Role of H-ras gene in chronic liver damage in mice, by using transgenic mice carrying a human c-H-ras protogene without mutations

Satoshi Tsunematsu, Hidetsugu Saito, Reiko Sato, Toshio Morizane, Hiromasa Ishii

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Hepatic tumors including hepatocellular carcinoma were generated by carbon tetrachloride in transgenic mice carrying a human c-H-ras gene (rasH2 mice). RasH2 mice express 2 to 3 times more ras protein (ras p21) in the liver than do non-Tg mice. When carbon tetrachloride was administered, the rasH2 mice produced about 5 times as many hepatic tumors than did the non-transgenic mice. However, neither the 10-100 times higher ras p21 expression required for murine fibroblast transformation by itself nor the mutational activation of the H-ras gene was observed in carbon tetrachloride-induced hepatic tumors. These results show that H-ras proto-oncogene expression in the murine liver, even if it is not high enough to transform cells, also causes liver tumors when CCl4 are repeatedly given.

Original languageEnglish
Pages (from-to)371-379
Number of pages9
JournalBiochemistry and Molecular Biology International
Volume42
Issue number2
Publication statusPublished - 1997 Jun 1

Keywords

  • H-ras
  • Hepatocellular caricmona
  • Neoplastic nodule
  • Over expression
  • Point mutation

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Genetics

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