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Strong, sustained hepatocellular proliferation precedes hepatocarcinogenesis in hepatitis-B surface-antigen transgenic mice

Academic Article
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Overview

authors

  • Huang, S. N.
  • Chisari, Francis

publication date

  • March 1995

journal

  • Hepatology  Journal

abstract

  • Hepatocyte turnover rates were studied in two lineages of transgenic mice that overproduce the hepatitis B virus (HBV) large envelope protein and retain filamentous hepatitis B surface antigen (HBsAg) particles in the endoplasmic reticulum, resulting in the formation of ground glass hepatocytes. The high producer lineage (50-4) develops a necroinflammatory liver disease that progresses to hepatocellular carcinoma (HCC), whereas the low producer lineage (107-5) displays no histopathologic changes other than ground glass hepatocytes. Bromodeoxyuridine (BrdU)-labeling studies of S-phase hepatocytes provide quantitative evidence for a strong, sustained proliferative response in the hepatocytes in lineage 50-4 that occurs after the onset of hepatocellular injury but long before the development of liver cell tumors. In contrast, the level of hepatocellular proliferation in lineage 107-5 is the same as nontransgenic controls. The findings support the concept that sustained hepatocellular proliferation plays an important role in the development of hepatocellular carcinoma (HCC).

subject areas

  • Animals
  • Cell Division
  • Hepatitis B Surface Antigens
  • Hepatitis B virus
  • Hepatitis, Animal
  • Liver
  • Liver Neoplasms, Experimental
  • Mice
  • Mice, Transgenic
  • S Phase
  • Tumor Cells, Cultured
  • Viral Envelope Proteins
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Identity

International Standard Serial Number (ISSN)

  • 0270-9139

Digital Object Identifier (DOI)

  • 10.1016/0270-9139(95)90508-1

PubMed ID

  • 7875658
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Additional Document Info

start page

  • 620

end page

  • 626

volume

  • 21

issue

  • 3

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