2019
Oligosaccharyltransferase Inhibition Reduces Receptor Tyrosine Kinase Activation and Enhances Glioma Radiosensitivity
Baro M, Sambrooks C, Quijano A, Saltzman WM, Contessa J. Oligosaccharyltransferase Inhibition Reduces Receptor Tyrosine Kinase Activation and Enhances Glioma Radiosensitivity. Clinical Cancer Research 2019, 25: 784-795. PMID: 29967251, PMCID: PMC6314911, DOI: 10.1158/1078-0432.ccr-18-0792.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsCell Cycle CheckpointsCell Line, TumorCell SurvivalDisease Models, AnimalDose-Response Relationship, DrugDose-Response Relationship, RadiationErbB ReceptorsGliomaHexosyltransferasesHumansMembrane ProteinsMiceRadiation ToleranceRadiation-Sensitizing AgentsReceptor Protein-Tyrosine KinasesSignal TransductionXenograft Model Antitumor AssaysConceptsNGI-1Cell cycle arrestDNA damageReceptor tyrosine kinase activationTyrosine kinase activationReceptor tyrosine kinasesSmall molecule inhibitorsEGFR family receptorsRTK signalingRTK activationXenograft tumor growthGlycosylation stateKinase activationTumor cell radiosensitivityExpression profilesProtein NTyrosine kinaseGlioma radiosensitivityParallel signalingTumor growthFamily activationCellular radiosensitivityFamily receptorsMechanistic roleProtein levels
2018
Oligosaccharyltransferase Inhibition Overcomes Therapeutic Resistance to EGFR Tyrosine Kinase Inhibitors
Lopez Sambrooks C, Baro M, Quijano A, Narayan A, Cui W, Greninger P, Egan R, Patel A, Benes CH, Saltzman WM, Contessa JN. Oligosaccharyltransferase Inhibition Overcomes Therapeutic Resistance to EGFR Tyrosine Kinase Inhibitors. Cancer Research 2018, 78: canres.0505.2018. PMID: 30026325, PMCID: PMC6125176, DOI: 10.1158/0008-5472.can-18-0505.Peer-Reviewed Original ResearchConceptsMutant NSCLCMutant non-small cell lung cancerNon-small cell lung cancerSignificant tumor growth delayEGFR-TKI treatmentCell lung cancerTyrosine kinase inhibitor resistanceEGFR tyrosine kinase inhibitor resistanceLung cancer cell linesNGI-1Tumor growth delayEffective therapeutic targetCell linesKinase inhibitor resistanceTumor cell viabilityH1975 xenograftsCancer cell linesTKI treatmentComplex transmembrane proteinsEGFR-TKILung cancerTumor responseCell cycle arrestPreclinical modelsTherapeutic strategies
2010
Cetuximab May Inhibit Tumor Growth and Angiogenesis Induced by Ionizing Radiation: A Preclinical Rationale for Maintenance Treatment After Radiotherapy
Pueyo G, Mesia R, Figueras A, Lozano A, Baro M, Vazquez S, Capella G, Balart J. Cetuximab May Inhibit Tumor Growth and Angiogenesis Induced by Ionizing Radiation: A Preclinical Rationale for Maintenance Treatment After Radiotherapy. The Oncologist 2010, 15: 976-986. PMID: 20798193, PMCID: PMC3228040, DOI: 10.1634/theoncologist.2008-0290.Peer-Reviewed Original ResearchConceptsEpidermal growth factor receptorKi-67 indexMicrovessel densityAggressive phenotypeTumor growthHigh Ki-67 indexCetuximab maintenance therapyMicroscopic residual diseaseBenefits of radiotherapyVascular endothelial growth factor (VEGF) secretionUntreated cellsGrowth factor secretionMechanism of actionCetuximab maintenanceGrowth factor receptorMaintenance therapyAdjuvant therapyPreclinical rationaleMaintenance treatmentResidual diseaseCarcinoma cell linesClinical evaluationExtracellular signal-related kinaseIrradiated cellsCetuximab