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      • Department of Molecular Biology and Genetics
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      Genetic aspects of hepatocellular carcinogenesis

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      Author(s)
      Ozturk, M.
      Date
      1999
      Source Title
      Seminars in Liver Disease
      Print ISSN
      0272-8087
      Volume
      19
      Issue
      3
      Pages
      235 - 242
      Language
      English
      Type
      Article
      Item Usage Stats
      207
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      Abstract
      Hepatocellular carcinoma (HCC) is linked etiologically to viruses (hepatitis B virus [HBV] and hepatitis C virus [HCV]), chemical carcinogens (i.e., aflatoxins), and other environmental and host factors causing chronic liver injury. Some hepatoblastomas may be linked to inherited gene mutations, but adult hereditary HCC appears to be rare. HCCs display gross genomic alterations, including DNA rearrangements associated with HBV DNA integration, loss of heterozygosity, and, less importantly, chromosomal amplifications and loss of imprinting. Many genes with somatic mutations have now been identified in these tumors. Most frequently involved genes are tumor suppressor genes such as p53, M6P/IGF2R, β-catenin, p16INK4A, and retinoblastoma genes. Most identified mutations are somatic, but germline mutations of p16INK4A, APC, and BRCA2 have also been reported. Oncogenic activation of several cellular genes such as cyclin D and cyclin A have been described in HCC, but the possible implication of candidate viral oncogenes (i.e., X protein of HBV) is still debated. A comprehensive analysis of all the genetic changes described for HCC demonstrates that at least four different growth regulatory pathways are altered in these tumors. However, each pathway appears to be implicated in a limited fraction of these tumors, suggesting that HCCs are genetically heterogenous neoplasms. This genetic heterogeneity correlates with the heterogeneity of etiologic factors implicated in HCC.
      Keywords
      β- catenin
      Cyclin D
      Hepatocellular carcinoma
      M6P/IGF2R
      P16INK4A
      p53
      Primary liver cancer
      Aflatoxin
      Beta catenin
      Carcinogen
      Cyclin a
      Cyclin d
      Protein p53
      Gene mutation
      Hepatitis b virus
      Hepatitis c virus
      Permalink
      http://hdl.handle.net/11693/25189
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