JAK1/STAT3 Activation through a Proinflammatory Cytokine Pathway Leads to Resistance to Molecularly Targeted Therapy in Non–Small Cell Lung Cancer
Shien K, Papadimitrakopoulou VA, Ruder D, Behrens C, Shen L, Kalhor N, Song J, Lee JJ, Wang J, Tang X, Herbst RS, Toyooka S, Girard L, Minna JD, Kurie JM, Wistuba II, Izzo JG. JAK1/STAT3 Activation through a Proinflammatory Cytokine Pathway Leads to Resistance to Molecularly Targeted Therapy in Non–Small Cell Lung Cancer. Molecular Cancer Therapeutics 2017, 16: 2234-2245. PMID: 28729401, PMCID: PMC5628136, DOI: 10.1158/1535-7163.mct-17-0148.Peer-Reviewed Original ResearchMeSH KeywordsAgedApoptosisCancer-Associated FibroblastsCarcinoma, Non-Small-Cell LungCell Line, TumorCytokinesDrug Resistance, NeoplasmEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansInterleukin-6Janus Kinase 1MaleMiddle AgedMolecular Targeted TherapyNeoplasm StagingOncostatin MReceptors, Oncostatin MSignal TransductionSTAT3 Transcription FactorConceptsNon-small cell lung cancerCancer-associated fibroblastsNSCLC cellsOSM receptorMajority of patientsCell lung cancerProinflammatory cytokine IL6Proinflammatory cytokine pathwaysSignificant therapeutic advancesClinical NSCLC samplesMol Cancer TherSTAT3-dependent mannerOSMR expressionDrug-induced apoptosisWorse prognosisPrognostic significanceLung cancerTherapeutic advancesCytokines IL6Molecule expressionNSCLC samplesCytokine pathwaysLung adenocarcinomaTargeted drugsParacrine mechanisms