Hepatocellular carcinoma tissues from HBsAg-negative patients with chronic alcoholic liver disease were investigated for the presence of hepatitis B virus DNA. Southern blot analyses of DNA extracted from the hepatocellular carcinomas were negative for hepatitis B virus DNA in all 17 patients examined, at a level of sensitivity of less than 0.01 genome equivalent per cell. Similarly, in liver tissues from another 30 patients with alcoholic cirrhosis without hepatocellular carcinoma, no hepatitis B virus DNA was detectable. We conclude that in our patients there is no molecular evidence for a contribution of hepatitis B virus infection to the development of hepatocellular carcinoma in alcoholic liver disease.
Epidemiologic evidence indicates that hepatitis B virus (HBV) infection is associated with a high risk for the development of hepatocellular carcinoma (HCC) (1-3). Furthermore, molecular hybridization analyses identified HBV DNA integrated into the cellular genome of most HCC tissues from HBV carriers (3-6). HBV DNA was also detected in patients with chronic HBsAg-negative liver disease, including alcoholic cirrhosis and HCC (7, 8). These findings implicate HBV infection in the pathogenesis of HCCs in patients with chronic HBsAg-negative liver disease and alcoholic cirrhosis. Because of the potential significance of these findings for the molecular biologic aspects of HCCs in alcoholic liver disease, we examined liver tissues from patients with alcoholic cirrhosis with and without HCC for the presence of HBV DNA by Southern blot hybridization.
MATERIALS AND METHODS
Patients and Tissues.
With the exception of two patients from Italy and one patient from Poland, all patients were