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
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