Cholangiocarcinomas in japanese and thai patients: Difference in etiology and incidence of point mutation of the c‐KI‐<i>ras</i> proto‐oncogene

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<jats:title>Abstract</jats:title><jats:p>Point‐mutational activation of the c‐Ki‐<jats:italic>ras</jats:italic> proto‐oncogene has been shown to be rare in human hepatocellular carcinoma, the most common primary liver cancer and one usually associated with chronic viral infection. To reveal the association of c‐Ki‐<jats:italic>ras</jats:italic> activation with cholangiocarcinogenesis under different etiological backgrounds, the incidence of point mutation at codons 12 and 13 of the c‐Ki‐<jats:italic>ras</jats:italic> proto‐oncogene was examined in three groups of human liver cancers with differentiation to biliary epithelial cells: Group 1, cholangiocellular carcinoma in Japanese with normal livers; Group 2, cholangiocellular carcinoma in Thais who had lived in an area where the liver fluke <jats:italic>Opisthorchis viverrini</jats:italic> is endemic; and Group 3, combined hepatocellular‐cholangiocellular carcinoma, a rare type showing features of both hepatocellular and biliary epithelial differentiation, in Japanese with chronic viral hepatitis with or without cirrhosis. The polymerase chain reaction and direct sequencing of its product were used to detect the mutation. Point mutation at codon 12 of the c‐Ki‐<jats:italic>ras</jats:italic> gene was detected in five (56%) of nine cases in Group 1. In contrast, the mutation was not detected in any of the cases in Groups 2 and 3. Therefore, point‐mutational activation of c‐Ki‐<jats:italic>ras</jats:italic> did not seem to be involved in the development of primary liver cancers associated with apparent chronic irritation of liver cells or biliary epithelial cells caused by exogenous liver‐fluke or viral infection. On the other hand, point‐mutational activation of the c‐Ki‐<jats:italic>ras</jats:italic> proto‐oncogene may be involved in cholangiocarcinogenesis in liver without preexisting liver‐fluke or viral infection. © 1992 Wiley‐Liss, Inc.</jats:p>

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