2019
Temozolomide Sensitizes MGMT-Deficient Tumor Cells to ATR Inhibitors
Jackson CB, Noorbakhsh SI, Sundaram RK, Kalathil AN, Ganesa S, Jia L, Breslin H, Burgenske DM, Gilad O, Sarkaria JN, Bindra RS. Temozolomide Sensitizes MGMT-Deficient Tumor Cells to ATR Inhibitors. Cancer Research 2019, 79: 4331-4338. PMID: 31273061, PMCID: PMC6810597, DOI: 10.1158/0008-5472.can-18-3394.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Agents, AlkylatingAntineoplastic Combined Chemotherapy ProtocolsAtaxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsCell Line, TumorCheckpoint Kinase 1DNA Breaks, Double-StrandedDNA DamageDNA Modification MethylasesDNA Repair EnzymesDrug SynergismFemaleHumansIsoxazolesMice, NudePyrazinesTemozolomideTumor Suppressor ProteinsXenograft Model Antitumor AssaysConceptsMGMT-deficient cells
2017
DNA polymerase beta participates in DNA End-joining
Ray S, Breuer G, DeVeaux M, Zelterman D, Bindra R, Sweasy JB. DNA polymerase beta participates in DNA End-joining. Nucleic Acids Research 2017, 46: 242-255. PMID: 29161447, PMCID: PMC5758893, DOI: 10.1093/nar/gkx1147.Peer-Reviewed Original ResearchConceptsDouble-strand breaksAlternative NHEJHomologous recombinationDNA polymerasePol βX-family DNA polymerasesFamily DNA polymerasesDNA polymerase betaDNA pol βDeleterious lesionsDNA endsGenomic instabilityNHEJ pathwayDNA proteinProcessing enzymesDefective repairCellular sensitivityCell deathStrand breaksPolymerase betaSubunit inhibitorPolymeraseSmall deletionsMechanistic insightsNHEJGBM radiosensitizers: dead in the water…or just the beginning?
Bindra RS, Chalmers AJ, Evans S, Dewhirst M. GBM radiosensitizers: dead in the water…or just the beginning? Journal Of Neuro-Oncology 2017, 134: 513-521. PMID: 28762004, DOI: 10.1007/s11060-017-2427-7.Peer-Reviewed Original ResearchConceptsPre-clinical evidenceNovel therapeutic approachesGBMs recurDevelopment of radiosensitizersClinical trialsTherapeutic approachesDNA damage response inhibitorsLocal controlPrimary siteDNA repair inhibitorsPotent agentOxidative stressRadiosensitizerRepair inhibitorsRadiosensitizationInhibitorsRadiotherapyClinicHypoxiaTrials
2009
Targeting the DNA damage response for cancer therapy
Powell SN, Bindra RS. Targeting the DNA damage response for cancer therapy. DNA Repair 2009, 8: 1153-1165. PMID: 19501553, DOI: 10.1016/j.dnarep.2009.04.011.Peer-Reviewed Original ResearchConceptsDNA damage responseCell cycle checkpointsDouble-strand breaksGenome integrityGenomic integrityHistone modificationsDamage responseCycle checkpointsDNA repairKey proteinsDNA damageAnti-cancer agentsHuman tumorsNew anti-cancer agentsPathwayCancer therapyTumor cellsCheckpointProteinTherapeutic interventionsRepairIntegrityDefectsCellsAppropriate response
2005
Hypoxia-Induced Phosphorylation of Chk2 in an Ataxia Telangiectasia Mutated–Dependent Manner
Gibson SL, Bindra RS, Glazer PM. Hypoxia-Induced Phosphorylation of Chk2 in an Ataxia Telangiectasia Mutated–Dependent Manner. Cancer Research 2005, 65: 10734-10741. PMID: 16322218, DOI: 10.1158/0008-5472.can-05-1160.Peer-Reviewed Original ResearchConceptsDNA repairAtaxia telangiectasiaSerine/threonine kinaseDNA damageRelated kinase ATMKinase ataxia telangiectasiaNBS1-dependent mannerDNA repair factorsPhosphorylation of Chk2Hypoxic growth conditionsKinase ATMThreonine kinaseChk2 activationReplication forksRepair factorsChk2Apoptotic pathwayCell survivalNovel pathwayCycle arrestPhosphorylationGrowth conditionsDependent mannerPathwayCellsGenetic instability and the tumor microenvironment: towards the concept of microenvironment-induced mutagenesis
Bindra RS, Glazer PM. Genetic instability and the tumor microenvironment: towards the concept of microenvironment-induced mutagenesis. Mutation Research/Fundamental And Molecular Mechanisms Of Mutagenesis 2005, 569: 75-85. PMID: 15603753, DOI: 10.1016/j.mrfmmm.2004.03.013.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell HypoxiaDNA DamageDNA RepairGenomic InstabilityMutagenesisNeoplasmsOxidative StressConceptsGenetic instabilitySuch genetic instabilityDNA repair pathwaysOxidative base damageSuch DNA lesionsGenome integrityTumor microenvironmentRepair pathwaysDNA strand breaksDNA lesionsBase damageDNA damageStrand breaksMutagenesisInduction of mutagenesisAdverse conditionsTumor progressionMicroenvironmentRecent studiesSignificant threatPotential mechanismsNumerous typesInductionPathway