2018
Association of Broad-Based Genomic Sequencing With Survival Among Patients With Advanced Non–Small Cell Lung Cancer in the Community Oncology Setting
Presley CJ, Tang D, Soulos PR, Chiang AC, Longtine JA, Adelson KB, Herbst RS, Zhu W, Nussbaum NC, Sorg RA, Agarwala V, Abernethy AP, Gross CP. Association of Broad-Based Genomic Sequencing With Survival Among Patients With Advanced Non–Small Cell Lung Cancer in the Community Oncology Setting. JAMA 2018, 320: 469-477. PMID: 30088010, PMCID: PMC6142984, DOI: 10.1001/jama.2018.9824.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnaplastic Lymphoma KinaseAntineoplastic AgentsCarcinoma, Non-Small-Cell LungDNA, NeoplasmFemaleGenes, erbB-1GenomicsGenotypeHumansImmunotherapyLung NeoplasmsMaleMiddle AgedMutationNeoplasm StagingReceptor Protein-Tyrosine KinasesRetrospective StudiesSequence Analysis, DNASurvival AnalysisConceptsAdvanced non-small cell lung cancerNon-small cell lung cancerCommunity oncology settingCell lung cancerLung cancerOncology settingRoutine testingNonsquamous non-small cell lung cancerTargeted treatmentPropensity score-matched survival analysisStage IIIB/IVFlatiron Health databaseIIIB/IVRetrospective cohort studyThird-line treatmentFirst-line treatmentMinority of patientsUnadjusted mortality ratesEGFR/ALKCohort studyOverall survivalSecondary outcomesUnmatched cohortPrimary outcomeAntineoplastic treatment
2015
Genetic landscape of metastatic and recurrent head and neck squamous cell carcinoma
Hedberg ML, Goh G, Chiosea SI, Bauman JE, Freilino ML, Zeng Y, Wang L, Diergaarde BB, Gooding WE, Lui VW, Herbst RS, Lifton RP, Grandis JR. Genetic landscape of metastatic and recurrent head and neck squamous cell carcinoma. Journal Of Clinical Investigation 2015, 126: 169-180. PMID: 26619122, PMCID: PMC4701554, DOI: 10.1172/jci82066.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedCarcinoma, Squamous CellDasatinibDiscoidin Domain ReceptorsFemaleHead and Neck NeoplasmsHumansInositol 1,4,5-Trisphosphate ReceptorsLymphatic MetastasisMaleMiddle AgedMutationNeoplasm Recurrence, LocalReceptor Protein-Tyrosine KinasesReceptors, MitogenSquamous Cell Carcinoma of Head and NeckConceptsDiscoidin domain receptor tyrosine kinase 2Neck squamous cell carcinomaSquamous cell carcinomaRecurrent tumorsWhole-exome sequencingSynchronous lymphCell carcinomaPrimary tumorDDR2 mutationsTumor pairsSrc family kinase inhibitorRecurrent/metastatic HNSCCPrimary index tumorSynchronous nodal metastasesHalf of patientsReceptor tyrosine kinase 2Tyrosine kinase 2American Cancer SocietyIndex primary tumorPotential therapeutic targetPrecision medicine approachLong-term survivalRespective primary tumorsSomatic nucleotide variantsNational Cancer Institute
2013
Identification of EGFR mutation, KRAS mutation, and ALK gene rearrangement in cytological specimens of primary and metastatic lung adenocarcinoma
Cai G, Wong R, Chhieng D, Levy GH, Gettinger SN, Herbst RS, Puchalski JT, Homer RJ, Hui P. Identification of EGFR mutation, KRAS mutation, and ALK gene rearrangement in cytological specimens of primary and metastatic lung adenocarcinoma. Cancer Cytopathology 2013, 121: 500-507. PMID: 23495083, DOI: 10.1002/cncy.21288.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdultAgedAged, 80 and overAnaplastic Lymphoma KinaseBiomarkers, TumorBone NeoplasmsCytodiagnosisDNA, NeoplasmErbB ReceptorsFeasibility StudiesFemaleGene RearrangementHumansIn Situ Hybridization, FluorescenceLiver NeoplasmsLung NeoplasmsMaleMiddle AgedMutationNeoplasm Recurrence, LocalPrognosisProto-Oncogene ProteinsProto-Oncogene Proteins p21(ras)Ras ProteinsReal-Time Polymerase Chain ReactionReceptor Protein-Tyrosine KinasesSoft Tissue NeoplasmsYoung AdultConceptsALK gene rearrangementMetastatic lung adenocarcinomaEGFR mutationsKRAS mutationsMetastatic tumorsEpidermal growth factor receptorLung adenocarcinomaCytological specimensGene rearrangementsMolecular testsMolecular alterationsKirsten rat sarcoma viral oncogene homolog (KRAS) mutationsALK gene rearrangement analysisAnaplastic lymphoma kinase (ALK) gene rearrangementEGFR T790M mutationRat sarcoma viral oncogene homolog mutationsCases of lungT790M mutationImportant therapeutic implicationsFine needle aspiratesGene rearrangement analysisCell block materialGrowth factor receptorRecurrent lungRecurrent adenocarcinomaAn 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
