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Genetics of Hepatocarcinogenesis in Mouse and Man

  • Tommaso A. Dragani
  • Giacomo Manenti
  • Manuela Gariboldi
  • F. Stefania Falvella
  • Marco A. Pierotti
  • Giuseppe Della Porta
Part of the NATO ASI Series book series (NSSA, volume 232)

Abstract

Mice genetically susceptible to hepatocarcinogenesis carry a germ-line genetic alteration, which has liver-specific effects. It should be considered as an initial step in the multistage process of hepatocarcinogenesis. Any other step could add to the genetic alteration, resulting in a high susceptibility to spontaneous and carcinogen induced liver tumorigenesis. A quantitative evaluation of carcinogen-induced liver tumors showed that the genetic alteration controls liver tumor growth, but not liver tumor frequency. Our recent observations indicate that Ha-ras gene mutations at codon 61 are frequently involved in the pathogenesis of liver tumors in mice genetically susceptible to hepatocarcinogenesis, but not in genetically resistant mice. Some rare human genetic syndromes are characterized by a high predisposition to hepatocellular carcinoma development, through the prior induction of cirrhosis. However, these syndromes do not represent the human counterparts of the genetic alterations responsible for their high susceptibility to hepatocarcinogenesis of the C3H and of the CBA mouse strains.

Keywords

Liver Tumor Glycogen Storage Disease Glycogen Storage Disease Type Porphyria Cutanea Tarda Resistant Mouse 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1992

Authors and Affiliations

  • Tommaso A. Dragani
    • 1
  • Giacomo Manenti
    • 1
  • Manuela Gariboldi
    • 1
  • F. Stefania Falvella
    • 1
  • Marco A. Pierotti
    • 1
  • Giuseppe Della Porta
    • 1
  1. 1.Division of Experimental Oncology AIstituto Nazionale TumoriMilanItaly

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