loss of heterozygosity. The mutated FPC gene on chromosome 5 q would be expected to be an early event to initiate the requisite hyperproliferation for adenoma formation. Adenomas will have undergone several gene or chromosome mutations before reaching the fully malignant state.
遗传性癌症疾病家族性结肠息肉病（FPC）不仅为研究结直肠癌的肿瘤进展提供了一个极好的模型，也为阐明一般致癌作用的分子机制提供了模型。本文综述了FPC肿瘤发生分子机制方面最近取得的显著进展。本综述包括FPC主要基因的定位信息以及肿瘤发生过程中的几种基因改变类型。这些基因改变之一是癌基因的激活，如ras基因的突变，另一个是肿瘤抑制基因的失活，如杂合性缺失。位于5号染色体q上的FPC基因突变预计是引发腺瘤形成所需的过度增殖的早期事件。腺瘤在达到完全恶性状态之前会经历几次基因或染色体突变。
