The past year was not a vintage year for advances in knowledge of malignant hepatic tumors. Nevertheless, important information, especially concerning the pathogenesis of hepatocellular carcinoma, did emerge and indicates new direction for research into hepatocarcinogenesis. Most exciting was the demonstration of a specific mutation of the putative tumor-suppressor gene,p53, in hepatocellular carcinomas from patients living in geographic regions where aflatoxin B1 is a risk factor, and of the carcinogenic potential of the hepatitis B virus X gene protein. An accurate assessment of the closeness of the association between hepatitis C virus infection and hepatocellular carcinoma in different populations awaits the determination of what proportion of the positive serum results for antibody to hepatitis C are false-positive. The interaction, if any, between hepatitis B and C viruses in the pathogenesis of hepatocellular carcinoma, and the mechanism whereby hepatitis C virus might induce malignant transformation of hepatocytes, remain uncertain. The cost effectiveness of surveillance programs designed to detect presymptomatic, resectable hepatocellular carcinomas is still being debated. Reports in the literature during the past year have not helped in resolving this issue because they contained data that supported both sides of the argument. No convincing evidence has yet emerged that either intravenous infusion of newer cytotoxic drugs, alone or in various combinations, or infusion of these drugs into the hepatic artery, with or without lipiodol targeting, or transcatheter hepatic artery embolization or chemoembolization, or hormonal manipulation have a positive effect on survival of patients with hepatocellular carcinoma.
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