Abstract
We compared the tumorigenic effects of the N-ras oncogene and the N-ras proto-oncogene in lymphoid and mammary tissues in an in vivo model. For this purpose, we generated transgenic mice with high levels of N-ras oncogene or N-ras proto-oncogene expression, driven by the complete mouse mammary tumor virus LTR (MMTV-LTR) (MMTV/N-ras(T) and MMTV/N-ras(N) constructs) and transgenic mice with low levels of N-ras oncogene or N-ras proto-oncogene expression, driven by a truncated MMTV-LTR (TMTV/N-ras(T) and TMTV/N-ras(N) constructs). We show that both, the N-ras proto-oncogene and the N-ras oncogene with a C:G → A:T mutation at codon 61, lead to identical tumor types: lymphoblastic T-cell lymphomas, cleaved B-cell lymphomas and poorly differentiated mammary carcinomas. Nevertheless, there were quantitative differences in tumor incidence and latency and in transgene expression among N-ras oncogene and N-ras proto-oncogene transgenics. Despite these differences in tumor kinetics, the predisposition to identical tumor types is in agreement with the idea that the N-ras oncogene and the N-ras proto-oncogene act through the same pathway for in vivo tumorigenesis in B-cells, T-cells or mammary epithelial cells.
Original language | English (US) |
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Pages (from-to) | 1053-1063 |
Number of pages | 11 |
Journal | Oncogene |
Volume | 13 |
Issue number | 5 |
State | Published - 1996 |
Externally published | Yes |
Keywords
- Lymphomas
- Mammary tumors
- Ras pathway
- Transgenic mice
ASJC Scopus subject areas
- Molecular Biology
- Genetics
- Cancer Research