Molecular aspects of human hepatocarcinogenesis mediated by inflammation: from hypercarcinogenic state to normo- or hypocarcinogenic state.

In spite of great efforts in the research relating to human hepatocarcinogenesis, its mechanism on the molecular level is yet to be determined. Chronic viral hepatitis may increase the chances of genetic events in hepatocytes of the host, by increasing the number of target cells or through proliferation of initiated hepatocytes, toward the eventual development of hepatocellular carcinoma. These conditions are referred to comprehensively as the 'hypercarcinogenic state'. Our goal, then, should be directed to the reversion of the 'hypercarcinogenic state' to the 'normo- or hypocarcinogenic state' so as to hopefully prevent or at least postpone the development of hepatocellular carcinoma.