2016
GSK-3α Is a Novel Target of CREB and CREB-GSK-3α Signaling Participates in Cell Viability in Lung Cancer
Park SA, Lee JW, Herbst RS, Koo JS. GSK-3α Is a Novel Target of CREB and CREB-GSK-3α Signaling Participates in Cell Viability in Lung Cancer. PLOS ONE 2016, 11: e0153075. PMID: 27049759, PMCID: PMC4822949, DOI: 10.1371/journal.pone.0153075.Peer-Reviewed Original Research
2015
E2F8 as a Novel Therapeutic Target for Lung Cancer
Park SA, Platt J, Lee JW, López-Giráldez F, Herbst RS, Koo JS. E2F8 as a Novel Therapeutic Target for Lung Cancer. Journal Of The National Cancer Institute 2015, 107: djv151. PMID: 26089541, PMCID: PMC4651101, DOI: 10.1093/jnci/djv151.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCCAAT-Enhancer-Binding ProteinsCell Line, TumorCell ProliferationCell SurvivalChromatin ImmunoprecipitationFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticHumansImmunoblottingKaplan-Meier EstimateLung NeoplasmsMiceMolecular Targeted TherapyNeoplastic Stem CellsPromoter Regions, GeneticRepressor ProteinsTissue Array AnalysisUbiquitin-Protein LigasesUp-RegulationXenograft Model Antitumor AssaysConceptsTarget genesCell cycle regulationNovel therapeutic targetPromoter activity assaysCell proliferationCancer cellsExpression of UHRF1Transcription activatorAntisense morpholinoChromatin immunoprecipitationCycle regulationTherapeutic targetEmbryonic developmentE2F membersHuman lung cancer cellsMicroarray analysisInvasion analysisLung cancer cellsDirect bindingTumor growthE2F8Activity assaysPublic databasesColony formationUHRF1
2012
Targeting the Apoptotic Pathway in Chondrosarcoma Using Recombinant Human Apo2L/TRAIL (Dulanermin), a Dual Proapoptotic Receptor (DR4/DR5) Agonist
Subbiah V, Brown RE, Buryanek J, Trent J, Ashkenazi A, Herbst R, Kurzrock R. Targeting the Apoptotic Pathway in Chondrosarcoma Using Recombinant Human Apo2L/TRAIL (Dulanermin), a Dual Proapoptotic Receptor (DR4/DR5) Agonist. Molecular Cancer Therapeutics 2012, 11: 2541-2546. PMID: 22914439, PMCID: PMC3496030, DOI: 10.1158/1535-7163.mct-12-0358.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisBone NeoplasmsCell SurvivalChondrosarcomaDNA Mutational AnalysisHumansImmunohistochemistryIsocitrate DehydrogenaseLung NeoplasmsMaleMiddle AgedProteomicsProto-Oncogene Proteins c-bcl-2Radiography, ThoracicReceptors, Death DomainRecombinant ProteinsSignal TransductionTNF-Related Apoptosis-Inducing LigandTomography, X-Ray ComputedTreatment OutcomeConceptsRecombinant human Apo2L/TRAILApo2L/TRAILRecent computed tomography scanSustained partial responseEvidence of diseaseComputed tomography scanP-ERK 1/2Partial responseProgressive diseaseNF-κBp65Receptor agonistTomography scanSubcentimeter nodulesPatient tumorsMetastatic chondrosarcomaP-mTORPatientsProlonged responseP-STAT3Proapoptotic receptor agonistsChondrosarcomaBcl-2DulanerminLungTumors
2010
Combination Treatment with MEK and AKT Inhibitors Is More Effective than Each Drug Alone in Human Non-Small Cell Lung Cancer In Vitro and In Vivo
Meng J, Dai B, Fang B, Bekele BN, Bornmann WG, Sun D, Peng Z, Herbst RS, Papadimitrakopoulou V, Minna JD, Peyton M, Roth JA. Combination Treatment with MEK and AKT Inhibitors Is More Effective than Each Drug Alone in Human Non-Small Cell Lung Cancer In Vitro and In Vivo. PLOS ONE 2010, 5: e14124. PMID: 21124782, PMCID: PMC2993951, DOI: 10.1371/journal.pone.0014124.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBenzimidazolesCarcinoma, Non-Small-Cell LungCell CycleCell Line, TumorCell SurvivalDose-Response Relationship, DrugDrug SynergismFemaleHeterocyclic Compounds, 3-RingHumansLung NeoplasmsMiceMice, Inbred BALB CMice, NudeMitogen-Activated Protein Kinase KinasesProto-Oncogene Proteins c-aktSignal TransductionSurvival AnalysisTumor BurdenXenograft Model Antitumor AssaysConceptsNon-small cell lung cancerCell lung cancerCombination of AZD6244Lung cancer cell linesCombination therapyLung cancerCancer cell linesTumor growthTumor tissueHuman non-small cell lung cancerLung cancer cell growthCell linesHuman lung cancer cell linesSingle drug treatmentSynergistic antitumor activityHuman lung tumorsAnimal survival timeMean animal survival timeCancer cell growthXenograft tumor growthP-AKT expressionLung tumorsDrug treatmentDrug combinationsSurvival time
1998
Paclitaxel/carboplatin administration along with antiangiogenic therapy in non-small-cell lung and breast carcinoma models
Herbst R, Takeuchi H, Teicher B. Paclitaxel/carboplatin administration along with antiangiogenic therapy in non-small-cell lung and breast carcinoma models. Cancer Chemotherapy And Pharmacology 1998, 41: 497-504. PMID: 9554595, DOI: 10.1007/s002800050773.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsBone Marrow CellsCarboplatinCarcinoma, Lewis LungCell SurvivalColony-Forming Units AssayCyclohexanesDrug SynergismDrug Therapy, CombinationFemaleMaleMammary Neoplasms, ExperimentalMiceMice, Inbred BALB CMice, Inbred C57BLMinocyclineNeovascularization, PathologicO-(Chloroacetylcarbamoyl)fumagillolPaclitaxelSesquiterpenesConceptsTNP-470/minocyclineEMT-6 mammary carcinomaBone marrow CFU-GMLewis lung carcinomaMarrow CFU-GMEMT-6 tumor cellsLung carcinomaMammary carcinomaCFU-GMNormal tissuesTumor cellsHigh-dose paclitaxelCell lung cancerCombination of paclitaxelToxicity of carboplatinEfficacy of chemotherapyTumor growth delayBreast carcinoma modelCytotoxicity of carboplatinEarly time pointsAgent regimenAntiangiogenic regimenCarboplatin administrationLung metastasesCell lung
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
1996
Lisofylline as a modifier of radiation therapy.
Wong J, Ara G, Keyes S, Herbst R, Coleman C, Teicher B. Lisofylline as a modifier of radiation therapy. Oncology Research Featuring Preclinical And Clinical Cancer Therapeutics 1996, 8: 513-8. PMID: 9160355.Peer-Reviewed Original ResearchConceptsEMT-6 cellsHypoxic EMT-6 cellsGy/minDose rate radiationTumor growth delay assayRate radiationEMT-6 murine mammary carcinomaSingle-dose radiationGrowth delay assayMurine mammary carcinomaHigh dose rate radiationLow dose rate radiationGamma radiation therapyRadiation survival curvesTumor cell survivalContinuous infusionMultiple dosesMammary carcinomaRadiation therapyPentoxifyllineLisofyllineRadiation settingsSurvival curvesDose radiationRadiation exposure