The sequential development of cirrhosis and hepatocellular carcinoma (HCC) in patients with post-transfusion hepatitis was a clue that led to the identification of hepatitis C virus (HCV) as a risk factor for HCC. The average time lag between transfusion-associated infection and cancer development was 30 years, with a range of 15-45 years. Using the polymerase chain reaction (PCR) technique, HCV-RNA has been almost invariably detected in serum and tumor tissue of anti-HCV-seropositive patients with HCC In many patients, HCV-RNA was found to belong to the more pathogenic type 1b. However, it is unlikely that HCV plays a direct role in liver tumorigenesis, since no reverse transcriptase activity has been found in infected livers. One current opinion is that HCV may promote cancer through cirrhosis, which is per se an important risk factor for this tumor: almost all patients with HCC have cirrhosis and up to 30% of them have coexisting serological evidence of hepatitis B virus (HBV) or alcohol abuse, further supporting the idea that both HCC and cirrhosis might result from the interplay of several risk factors. However, there are also data suggesting that HCV may interact with cellular genes regulating cell growth and differentiation independently of the onset of cirrhosis.
|Number of pages||8|
|Journal||Recent results in cancer research. Fortschritte der Krebsforschung. Progres dans les recherches sur le cancer|
|Publication status||Published - 1998|