2021
Clinical Activity and Safety of Cediranib and Olaparib Combination in Patients with Metastatic Pancreatic Ductal Adenocarcinoma without BRCA Mutation
Kim J, Cardin DB, Vaishampayan UN, Kato S, Grossman SR, Glazer P, Shyr Y, Ivy SP, LoRusso P. Clinical Activity and Safety of Cediranib and Olaparib Combination in Patients with Metastatic Pancreatic Ductal Adenocarcinoma without BRCA Mutation. The Oncologist 2021, 26: e1104-e1109. PMID: 33742489, PMCID: PMC8265343, DOI: 10.1002/onco.13758.Peer-Reviewed Original ResearchConceptsMetastatic pancreatic adenocarcinomaHomologous recombination DNA repair deficiencyMetastatic pancreatic ductal adenocarcinomaPancreatic ductal adenocarcinomaOlaparib combinationStable diseaseBRCA mutationsAdverse eventsDuctal adenocarcinomaCommon treatment-related adverse eventsVascular endothelial growth factor receptor inhibitorEndothelial growth factor receptor inhibitorTreatment-related adverse eventsGrowth factor receptor inhibitorsPrior systemic chemotherapyMedian overall survivalObjective response rateGermline BRCA mutationsBest overall responseExpression of BRCA1/2Restaging scanCancer cell linesPrimary endpointStudy drugSystemic chemotherapyClinical Efficacy of Olaparib in IDH1/IDH2-Mutant Mesenchymal Sarcomas
Eder JP, Doroshow DB, T. K, Keedy VL, Sklar JS, Glazer P, Bindra R, Shapiro GI. Clinical Efficacy of Olaparib in IDH1/IDH2-Mutant Mesenchymal Sarcomas. JCO Precision Oncology 2021, 5: 466-472. PMID: 34994649, PMCID: PMC9848565, DOI: 10.1200/po.20.00247.Peer-Reviewed Original ResearchConceptsPulmonary epithelioid hemangioendotheliomaStable diseaseEpithelioid hemangioendotheliomaClinical benefitClinical benefit rateOpen-label studyPrimary end pointPoly (ADP-ribose) polymerase inhibitionDefective homologous recombination (HR) repairMesenchymal sarcomaObjective responsePartial responseClinical efficacyPatient populationBenefit rateCombination trialsPatientsSolid tumorsIDH1/2-mutant tumorsIDH1/2 mutationsPARP inhibitorsEnd pointPARP inhibitionTumorsOlaparib
2017
A cell-penetrating antibody inhibits human RAD51 via direct binding
Turchick A, Hegan DC, Jensen RB, Glazer PM. A cell-penetrating antibody inhibits human RAD51 via direct binding. Nucleic Acids Research 2017, 45: 11782-11799. PMID: 29036688, PMCID: PMC5714174, DOI: 10.1093/nar/gkx871.Peer-Reviewed Original ResearchConceptsHomology-directed repairMolecular basisDirect bindingSynthetic lethal killingPre-clinical developmentBRCA2-deficient cancer cellsCell-penetrating antibodiesAnti-cancer agentsLupus autoantibodiesHuman Rad51DNA repairDNA bindingRAD51N-terminusCancer cellsSilico molecular modelingFunction mutationsCancer therapySpecific inhibitorDNANovel inhibitorsAttractive targetComplementarity-determining regionsMolecular modelingCell penetration
2000
Specific Mutations Induced by Triplex-Forming Oligonucleotides in Mice
Vasquez K, Narayanan L, Glazer P. Specific Mutations Induced by Triplex-Forming Oligonucleotides in Mice. Science 2000, 290: 530-533. PMID: 11039937, DOI: 10.1126/science.290.5491.530.Peer-Reviewed Original ResearchConceptsSomatic cellsSpecific genomic sitesEmbryonic stem cell technologyDuplex DNA sequencesGene functionGreater mutation frequenciesGenomic sitesGenome modificationChromosomal copyDNA sequencesSequence-controlled oligomersReporter geneStem cell technologyControl genesGerm-line mutationsGenesSpecific mutationsSupF geneControl oligomersMutationsMutation frequencyTransgenic miceOligonucleotideCellsMutation detectionMutant p53 protein overexpression in women with ipsilateral breast tumor recurrence following lumpectomy and radiation therapy
Turner B, Gumbs A, Carbone C, Carter D, Glazer P, Haffty B. Mutant p53 protein overexpression in women with ipsilateral breast tumor recurrence following lumpectomy and radiation therapy. Cancer 2000, 88: 1091-1098. PMID: 10699900, DOI: 10.1002/(sici)1097-0142(20000301)88:5<1091::aid-cncr21>3.0.co;2-y.Peer-Reviewed Original ResearchConceptsIpsilateral breast tumor recurrenceMutant p53 protein overexpressionBreast carcinoma patientsP53 protein overexpressionBreast tumor recurrenceDistant disease-free survivalDisease-free survivalCase-control studyPrimary breast tumorsCarcinoma patientsMutant p53 proteinBreast tumor relapseRadiation therapyTumor recurrenceBreast tumorsFree survivalProtein overexpressionPrognostic significanceP53 proteinEstrogen receptorTumor relapseIndex caseP53 mutationsControl casesP53 protein immunoreactivityActivation of human γ-globin gene expression via triplex-forming oligonucleotide (TFO)-directed mutations in the γ-globin gene 5′ flanking region
