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Molecular pathogenesis of hepatocellular carcinoma in hepatitis B virus transgenic mice

Academic Article
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  • Identity
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Overview

authors

  • Chisari, Francis
  • Klopchin, K.
  • Moriyama, T.
  • Pasquinelli, C.
  • Dunsford, H. A.
  • Sell, S.
  • Pinkert, C. A.
  • Brinster, R. L.
  • Palmiter, R. D.

publication date

  • December 1989

journal

  • Cell  Journal

abstract

  • Transgenic mice that overproduce the hepatitis B virus large envelope polypeptide and accumulate toxic quantities of hepatitis B surface antigen (HBsAg) within the hepatocyte develop severe, prolonged hepatocellular injury that initiates a programmed response within the liver, characterized by inflammation, regenerative hyperplasia, transcriptional deregulation, and aneuploidy. This response inexorably progresses to neoplasia. The incidence of hepatocellular carcinoma in this model corresponds to the frequency, severity, and age of onset of liver cell injury, which itself corresponds to the intrahepatic concentration of HBsAg and is influenced by genetic background and sex. Thus, the inappropriate expression of a single structural viral gene is sufficient to cause malignant transformation in this model. These results suggest that severe, prolonged cellular injury induces a preneoplastic proliferative response that fosters secondary genetic events that program the cell for unrestrained growth.

subject areas

  • Aging
  • Animals
  • Cell Line
  • Cell Transformation, Neoplastic
  • Female
  • Flow Cytometry
  • Gene Expression
  • Hepatitis B Surface Antigens
  • Hepatitis B virus
  • Liver
  • Liver Neoplasms, Experimental
  • Male
  • Mice
  • Mice, Transgenic
  • Plasmids
  • Sex Factors
  • Viral Envelope Proteins
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Identity

International Standard Serial Number (ISSN)

  • 0092-8674

Digital Object Identifier (DOI)

  • 10.1016/0092-8674(89)90770-8

PubMed ID

  • 2598264
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Additional Document Info

start page

  • 1145

end page

  • 1156

volume

  • 59

issue

  • 6

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