2007
Vandetanib (ZD6474): an orally available receptor tyrosine kinase inhibitor that selectively targets pathways critical for tumor growth and angiogenesis
Herbst RS, Heymach JV, O’Reilly M, Onn A, Ryan AJ. Vandetanib (ZD6474): an orally available receptor tyrosine kinase inhibitor that selectively targets pathways critical for tumor growth and angiogenesis. Expert Opinion On Investigational Drugs 2007, 16: 239-249. PMID: 17243944, DOI: 10.1517/13543784.16.2.239.Peer-Reviewed Original ResearchConceptsTumor typesHereditary medullary thyroid cancerReceptor tyrosine kinase inhibitorsPhase III trialsProgression-free survivalDaily oral administrationPhase II evaluationPhase I studiesMedullary thyroid cancerTyrosine kinase inhibitorsSolid tumor typesTumor cell proliferationRefractory NSCLCAdvanced NSCLCIII trialsI studiesII evaluationThyroid cancerOral administrationAvailable agentsClinical developmentPharmacokinetic profileTumor growthVandetanibTumor angiogenesis
2002
Angiogenesis inhibitors in lung cancer
Kim ES, Herbst RS. Angiogenesis inhibitors in lung cancer. Current Oncology Reports 2002, 4: 325-333. PMID: 12044242, DOI: 10.1007/s11912-002-0008-0.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAngiostatinsCarcinoma, Non-Small-Cell LungCollagenCyclohexanesEndostatinsHumansLung NeoplasmsO-(Chloroacetylcarbamoyl)fumagillolPeptide FragmentsPlasminogenReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, Vascular Endothelial Growth FactorSesquiterpenesSurvival RateThalidomideConceptsLung cancerAngiogenesis inhibitorsSurvival rateMajor public health problemVascular endothelial growth factor receptorOngoing randomized studiesCell lung cancerEndothelial growth factor receptorTraditional cytotoxic therapiesCancer-related deathImproved survival ratesPublic health problemSevere side effectsInhibitors of angiogenesisEndogenous angiogenesis inhibitorGrowth factor receptorMetastatic diseaseRandomized studyChemotherapy dosesClinical benefitCytotoxic therapyCyclooxygenase inhibitorRadiation therapySide effectsHealth problems
2000
Treatment for malignant pleural effusion of human lung adenocarcinoma by inhibition of vascular endothelial growth factor receptor tyrosine kinase phosphorylation.
Yano S, Herbst RS, Shinohara H, Knighton B, Bucana CD, Killion JJ, Wood J, Fidler IJ. Treatment for malignant pleural effusion of human lung adenocarcinoma by inhibition of vascular endothelial growth factor receptor tyrosine kinase phosphorylation. Clinical Cancer Research 2000, 6: 957-65. PMID: 10741721.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAngiogenesis InhibitorsAnimalsCapillary PermeabilityCell DivisionCell LineEndothelial Growth FactorsEndothelium, VascularGene Expression RegulationHumansImmunohistochemistryIn Situ HybridizationLung NeoplasmsLymphokinesMaleMiceMice, Inbred BALB CMice, NudeNeoplasm TransplantationNeovascularization, PathologicPhosphorylationPhthalazinesPleural Effusion, MalignantPyridinesReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, Vascular Endothelial Growth FactorTransplantation, HeterologousTumor Cells, CulturedVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsMalignant pleural effusionReceptor tyrosine kinase inhibitorsPleural effusionPTK 787Human dermal microvascular endothelial cellsTyrosine kinase inhibitorsPC14PE6 cellsDermal microvascular endothelial cellsMicrovascular endothelial cellsVEGF/VPFOral treatmentLung lesionsGrowth factor receptor tyrosine kinase inhibitorsAdvanced human lung cancerPlatelet-derived growth factor receptor tyrosine kinase inhibitorVEGF/VPF proteinEndothelial cellsKinase inhibitorsVascular endothelial growth factor/vascular permeability factorHuman lung cancerNude mouse modelHuman lung adenocarcinomaHuman lung adenocarcinoma cellsVascular permeability factorHuman lung carcinoma cells