2008
Increased EGFR Gene Copy Number Detected by Fluorescent In Situ Hybridization Predicts Outcome in Non–Small-Cell Lung Cancer Patients Treated With Cetuximab and Chemotherapy
Hirsch FR, Herbst RS, Olsen C, Chansky K, Crowley J, Kelly K, Franklin WA, Bunn PA, Varella-Garcia M, Gandara DR. Increased EGFR Gene Copy Number Detected by Fluorescent In Situ Hybridization Predicts Outcome in Non–Small-Cell Lung Cancer Patients Treated With Cetuximab and Chemotherapy. Journal Of Clinical Oncology 2008, 26: 3351-3357. PMID: 18612151, PMCID: PMC3368372, DOI: 10.1200/jco.2007.14.0111.Peer-Reviewed Original ResearchMeSH KeywordsAgedAnalysis of VarianceAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorCarcinoma, Non-Small-Cell LungCetuximabFemaleGene Expression Regulation, NeoplasticGenes, erbB-1HumansIn Situ HybridizationIn Situ Hybridization, FluorescenceLung NeoplasmsMaleMiddle AgedMultivariate AnalysisNeoplasm StagingPatient SelectionPredictive Value of TestsPrognosisProportional Hazards ModelsReference ValuesRisk AssessmentSurvival AnalysisTreatment OutcomeConceptsCell lung cancer patientsLung cancer patientsFISH-negative patientsEGFR FISHNSCLC patientsCancer patientsSurvival timeMedian progression-free survival timeProgression-free survival timeEGFR tyrosine kinase inhibitorsDisease control rateChemotherapy-naive patientsAdvanced-stage NSCLCMedian survival timeEpidermal growth factor receptor (EGFR) gene copy numberFISH-positive patientsAvailable tumor tissueEGFR gene copy numberTyrosine kinase inhibitorsFISH-positive tumorsPhase II selection trialFISH-positive groupConcurrent chemotherapyConcurrent therapyPredictive factors
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 cellsDifferential expression of E-cadherin and type IV collagenase genes predicts outcome in patients with stage I non-small cell lung carcinoma.
Herbst RS, Yano S, Kuniyasu H, Khuri FR, Bucana CD, Guo F, Liu D, Kemp B, Lee JJ, Hong WK, Fidler IJ. Differential expression of E-cadherin and type IV collagenase genes predicts outcome in patients with stage I non-small cell lung carcinoma. Clinical Cancer Research 2000, 6: 790-7. PMID: 10741698.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedCadherinsCarcinoma, Non-Small-Cell LungDisease-Free SurvivalFemaleGene Expression Regulation, NeoplasticHumansIn Situ HybridizationLung NeoplasmsMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9Middle AgedMultivariate AnalysisNeoplasm MetastasisNeoplasm Recurrence, LocalNeoplasm StagingPredictive Value of TestsSurvival AnalysisConceptsE-cadherin ratioLung cancerType IV collagenaseLung carcinomaDisease outcomeStage I non-small cell lung carcinomaPrimary non-small cell lung cancerNon-small cell lung cancerE-cadherinKaplan-Meier survival analysisNon-small cell lung carcinomaD. Anderson Cancer CenterResectable lung cancerDisease-free survivalSignificant prognostic factorsLonger overall survivalCell lung cancerDisease recurrence rateRoutine histopathological examinationCox univariate analysisAnderson Cancer CenterCell lung carcinomaVascular endothelial growth factor/vascular permeability factorHuman lung cancerBasic fibroblast growth factor
1997
Reversal of in vivo drug resistance by the transforming growth factor‐β inhibitor decorin
Teicher B, Maehara Y, Kakeh Y, Ara G, Keyes S, Wong J, Herbst R. Reversal of in vivo drug resistance by the transforming growth factor‐β inhibitor decorin. International Journal Of Cancer 1997, 71: 49-58. PMID: 9096665, DOI: 10.1002/(sici)1097-0215(19970328)71:1<49::aid-ijc10>3.0.co;2-4.Peer-Reviewed Original ResearchConceptsEMT-6/CDDP tumorTumor cell survivalParent tumorResistant tumorsDrug resistanceAdministration of decorinCell survivalEMT-6/CTXPlasma TGF-beta levelsTGF-beta proteinGranulocyte-macrophage colony-stimulating factorSitu hybridizationTGF-beta levelsVivo drug resistanceHigher plasma levelsTGF-beta mRNATumor-bearing animalsMurine mammary tumorsGrowth factorColony-stimulating factorDrug responseDecorinCytotoxic therapyPlasma levelsTumor levels