M. Kojima et al., KI-RAS POINT MUTATION IN DIFFERENT TYPES OF COLORECTAL CARCINOMAS IN EARLY STAGES, Diseases of the colon & rectum, 40(2), 1997, pp. 161-167
PURPOSE: The aim of this study was to elucidate pathways of carcinogen
esis in the colon and rectum by investigating Ki-ras point mutation in
different types of colorectal carcinomas in the early stage. METHODS:
We analyzed rates of Ki-ras codon 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). RESULTS: Frequency of
Ki-ras mutations in superficial-type carcinomas was 14.3 percent (3/21
), which nas significantly lower than 50 percent (17/34) in small poly
poid carcinomas and 40.5 percent (17/42) in advanced carcinomas. These
data suggest that another pathway of colorectal carcinogenesis that d
oes not involve Ki-ras point mutation might exist. Among the 17 small
polypoid carcinomas with Ki-ras point mutation in which both adenomato
us 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 adenoma
tous tissue; in the other three cases, Ki-ras point mutation was prese
nt only in adenomatous tissue but not in carcinomatous tissue. CONCLUS
IONS: These data suggest that carcinoma in a small polypoid lesion doe
s not always develop from pre-existing adenoma with Ki-ras point mutat
ion; in a small number of the polypoid-type early carcinomas, polyclon
al composition concerning the Ki-ras gene may exist.