| Autor: |
Fedorov LM; Institut für Medizinische Strahlenkunde und Zellforschung, Bayerische Julius-Maximilians-Universität, D-97078 Würzburg, Germany., Tyrsin OY, Papadopoulos T, Camarero G, Götz R, Rapp UR |
| Jazyk: |
angličtina |
| Zdroj: |
Cancer research [Cancer Res] 2002 Nov 01; Vol. 62 (21), pp. 6297-303. |
| Abstrakt: |
The efficiency of tumor induction by oncogenes is influenced by modifier genes that determine individual susceptibility. We have used a transgenic mouse model to examine the role of a candidate susceptibility gene, bcl-2, for development of Raf oncogene-induced lung adenomas. Loss of bcl-2 greatly retarded tumor development without affecting tumor phenotype. Tumor tissues from bcl-2 positive and negative mice were compared for the fraction of S phase cells by staining for proliferating cell nuclear antigen and for the fraction of apoptotic cells by terminal deoxynucleotidyl transferase-mediated nick end labeling assay. The data indicate that the increased tumor latency in the absence of bcl-2 results primarily from an increased apoptotic rate but also involves a decrease in tumor cell proliferation. Both effects can be rescued by breeding with H2K-bcl-2 transgenic mice demonstrating that loss of bcl-2 was the major genetic factor determining tumor resistance. These findings suggest that bcl-2 is a major susceptibility gene for development of lung cancer in mice and perhaps in humans. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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