Background/Aims: In the carcinogenic process, several markers have been defined as an evidence of genetic damage. The ras gene fami]y is one of these markers. Point mutation of a certain area of ras gene may represent the specific target of certain carcinogen. To elucidate the mechanism of ras gene activation in gastric carcinogenesis, we conducted this study. The goal of this study was to detect the frequency of K-ras, and H-ras point mutation in Korean gastric carcinoma patients. Methods: Experimental specimens were taken by gastrofiberscopic biopsy from 29 gastric cancer patients and DNA was extracted from the specimen. Intact genomic DNA was extracted from 17 cases and PCR was done with each pair of primers for K-ras 12th and 13th codon, 61st codon, H-ras 12th and 13th codon, 61st codon. These PCR products were selectively hybridized with detecting probes of various mutation. Results: One point mutation was found at K-ras 12th, 13th codon where glycine was substituted by aspartic acid. No other mutation was found at K-ras 6ist, H-ras 12th, 13th and H-ras 61st codon. The patient who showed mutation at K-ras codon 12 was confirmed as moderately differentiated adenocarcinoma. Conclusions: Point mutation of ras gene might be related in gastric carcinoma of the Koreans. In near future, studies for detection of ras gene mutation need to be done in a larger scale in precancerous lesions, and early, advanced and metastatic gastric cancers according to cell differentiation. (Korean J Gastroenterol 1996; 28:151 - 163)