Parallel epigenetic and genetic changes in the pathogenesis of hepatitis virus-associated hepatocellular carcinoma.
Hepatocellular carcinoma (HCC) is one of the most frequent tumor types in the world, with short survival times and few treatment options. Hepatitis B virus (HBV) and hepatitis C virus (HCV) are major etiologic agents of HCC, although the associated mechanisms are incompletely understood. The available evidence suggests that both viruses promote tumorigenesis by up-regulating genes that promote hepatocellular growth and survival, and by down-regulating other genes that act as tumor suppressors and negative growth regulatory molecules. Significantly, a number of the pathways that are altered by these viruses are the same ones that accumulate genetic alterations during tumor progression. This suggests that the pathways that promote virus persistence and replication may also promote cell growth and survival. From the perspective of the virus, this promotes chronic infection, while from the perspective of the host, this promotes tumorigenesis.
Feitelson
Mark A
MA
Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Room 222 Alumni Hall, 1020 Locust Street, Philadelphia, PA 19107, USA. mark.feitelson@jefferson.edu
D006528:Carcinoma, Hepatocellular / Q000235:genetics* / Q000821:virology; D044127:Epigenesis, Genetic; D016174:Hepacivirus / Q000472:pathogenicity; D006515:Hepatitis B virus / Q000472:pathogenicity; D019694:Hepatitis B, Chronic / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000235:genetics*; D006801:Humans; D008113:Liver Neoplasms / Q000235:genetics* / Q000821:virology