| First Author | Diaz R | Year | 2004 |
| Journal | Carcinogenesis | Volume | 25 |
| Issue | 4 | Pages | 535-9 |
| PubMed ID | 14633661 | Mgi Jnum | J:89348 |
| Mgi Id | MGI:3039967 | Doi | 10.1093/carcin/bgh026 |
| Citation | Diaz R, et al. (2004) Complex effects of Ras proto-oncogenes in tumorigenesis. Carcinogenesis 25(4):535-9 |
| abstractText | Ras proteins have been found mutated in about one-third of human tumors. In vitro, Ras has been shown to regulate distinct and contradictory effects, such as cellular proliferation and apoptosis. Nonetheless, the effects that the wild-type protein elicits in tumorigenesis are poorly understood. Depending on the type of tissue, Ras proto-oncogenes appear to either promote or inhibit the tumor phenotype. In this report, we treated wild-type and N-ras knockout mice with 3-methylcholanthrene (MCA) to induce fibrosarcomas and found that MCA is more carcinogenic in wild-type mice than in knockout mice. After injecting different doses of a tumorigenic cell line, the wild-type mice exhibited a shorter latency of tumor development than the knockouts, indicating that there are N-ras-dependent differences in the stromal cells. Likewise, we have analyzed B-cell lymphomas induced by either N-methylnitrosourea or by the N-ras oncogene in mice that over-express the N-ras proto-oncogene and found that the over-expression of wild-type N-ras is able to increase the incidence of these lymphomas. Considered together, our results indicate that Ras proto-oncogenes can enhance or inhibit the malignant phenotype in vivo in different systems. |
