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Publication : Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context.

First Author  Guerra C Year  2003
Journal  Cancer Cell Volume  4
Issue  2 Pages  111-20
PubMed ID  12957286 Mgi Jnum  J:86101
Mgi Id  MGI:2678676 Doi  10.1016/s1535-6108(03)00191-0
Citation  Guerra C, et al. (2003) Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context. Cancer Cell 4(2):111-20
abstractText  We have targeted a K-ras allele in mouse embryonic stem (ES) cells to express a K-Ras(V12) oncoprotein along with a marker protein (beta-geo) from a single bicistronic transcript. Expression of this oncogenic allele requires removal of a knocked in STOP transcriptional cassette by Cre recombinase. Primary mouse embryonic fibroblasts expressing this K-ras(V12) allele do not undergo proliferative senescence and proliferate as immortal cells. In mice, expression of K-ras(V12) throughout the body fails to induce unscheduled proliferation or other growth abnormalities for up to eight months. Only a percentage of K-ras(V12)-expressing lung bronchiolo-alveolar cells undergo malignant transformation leading to the formation of multiple adenomas and adenocarcinomas. These results indicate that neoplastic growth induced by an endogenous K-ras oncogene depends upon cellular context.
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