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Chronic hepatitis B in hepatocarcinogenesis
  1. N H Park2,
  2. I H Song3,
  3. Y-H Chung1
  1. 1Division of Gastroenterology, Department of Internal Medicine, University of Ulsan, College of Medicine, Asan Medical Centre, Seoul, Korea
  2. 2Division of Gastroenterology, Department of Internal Medicine, University of Ulsan College of Medicine, Ulsan University Hospital, Ulsan
  3. 3Division of Gastroenterology, Department of Internal Medicine, Dankook University College of Medicine, Cheonan, Korea
  1. Correspondence to:
 DrY-H Chung
 Division of Gastroenterology, Department of Internal Medicine, University of Ulsan College of Medicine, Asan Medical Centre, 388-1 Pungnap-dong, Sonpa-gu, Seoul 138-736 Korea; yhchung@www.amc.seoul.kr

Abstract

Hepatocellular carcinoma (HCC) is the fifth most common cancer in the world, and has a wide geographical variation. Eighty per cent of HCC is attributed to hepatitis B virus (HBV). The predominant carcinogenic mechanism of HBV associated HCC is through the process of liver cirrhosis, but direct oncogenic effects of HBV may also contribute. Prevention of HBV infections as well as effective treatment of chronic hepatitis B is still needed for the global control of HBV associated HCC. Continued investigation of the mechanisms of hepatocarcinogenesis will refine our current understanding of the molecular and cellular basis for neoplastic transformation in the liver.

  • HCC, hepatocellular carcinoma
  • HBV, hepatitis B virus
  • CREB, cAMP response element binding protein
  • NF-κB, nuclear factor κ B
  • TNF, tumour necrosis factor
  • CDK, cyclin dependent kinase
  • VEGF, vascular endothelial growth factor
  • MMP, metalloproteinase
  • IGF, insulin growth factor
  • hepatocellular carcinoma
  • hepatitis b virus
  • hepatitis B x protein (HBx)
  • transactivation

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Footnotes

  • Funding: none.

  • Conflicts of interest: none declared.

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