Guerra, CarmenMijimolle, NievesDhawahir, AlmaDubus, PierreBarradas, MartaSerrano, ManuelCampuzano Uceda, María VictoriaBarbacid, Mariano2016-02-182016-02-182003Guerra C, Mijimolle N, Dhawahir A, Dubus P, Barradas M, Serrano M et al. Tumor induction by an endogenous K-ras oncogene is highly dependent on cellular context. Cancer cell. 2003; 4(2): 111-120. DOI 10.1016/S1535-6108(03)00191-01535-6108http://hdl.handle.net/10230/25890We 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 contextapplication/pdfeng© Elsevier. This is the published version of an article http://dx.doi.org/10.1016/S1535-6108(03)00191-0 that appeared in the journal Cancer cell. It is published in an Open Archive under an Elsevier user license. Details of this licence are available here: http://www.elsevier.com/about/open-access/open-access-policies/oa-license-policy/elsevier-user-licenseProteïnesCèl·lules -- Divisióinfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1016/S1535-6108(03)00191-0info:eu-repo/semantics/openAccess