Xu X, Glazer P, Wang G. Activation of human γ-globin gene expression via triplex-forming oligonucleotide (TFO)-directed mutations in the γ-globin gene 5′ flanking region. Gene 2000, 242: 219-228. PMID: 10721715, DOI: 10.1016/s0378-1119(99)00522-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceBinding SitesCell LineDNADNA-Binding ProteinsGene Expression RegulationGlobinsHeLa CellsHost Cell Factor C1HumansK562 CellsMolecular Sequence DataMutagenesis, Site-DirectedMutationOctamer Transcription Factor-1OligonucleotidesProtein BindingRegulatory Sequences, Nucleic AcidTranscription FactorsTumor Cells, CulturedConceptsGamma-globin gene expressionGamma-globin geneGene expressionHuman γ-globin gene expressionVivo gene expression assaysΓ-globin gene expressionGenetic diseasesAgamma-globin geneMouse erythroleukemia cellsTarget gene expressionTarget siteBeta-globin disordersFetal hemoglobin (HPFH) conditionBeta-globin geneSingle base changeGene expression assaysProtein binding assaysTranscription factorsHuman normal fibroblast cellsDNA sequencing analysisCommon genetic diseaseFlanking regionsExpression assaysErythroleukemia cellsTriplex-forming oligonucleotides
1999
Different mutator phenotypes in Mlh1- versus Pms2-deficient mice
Yao X, Buermeyer A, Narayanan L, Tran D, Baker S, Prolla T, Glazer P, Liskay R, Arnheim N. Different mutator phenotypes in Mlh1- versus Pms2-deficient mice. Proceedings Of The National Academy Of Sciences Of The United States Of America 1999, 96: 6850-6855. PMID: 10359802, PMCID: PMC22005, DOI: 10.1073/pnas.96.12.6850.Peer-Reviewed Original ResearchConceptsMismatch repairMutator phenotypeMutation rateDifferent chromosomal locationsSingle-molecule PCRDinucleotide repeat lociMutation frequencyDNA mismatch repairMononucleotide repeat tractsChromosomal locationCellular processesDNA repair capacityHigh mutation frequencyDifferent mutator phenotypesMultiple genetic alterationsKnockout strainRepeat tractMlh1pMLH1 MMR geneRepeat lociGenetic alterationsDifferent tumor spectrumRepair capacityTumor developmentMMR genes
1997
Elevated levels of mutation in multiple tissues of mice deficient in the DNA mismatch repair gene Pms2
Narayanan L, Fritzell J, Baker S, Liskay R, Glazer P. Elevated levels of mutation in multiple tissues of mice deficient in the DNA mismatch repair gene Pms2. Proceedings Of The National Academy Of Sciences Of The United States Of America 1997, 94: 3122-3127. PMID: 9096356, PMCID: PMC20332, DOI: 10.1073/pnas.94.7.3122.Peer-Reviewed Original ResearchConceptsDNA mismatch repair gene PMS2Multiple tissuesMutation reporter geneMismatch repair gene PMS2Role of mutagenesisMammalian homologGenomic integrityReporter geneRepeat sequencesPMS2 locusMononucleotide repeat sequencesGenetic instabilityLimited tissue distributionDNA mismatch repair genesRepair genesHereditary colon cancerNormal developmentSlippage errorsGenesMutagenic treatmentEssential roleMismatch repair genesMutagenesisMutation frequencyHybrid transgenic mice
1996
Other transgenic mutation assays: Tissue specificity of spontaneous point mutations in λsupF transgenic mice
Leach E, Narayanan L, Havre P, Gunther E, Yeasky T, Glazer P. Other transgenic mutation assays: Tissue specificity of spontaneous point mutations in λsupF transgenic mice. Environmental And Molecular Mutagenesis 1996, 28: 459-464. PMID: 8991078, DOI: 10.1002/(sici)1098-2280(1996)28:4<459::aid-em23>3.0.co;2-d.Peer-Reviewed Original Research
1986
Detection and analysis of UV-induced mutations in mammalian cell DNA using a lambda phage shuttle vector.
Glazer P, Sarkar S, Summers W. Detection and analysis of UV-induced mutations in mammalian cell DNA using a lambda phage shuttle vector. Proceedings Of The National Academy Of Sciences Of The United States Of America 1986, 83: 1041-1044. PMID: 2937054, PMCID: PMC323006, DOI: 10.1073/pnas.83.4.1041.Peer-Reviewed Original ResearchConceptsMammalian cellsStable mouse L cell lineLambda phage shuttle vectorMouse cell DNACell DNAMammalian cell DNASupF geneMouse L cell lineDNA sequence analysisLambda phage vectorL cell lineMutant phageMouse cellsSequence analysisShuttle vectorUV-induced mutationsMultiple copiesUV mutagenesisPhage vectorEscherichia coliMutagenesisViable phagePhagesGenesT transition
1985
Direct and inducible mutagenesis in mammalian cells.
Summers W, Sarkar S, Glazer P. Direct and inducible mutagenesis in mammalian cells. Cancer Surveys 1985, 4: 517-28. PMID: 3916654.Peer-Reviewed Original ResearchConceptsMammalian cellsAnimal cellsAnimal virusesSimple eukaryotesInducible mutagenesisMutant geneSequence analysisShuttle vectorMutagenic pathwayMutagenesisDNA damageViral genomeWeigle mutagenesisMutagenic mechanismsDirect sequence analysisProkaryotesCellsBacteriaEukaryotesGenomeSimilar sitesRecent dataGenesExtrapolation of resultsPhages