2018
ADAURA: Phase III, Double-blind, Randomized Study of Osimertinib Versus Placebo in EGFR Mutation-positive Early-stage NSCLC After Complete Surgical Resection
Wu YL, Herbst R, Mann H, Rukazenkov Y, Marotti M, Tsuboi M. ADAURA: Phase III, Double-blind, Randomized Study of Osimertinib Versus Placebo in EGFR Mutation-positive Early-stage NSCLC After Complete Surgical Resection. Clinical Lung Cancer 2018, 19: e533-e536. PMID: 29789220, DOI: 10.1016/j.cllc.2018.04.004.Peer-Reviewed Original ResearchConceptsCell lung cancerDisease recurrenceLung cancerMutation statusSurvival rateEpidermal growth factor receptor tyrosine kinase inhibitorsGrowth factor receptor tyrosine kinase inhibitorsComplete surgical tumor resectionDisease-free survival ratesT790M mutation statusReceptor tyrosine kinase inhibitorsMaximum treatment durationStage IB-IIIAPlacebo-controlled studyDisease-free survivalEarly-stage NSCLCComplete surgical resectionOverall survival rateHealth-related qualityHealth resource useSurgical tumor resectionEGFR mutation statusTyrosine kinase inhibitorsCentral confirmationVersus Placebo
2017
Factors associated with better overall survival (OS) in patients with previously treated, PD-L1–expressing, advanced NSCLC: Multivariate analysis of KEYNOTE-010.
Herbst R, Baas P, Kim D, Felip E, Perez-Gracia J, Han J, Molina J, Kim J, Dubos Arvis C, Ahn M, Majem M, Fidler M, Castro G, Garrido M, Ellison M, Samkari A, Lubiniecki G, Garon E. Factors associated with better overall survival (OS) in patients with previously treated, PD-L1–expressing, advanced NSCLC: Multivariate analysis of KEYNOTE-010. Journal Of Clinical Oncology 2017, 35: 9090-9090. DOI: 10.1200/jco.2017.35.15_suppl.9090.Peer-Reviewed Original ResearchOverall survivalKEYNOTE-010Advanced NSCLCPD-L1Multivariate analysisPembrolizumab armBetter OSHazard ratioCox proportional hazards regression modelNormal baseline lactate dehydrogenaseProportional hazards regression modelsBaseline lactate dehydrogenasePD-L1 TPSPositive advanced NSCLCSuperior overall survivalBetter overall survivalIndependent central reviewHazards regression modelsLactate dehydrogenaseEGFR mutation statusNonsquamous histologyRECIST v1.1Smoking statusTumor characteristicsCentral review
2013
An Epithelial–Mesenchymal Transition Gene Signature Predicts Resistance to EGFR and PI3K Inhibitors and Identifies Axl as a Therapeutic Target for Overcoming EGFR Inhibitor Resistance
Byers LA, Diao L, Wang J, Saintigny P, Girard L, Peyton M, Shen L, Fan Y, Giri U, Tumula PK, Nilsson MB, Gudikote J, Tran H, Cardnell RJ, Bearss DJ, Warner SL, Foulks JM, Kanner SB, Gandhi V, Krett N, Rosen ST, Kim ES, Herbst RS, Blumenschein GR, Lee JJ, Lippman SM, Ang KK, Mills GB, Hong WK, Weinstein JN, Wistuba II, Coombes KR, Minna JD, Heymach JV. An Epithelial–Mesenchymal Transition Gene Signature Predicts Resistance to EGFR and PI3K Inhibitors and Identifies Axl as a Therapeutic Target for Overcoming EGFR Inhibitor Resistance. Clinical Cancer Research 2013, 19: 279-290. PMID: 23091115, PMCID: PMC3567921, DOI: 10.1158/1078-0432.ccr-12-1558.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAxl Receptor Tyrosine KinaseCarcinoma, Non-Small-Cell LungCell Line, TumorCluster AnalysisDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionErbB ReceptorsGene Expression ProfilingHumansLung NeoplasmsMiceNeoplasm MetastasisPhosphoinositide-3 Kinase InhibitorsProtein Kinase InhibitorsProteomeProteomicsProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesRecurrenceReproducibility of ResultsConceptsEpithelial-mesenchymal transitionPotential therapeutic targetEGFR inhibitor resistanceTherapeutic targetEMT signatureInhibitor resistanceMesenchymal transition gene signatureMesenchymal cellsCell linesBiomarker-Integrated ApproachesPI3K/Akt pathway inhibitorNon-small cell lung carcinoma cell lineEGFR mutation statusReceptor tyrosine kinase AXLNSCLC cell linesPI3K/Akt inhibitorCell lung carcinoma cell lineGene expression profilesTyrosine kinase AXLLung carcinoma cell linePI3K inhibitorsDrug response analysisAkt pathway inhibitorCarcinoma cell linesErlotinib resistance