2019
Siglec-15 as an immune suppressor and potential target for normalization cancer immunotherapy
Wang J, Sun J, Liu LN, Flies DB, Nie X, Toki M, Zhang J, Song C, Zarr M, Zhou X, Han X, Archer KA, O’Neill T, Herbst RS, Boto AN, Sanmamed MF, Langermann S, Rimm DL, Chen L. Siglec-15 as an immune suppressor and potential target for normalization cancer immunotherapy. Nature Medicine 2019, 25: 656-666. PMID: 30833750, PMCID: PMC7175920, DOI: 10.1038/s41591-019-0374-x.Peer-Reviewed Original ResearchConceptsNormalization cancer immunotherapyTumor microenvironmentSiglec-15Antibody blockadeCancer immunotherapyImmune suppressorMyeloid cellsAntigen-specific T cell responsesB7-H1/PDTumor-infiltrating myeloid cellsB7-H1 moleculesAnti-tumor immunityT cell responsesPotential targetImmune evasion mechanismsInhibits tumor growthMacrophage colony-stimulating factorColony-stimulating factorB7-H1Evasion mechanismsMouse modelHuman cancer cellsTumor growthCell responsesGenetic ablation
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
2007
Targeted therapy of orthotopic human lung cancer by combined vascular endothelial growth factor and epidermal growth factor receptor signaling blockade
Wu W, Onn A, Isobe T, Itasaka S, Langley RR, Shitani T, Shibuya K, Komaki R, Ryan AJ, Fidler IJ, Herbst RS, O'Reilly MS. Targeted therapy of orthotopic human lung cancer by combined vascular endothelial growth factor and epidermal growth factor receptor signaling blockade. Molecular Cancer Therapeutics 2007, 6: 471-483. PMID: 17308046, DOI: 10.1158/1535-7163.mct-06-0416.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAngiogenesis InhibitorsAnimalsApoptosisBlotting, WesternCarcinoma, Squamous CellCell Line, TumorCell ProliferationEndothelium, VascularErbB ReceptorsFlow CytometryHumansLung NeoplasmsMaleMiceMice, Inbred BALB CMice, Inbred CBANeovascularization, PathologicPhosphorylationPiperidinesProto-Oncogene Proteins c-aktQuinazolinesSignal TransductionVascular Endothelial Growth Factor Receptor-2Xenograft Model Antitumor AssaysConceptsVascular endothelial growth factorVEGF receptor 2EGF receptorEpidermal growth factorLung cancerHuman lung cancerEndothelial growth factorGrowth factorMitogen-activated protein kinaseNon-small cell lung cancerOrthotopic human lung cancerProtein tyrosine kinase inhibitorEndothelial cellsTumor-associated endothelial cellsHuman lung cancer specimensAdvanced lung cancerSelective protein tyrosine kinase inhibitorCell lung cancerLung cancer patientsOrthotopic mouse modelEndothelial cell tube formationLung cancer specimensHuman lung adenocarcinoma cellsTyrosine kinase inhibitorsSmall molecule inhibitors
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
1999
The proteasome inhibitor PS-341 in cancer therapy.
Teicher B, Ara G, Herbst R, Palombella V, Adams J. The proteasome inhibitor PS-341 in cancer therapy. Clinical Cancer Research 1999, 5: 2638-45. PMID: 10499643.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsBoronic AcidsBortezomibBreast NeoplasmsCisplatinCyclophosphamideDipeptidesDrug SynergismHumansMammary Neoplasms, ExperimentalMiceMice, Inbred BALB CProtease InhibitorsPyrazinesRadiation-Sensitizing AgentsTumor Cells, CulturedUbiquitinsConceptsProteasome inhibitor PS-341PS-341EMT-6/CDDP tumorAdditive tumor growth delayCancer therapyEMT-6/CTXTumor cell survival assayTumor growth delay assayLewis lung carcinomaColony-forming unit-granulocyte macrophageTumor growth delayGrowth delay assayHuman breast carcinoma cellsMCF-7 human breast carcinoma cellsUnit-granulocyte macrophageTumor cell killingCell survival assayBreast carcinoma cellsMetastatic diseaseInteresting new targetLung carcinomaRadiation therapyVivo resistanceGrowth delayParent tumor
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 lungAcute in vivo resistance in high-dose therapy.
Teicher BA, Ara G, Keyes SR, Herbst RS, Frei E. Acute in vivo resistance in high-dose therapy. Clinical Cancer Research 1998, 4: 483-91. PMID: 9516940.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsCarboplatinCyclophosphamideDisease Models, AnimalDose-Response Relationship, DrugDrug Resistance, MultipleDrug Resistance, NeoplasmFemaleMammary Neoplasms, ExperimentalMelphalanMiceMice, Inbred BALB CNeoplasm TransplantationPaclitaxelThiotepaConceptsTumor growth delayAdditive tumor growth delayHigh-dose cyclophosphamideHigh-dose melphalanGrowth delaySecond highest doseHigh doseSequential high-dose chemotherapyTumor cell survival assayEMT-6 mammary carcinomaTumor growth delay studiesBone marrow colony-forming unitsHigh-dose therapyMarrow colony-forming unitsHigh-dose chemotherapyBone marrow CFU-GMHigh-dose treatmentGrowth delay studiesTumor-bearing miceMarrow CFU-GMSolid tumor modelsCell survival assayCombination regimensMammary carcinomaCyclophosphamide
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 levelsTransforming growth factor-beta 1 overexpression produces drug resistance in vivo: reversal by decorin.
Teicher BA, Ikebe M, Ara G, Keyes SR, Herbst RS. Transforming growth factor-beta 1 overexpression produces drug resistance in vivo: reversal by decorin. In Vivo 1997, 11: 463-72. PMID: 9509296.Peer-Reviewed Original ResearchConceptsBone marrow CFU-GMMarrow CFU-GMAdministration of decorinParent tumorCFU-GMTumor linesBALB/c miceEffects of secretionsC micePlasma levelsVivo resistanceMonolayer culturesSolid tumorsTherapeutic resistanceTumorsTumor modelDrug resistanceDrug sensitivityDosage rangeThiotepaMelphalanCell linesCisplatinAdministrationAnimalsPEG-hemoglobin: effects on tumor oxygenation and response to chemotherapy.
Teicher B, Ara G, Herbst R, Takeuchi H, Keyes S, Northey D. PEG-hemoglobin: effects on tumor oxygenation and response to chemotherapy. In Vivo 1997, 11: 301-11. PMID: 9292296.Peer-Reviewed Original ResearchConceptsPEG-hemoglobinTumor growth delayMammary carcinomaTumor cell killingSolid tumorsTumor oxygenationGrowth delayDose of chemotherapyEMT-6 murine mammary carcinomaBone marrow CFU-GMEfficacy of chemotherapyEMT-6 tumorsMurine mammary carcinomaTumor-bearing miceCFU-GM survivalMarrow CFU-GMCell killingOxygen delivery agentEMT-6 tumor-bearing miceChemotherapy administrationLung metastasesMultiple dosesSingle dosesChemotherapyCFU-GM