HEPATOCELLULAR-CARCINOMA

The mechanisms of hepatic carcinogenesis remain a major focus of resea rch. Progress has been made in the identification of genetic changes o ccurring in premalignant liver, with evidence that dysplastic liver is neoplastic. Significantly, oncogenic changes are also present in cirr hotic liver. With respect to metabolic pathways relevant to hepatocell ular carcinoma, there is increasing emphasis on the balance between th e proliferative effects of insulinlike growth factors and the antineop lastic effects of transforming growth factor-beta. These and other stu dies are elucidating the histologic, genetic, and related metabolic st eps that are relevant to malignant transformation. Clinically, dysplas ia present on liver biopsy has been used to identify patients at incre ased risk of developing hepatocellular carcinoma. This predictive test ing has implications for the treatment of patients with compensated ci rrhosis. Additionally, there is tantalizing and controversial evidence that treatment of hepatitis C-related cirrhosis with interferon may r educe the risk of hepatocellular carcinoma.