Ki -ras point mutation in different types of colorectal carcinomas in early stages

Publisher Website
Google Scholar
Abstract
The aim of this study was to elucidate pathways of carcinogenesis in the colon and rectum by investigating Ki-raspoint mutation in different types of colorectal carcinomas in the early stage. We analyzed rates of Ki-rascodon 12 mutations in 34 small, polypoid-type carcinomas (Tis or T1), 21 superficial-type carcinomas (Tis or T1), and 42 advanced carcinomas (T2, T3, and T4). Frequency of Ki-rasmutations in superficial-type carcinomas was 14.3 percent (3/21), which was significantly lower than 50 percent (17/34) in small polypoid carcinomas and 40.5 percent (17/42) in advanced carcinomas. These data suggest that another pathway of colorectal carcinogenesis that does not involve Ki-raspoint mutation might exist. Among the 17 small polypoid carcinomas with Ki-raspoint mutation in which both adenomatous and carcinomatous tissue were examined, 12 showed a mutation of the same type in both carcinomatous and adenomatous tissues. In two cases, mutation was present only in carcinomatous tissue and not in adenomatous tissue; in the other three cases, Ki-raspoint mutation was present only in adenomatous tissue but not in carcinomatous tissue. These data suggest that carcinoma in a small polypoid lesion does not always develop from pre-existing adenoma with Ki-raspoint mutation; in a small number of the polypoid-type early carcinomas, polyclonal composition concerning the Ki-rasgene may exist.