Sustained ERK inhibition maximizes responses of BrafV600E thyroid cancers to radioiodine
Nagarajah J, Le M, Knauf JA, Ferrandino G, Montero-Conde C, Pillarsetty N, Bolaender A, Irwin C, Krishnamoorthy GP, Saqcena M, Larson SM, Ho AL, Seshan V, Ishii N, Carrasco N, Rosen N, Weber WA, Fagin JA. Sustained ERK inhibition maximizes responses of BrafV600E thyroid cancers to radioiodine. Journal Of Clinical Investigation 2016, 126: 4119-4124. PMID: 27669459, PMCID: PMC5096947, DOI: 10.1172/jci89067.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SubstitutionAnimalsBenzimidazolesExtracellular Signal-Regulated MAP KinasesIodidesIodine RadioisotopesMAP Kinase Signaling SystemMiceMice, Mutant StrainsMutation, MissenseProto-Oncogene Proteins B-rafThyroid NeoplasmsConceptsThyroid cancerThyroid differentiation genesBRAF-mutant thyroid cancerIodide uptakeCancer cellsERK inhibitionERK signalingMEK inhibitor selumetinibThyroid cellsThyroid cancer cellsRAI therapyMaximal responseRadioiodide therapyCancerThyroid hormone biosynthesisOncogenic BRAFIodide accumulationPotent inhibitionDifferentiation genesTherapyMAPK signalingInhibitionIodide transportSignalingERK