Miki Y, Nishisho I, Miyoshi Y, Nakamura Y
Dept. of Biochemistry, Cancer Institute.
Gan To Kagaku Ryoho. 1991 Apr;18(4):515-21.
This report reviewed recent remarkable progresses on the cytomolecular mechanisms in colorectal carcinogenesis. Colorectal carcinoma is a good model for the study of multi-step progression, because we can obtain adenomatous polyps which are considered as a precancerous form. Furthermore, a familial syndrome, which is characterized by numerous adenomas of the colon, is available for linkage analysis. Recently, the p53 and DCC genes have been identified as candidate tumor suppressor genes on chromosome 17p and 18q respectively. In this paper, we present the multiple genetic alterations in colorectal carcinoma, including activation of K-ras gene and inactivation of tumor suppressor gene such as p53 and DCC genes as well as loss of heterozygosity and approach to the gene responsible for adenomatous polyposis coli by reverse genetics.
本报告回顾了近年来结直肠癌发生的细胞分子机制方面的显著进展。结直肠癌是研究多步骤进展的良好模型，因为我们可以获得被视为癌前形式的腺瘤性息肉。此外，一种以结肠大量腺瘤为特征的家族性综合征可用于连锁分析。最近，p53和DCC基因已分别被确定为17号染色体短臂和18号染色体长臂上的候选抑癌基因。在本文中，我们介绍了结直肠癌中的多种基因改变，包括K-ras基因的激活、p53和DCC等抑癌基因的失活以及杂合性缺失，以及通过反向遗传学方法寻找与腺瘤性息肉病相关的基因。
