2019
DNMT3A co-mutation in an IDH1-mutant glioblastoma
Fomchenko EI, Erson-Omay EZ, Zhao A, Bindra RS, Huttner A, Fulbright RK, Moliterno J. DNMT3A co-mutation in an IDH1-mutant glioblastoma. Molecular Case Studies 2019, 5: a004119. PMID: 31371348, PMCID: PMC6672028, DOI: 10.1101/mcs.a004119.Peer-Reviewed Original ResearchMeSH KeywordsAdultBiomarkers, TumorBrain NeoplasmsDNA (Cytosine-5-)-MethyltransferasesDNA MethylationDNA Methyltransferase 3ADNA Modification MethylasesEpigenesis, GeneticGene Expression ProfilingGene Expression Regulation, NeoplasticGlioblastomaGliomaHumansIsocitrate DehydrogenaseMaleMutationMutation, MissensePromoter Regions, GeneticConceptsIDH1-mutant glioblastomaEpigenetic controlHistone modificationsTranscriptional regulationDNA methylationExpression profilesGlioblastoma biologySomatic mutationsDe novoMutationsMutant glioblastomasTumor landscapeMutational profileTargeted therapeutic approachesGlioblastomaImportant roleMethylationDNMT3ABiologyGliomagenesisMissenseRegulationNovoPrimary brain tumorsTherapeutic approaches
2010
Inhibition of poly(ADP-ribose) polymerase down-regulates BRCA1 and RAD51 in a pathway mediated by E2F4 and p130
Hegan DC, Lu Y, Stachelek GC, Crosby ME, Bindra RS, Glazer PM. Inhibition of poly(ADP-ribose) polymerase down-regulates BRCA1 and RAD51 in a pathway mediated by E2F4 and p130. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 2201-2206. PMID: 20133863, PMCID: PMC2836641, DOI: 10.1073/pnas.0904783107.Peer-Reviewed Original ResearchMeSH KeywordsCell Line, TumorColonic NeoplasmsCrk-Associated Substrate ProteinDNA RepairDown-RegulationE2F4 Transcription FactorEnzyme InhibitorsGenes, BRCA1HumansPhenanthrenesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesPromoter Regions, GeneticRad51 RecombinaseRadiation-Sensitizing AgentsRNA, Small InterferingConceptsHomology-dependent repairBase excision repair factorsExcision repair factorsPARP inhibitionRole of PARPPARP inhibitorsRepair factorsExpression of BRCA1DNA repairDNA breaksHypoxic cancer cellsRAD51SiRNA knockdownDNA damagePARP-1P130 expressionCancer therapyP130Cancer cellsPARPRad51 promoterHPV E7BRCA1E7 expressionSiRNAs
2007
Co-repression of mismatch repair gene expression by hypoxia in cancer cells: Role of the Myc/Max network
Bindra RS, Glazer PM. Co-repression of mismatch repair gene expression by hypoxia in cancer cells: Role of the Myc/Max network. Cancer Letters 2007, 252: 93-103. PMID: 17275176, DOI: 10.1016/j.canlet.2006.12.011.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell Cycle ProteinsCell HypoxiaCell Line, TumorDNA Mismatch RepairDown-RegulationGene Expression Regulation, NeoplasticGenomic InstabilityHumansHypoxia-Inducible Factor 1MutL Protein Homolog 1MutS Homolog 2 ProteinNeoplasmsNuclear ProteinsPromoter Regions, GeneticProto-Oncogene Proteins c-mycRepressor ProteinsConceptsHypoxia-inducible factorHypoxia-induced genetic instabilityGene expressionGenetic instabilityRepair genesStress response pathwaysC-Myc/MaxStress response factorsMismatch repair genesCancer cellsRepair gene expressionMax complexesCoordinated repressionKey genesDNA repairMMR pathwayProximal promoterMicroenvironmental stressMax networkMMR gene expressionDeficient cellsGenesRepressionEssential roleMMR genes
2006
Basal repression of BRCA1 by multiple E2Fs and pocket proteins at adjacent E2F sites
Bindra RS, Glazer PM. Basal repression of BRCA1 by multiple E2Fs and pocket proteins at adjacent E2F sites. Cancer Biology & Therapy 2006, 5: 1400-1407. PMID: 17106239, DOI: 10.4161/cbt.5.10.3454.Peer-Reviewed Original ResearchConceptsAdjacent E2F sitesE2F siteP107 complexesPocket proteinsQuantitative chromatin immunoprecipitation analysisBRCA1 promoterE2F-dependent repressionPocket proteins p130Chromatin immunoprecipitation analysisBRCA1 expressionProximal promoter regionCritical tumor suppressor genesUnderstanding of regulationTumor suppressor geneAdjacent promoter elementsTumor microenvironmental stressE2F complexesProtein p130Transcriptional regulationBasal repressionPromoter occupancyLog-phase cellsBasal repressorPromoter elementsTarget genesRepression of RAD51 gene expression by E2F4/p130 complexes in hypoxia
Bindra RS, Glazer PM. Repression of RAD51 gene expression by E2F4/p130 complexes in hypoxia. Oncogene 2006, 26: 2048-2057. PMID: 17001309, DOI: 10.1038/sj.onc.1210001.Peer-Reviewed Original ResearchConceptsDNA repair pathwaysE2F siteRepair pathwaysHypoxia-induced genetic instabilityGenetic instabilityCoordinated transcriptional programRepair genesHypoxic stressRecombinational repair genesDownregulation of Rad51RAD51 gene expressionTranscriptional programsProximal promoterGene expressionNuclear accumulationMechanistic basisDNA mismatch repair genesRAD51BRCA1 promoterGenesPromoterMismatch repair genesBRCA1 geneNew therapeutic strategiesSimilar mechanism
2005
Hypoxia-Induced Down-regulation of BRCA1 Expression by E2Fs
Bindra RS, Gibson SL, Meng A, Westermark U, Jasin M, Pierce AJ, Bristow RG, Classon MK, Glazer PM. Hypoxia-Induced Down-regulation of BRCA1 Expression by E2Fs. Cancer Research 2005, 65: 11597-11604. PMID: 16357170, DOI: 10.1158/0008-5472.can-05-2119.Peer-Reviewed Original ResearchMeSH KeywordsBRCA1 ProteinBreast NeoplasmsCell HypoxiaChromatin ImmunoprecipitationColonic NeoplasmsDNA RepairDown-RegulationE2F Transcription FactorsGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitLuciferasesLung NeoplasmsPromoter Regions, GeneticRecombination, GeneticReverse Transcriptase Polymerase Chain ReactionRNA, MessengerTranscription, GeneticTumor Cells, CulturedConceptsHomologous recombinationBRCA1 expressionGenetic instabilityError-prone NHEJ pathwayAdjacent E2F sitesHomologous recombination pathwayImpaired homologous recombinationNonhomologous end-joining repair pathwayGenetic mutationsTranscriptional repressionE2F sitePromoter occupancyTranscriptional responseDNA repairNHEJ pathwayRepair pathwaysNovel linkE2FRecombination pathwayBRCA1 promoterSporadic cancersIntriguing mechanismBRCA1 inactivationDynamic redistributionRepression