| First Author | Tsunematsu S | Year | 1997 |
| Journal | Biochem Mol Biol Int | Volume | 42 |
| Issue | 2 | Pages | 371-9 |
| PubMed ID | 9238536 | Mgi Jnum | J:43885 |
| Mgi Id | MGI:1099094 | Doi | 10.1080/15216549700202771 |
| Citation | Tsunematsu S, et al. (1997) 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. Biochem Mol Biol Int 42(2):371-9 |
| abstractText | 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 CC1(4) are repeatedly given. |
