Tumorigenesis Driven by BRAFV600E Requires Secondary Mutations that Overcome it's Feedback Inhibition of RAC1 and Migration.
Gadal S, Boyer J, Roy S, Outmezguine N, Sharma M, Li H, Fan N, Chan E, Romin Y, Barlas A, Chang Q, Pancholi P, Timaul N, Overholtzer M, Yaeger R, Manova-Todorova K, de Stanchina E, Bosenberg M, Rosen N. Tumorigenesis Driven by BRAFV600E Requires Secondary Mutations that Overcome it's Feedback Inhibition of RAC1 and Migration. Cancer Research 2025 PMID: 39992718, DOI: 10.1158/0008-5472.can-24-2220.Peer-Reviewed Original ResearchInhibition of Rac1Rac1 activationLevels of ERK activationSecondary mutationsBRAFV600E mutationInhibition of Rac1 activityMutant Rac1Cell motilityRac1ERK activationMesenchymal migrationFeedback inhibitionRestored migrationMutationsGenetically engineered mouse modelsCell proliferationSelection of lesionsTumor evolutionPTEN inactivationTumorigenesisOncogenic driversBRAFV600EMalignant transformationBenign neviMouse model
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