High-throughput mutation profiling of CTCL samples reveals KRAS and NRAS mutations sensitizing tumors toward inhibition of the RAS/RAF/MEK signaling cascade
Kießling M, Oberholzer PA, Mondal C, Karpova MB, Zipser MC, Lin WM, Girardi M, MacConaill LE, Kehoe SM, Hatton C, French LE, Garraway LA, Polier G, Süss D, Klemke CD, Krammer PH, Gülow K, Dummer R. High-throughput mutation profiling of CTCL samples reveals KRAS and NRAS mutations sensitizing tumors toward inhibition of the RAS/RAF/MEK signaling cascade. Blood 2011, 117: 2433-2440. PMID: 21209378, PMCID: PMC3952811, DOI: 10.1182/blood-2010-09-305128.Peer-Reviewed Original ResearchMeSH KeywordsBiopsyHigh-Throughput Screening AssaysHumansLymphoma, T-Cell, CutaneousMitogen-Activated Protein Kinase KinasesMutationMycosis FungoidesNeoplasm StagingProtein Kinase InhibitorsProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Raf KinasesRas ProteinsSezary SyndromeSignal TransductionConceptsCutaneous T-cell lymphomaStage IV patientsHUT78 cellsIV patientsPleomorphic cutaneous T-cell lymphomaHigh-throughput mutation profilingMEK inhibitorsCTCL cell line Hut78T-cell lymphomaRAS/RAF/MEKCTCL cell linesOncogenic mutationsCommon oncogenic mutationsCTCL patientsOverall survivalSézary syndromeMycosis fungoidesBiopsy specimensPatients profitPreclinical resultsMEK inhibitor U0126NRAS mutationsLymphoid cellsCTCL samplesRAS mutations