MOLECULAR PATHOGENESIS OF HEPATOCELLULAR CARCINOMA
Metodieva SN
*Corresponding Author: Corresponding Author: S. Nikolova Metodieva, Department of Medical Genetics, Medical Faculty, Medical University Sofia, 2 Zdrave str., 1413, Sofia, Bulgaria; Tel/Fax: + 359-2-9520-357; E-mail: svetlana.metodieva@ yahoo.com
page: 15

Abstract

 

The most important risk factors for the development of human hepatocellular carcinoma (HCC) are chronic infec tion with hepatitis B virus (HBV) and/or hepatitis C virus (HCV), high dietary exposure to hepatic carcinogen afla toxin B1 and alcohol abuse. Hepatitis B virus exerts its effects through integration of the viral DNA into the hepa tocyte genome, or through acting as transcriptional regu lator for several cellular proto-oncogenes and tumor-sup pressor genes. Hepatitis C virus may affect hepatocytes via the transcriptional regulation activity of the HCV core protein or via the HCV non structural proteins NS5A, NS5B and NS2, interfering with the regulation of cell cycle and apoptosis. Environmental exposure to aflatoxin B1 can cause a specific missense mutation in codon 249 of the p53 tumor-suppressor gene. Habitual alcohol consump tion leads to production of reactive oxygen species and peroxidation damage to DNA. The objective of this review is to make you acquainted with the most common risk factors and the most frequent genetic aberrations associ ated with the development of HCC.

Key words: Aflatoxin; Alcohol; Hepatitis; Hepato cellular carcinoma (HCC)





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