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World J Gastroenterol. Sep 21, 2014; 20(35): 12367-12371
Published online Sep 21, 2014. doi: 10.3748/wjg.v20.i35.12367
Published online Sep 21, 2014. doi: 10.3748/wjg.v20.i35.12367
Hepatitis C-associated liver carcinogenesis: Role of PML nuclear bodies
Kerstin Herzer, Guido Gerken, Department for Gastroenterology and Hepatology, University Hospital Essen, 45122 Essen, Germany
Kerstin Herzer, Department of General-, Visceral- und Transplantation Surgery, University Hospital Essen, 45122 Essen, Germany
Thomas G Hofmann, Cellular Senescence Group, DKFZ-ZMBH Alliance, Deutsches Krebsforschungszentrum (dkfz.), 69120 Heidelberg, Germany
Author contributions: Herzer K and Hofmann TG designed and wrote the manuscript; Gerken G contributed in supplementing the manuscript.
Correspondence to: Kerstin Herzer, MD, Department for Gastroenterology and Hepatology, University Hospital Essen, Hufeland str. 55, 45122 Essen, Germany. kerstin.herzer@uk-essen.de
Telephone: +49-201-7236579 Fax: +49-201-7236926
Received: November 14, 2013
Revised: December 31, 2013
Accepted: July 24, 2014
Published online: September 21, 2014
Revised: December 31, 2013
Accepted: July 24, 2014
Published online: September 21, 2014
Core Tip
Core tip: Escape from immune response and non-responsiveness to interferon-therapy are frequently observed in hepatitis C virus (HCV) infection. HCV infection leads to severe liver disease like cirrhosis and hepatocellular carcinoma and is the major cause for hepatocellular carcinoma and liver transplantation in the western world. Interestingly, HCV interferes with tumor suppressor promyelocytic leukemia (PML) function in apoptosis. PML localises to multi-protein complexes termed nuclear bodies (NBs). The number and the size of PML NBs are increased upon interferon-treatment and PML NBs represent preferential targets in viral infection. Accordingly, PML plays an important role in the antiviral action of interferons.