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Role of H‐ras gene in chronic liver damage in mice. By using transgenic mice carrying a human c‐H‐ras proto‐oncogene without mutations
Author(s) -
Tsunematsu Satoshi,
Saito Hidetsugu,
Sato Reiko,
Morizane Toshio,
Ishii Hiromasa
Publication year - 1997
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549700202771
Subject(s) - carbon tetrachloride , oncogene , genetically modified mouse , transgene , gene , ccl4 , hepatocellular carcinoma , biology , cancer research , microbiology and biotechnology , chemistry , biochemistry , cell cycle , organic chemistry
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.