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oai:repisalud.isciii.es:20.500.12105/230912024-11-29T13:45:03Zcom_20.500.12105_2173com_20.500.12105_2051col_20.500.12105_19597

00925njm 22002777a 4500 dc Guerra, Carmen author Mijimolle, Nieves author Dhawahir, Alma author Dubus, Pierre author Barradas, Marta author Serrano, Manuel author Campuzano, Victoria author Barbacid, Mariano author 2003-08 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. Cancer Cell . 2003 ;4(2):111-20 1535-6108 https://hdl.handle.net/20.500.12105/23091 12957286 10.1016/s1535-6108(03)00191-0 Cancer cell Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context.