Guerra, CarmenMijimolle, NievesDhawahir, AlmaDubus, PierreBarradas, MartaSerrano, ManuelCampuzano, VictoriaBarbacid, Mariano2024-09-162024-09-162003-08Cancer Cell . 2003 ;4(2):111-201535-6108https://hdl.handle.net/20.500.12105/23091We 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.engVoRhttp://creativecommons.org/licenses/by-nc-nd/4.0/Cell Transformation, NeoplasticProtein Serine-Threonine KinasesAnimalsCell DivisionCell Line, TransformedCellular SenescenceChromosome AberrationsCyclin-Dependent Kinase Inhibitor p16FibroblastsGene TargetingGenes, rasGenetic VectorsMAP Kinase Signaling SystemMiceMice, TransgenicNeoplasmsOncogene Protein p21(ras)Proto-Oncogene ProteinsProto-Oncogene Proteins c-aktReverse Transcriptase Polymerase Chain ReactionStem CellsSurvival RateTumor Suppressor Protein p14ARFTumor Suppressor Protein p53Attribution-NonCommercial-NoDerivatives 4.0 Internacional129572864211110.1016/s1535-6108(03)00191-0Cancer cellopen access