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. 2003 Aug;4(2):111-20.
doi: 10.1016/s1535-6108(03)00191-0.

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

Carmen Guerra  1 , Nieves Mijimolle, Alma Dhawahir, Pierre Dubus, Marta Barradas, Manuel Serrano, Victoria Campuzano, Mariano Barbacid
Affiliations
Free article

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

Carmen Guerra et al. Cancer Cell. 2003 Aug.
Free article

Abstract

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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