2020
Ku80-Targeted pH-Sensitive Peptide–PNA Conjugates Are Tumor Selective and Sensitize Cancer Cells to Ionizing Radiation
Kaplan AR, Pham H, Liu Y, Oyaghire S, Bahal R, Engelman DM, Glazer PM. Ku80-Targeted pH-Sensitive Peptide–PNA Conjugates Are Tumor Selective and Sensitize Cancer Cells to Ionizing Radiation. Molecular Cancer Research 2020, 18: 873-882. PMID: 32098827, PMCID: PMC7272299, DOI: 10.1158/1541-7786.mcr-19-0661.Peer-Reviewed Original ResearchConceptsCancer cellsTumor cellsLocal tumor irradiationTumor-selective radiosensitizationMouse tumor modelsKu80 expressionNovel agentsTumor irradiationTumor growthTumor microenvironmentTumor modelRadiation treatmentTherapeutic agentsSubcutaneous mouse tumor modelTumorsMiceCancer therapyHealthy tissueAcute toxicitySpecific targetingSelective effectPNA antisenseTumor-SelectiveAcidic culture conditionsSensitize cancer cells
2000
Triple-Helix Formation Induces Recombination in Mammalian Cells via a Nucleotide Excision Repair-Dependent Pathway
Faruqi A, Datta H, Carroll D, Seidman M, Glazer P. Triple-Helix Formation Induces Recombination in Mammalian Cells via a Nucleotide Excision Repair-Dependent Pathway. Molecular And Cellular Biology 2000, 20: 990-1000. PMID: 10629056, PMCID: PMC85216, DOI: 10.1128/mcb.20.3.990-1000.2000.Peer-Reviewed Original ResearchAnimalsBase SequenceCell Line, TransformedChromosome MappingColonic NeoplasmsCOS CellsDNA RepairDNA-Binding ProteinsGenes, ReporterGenes, SuppressorHumansModels, GeneticMutagenesisNucleic Acid ConformationOligodeoxyribonucleotidesRecombinant ProteinsRecombination, GeneticRNA, TransferRNA-Binding ProteinsSequence DeletionTransfectionTumor Cells, CulturedXeroderma Pigmentosum Group A ProteinActivation 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
1998
Expression of AP-2 transcription factors in human breast cancer correlates with the regulation of multiple growth factor signalling pathways.
Turner B, Zhang J, Gumbs A, Maher M, Kaplan L, Carter D, Glazer P, Hurst H, Haffty B, Williams T. Expression of AP-2 transcription factors in human breast cancer correlates with the regulation of multiple growth factor signalling pathways. Cancer Research 1998, 58: 5466-72. PMID: 9850080.Peer-Reviewed Original ResearchMeSH KeywordsBinding SitesBreastBreast NeoplasmsDNA-Binding ProteinsEpitheliumFemaleHumansImmunohistochemistryPrognosisPromoter Regions, GeneticReceptor, ErbB-2Receptor, IGF Type 1Receptors, EstrogenReceptors, Growth FactorReceptors, ProgesteroneSignal TransductionTranscription Factor AP-2Transcription FactorsTumor Cells, CulturedUp-RegulationConceptsAP-2 transcription factorsAP-2-binding sitesTranscription factorsAP-2gammaAP-2alphaAP-2 gene familyAP-2 geneAP-2 family membersInsulin-like growth factor I receptorAP-2 familySignal transduction moleculesAP-2 proteinsAP-2alpha proteinMammalian developmentGene familyHuman breast cancerGrowth factor receptorTransduction moleculesProximal promoterBreast cancerReceptor promoterMultiple growth factorsBreast cancer cell linesCell growthAP-2gamma expressionMutagenesis induced by the tumor microenvironment
Yuan J, Glazer P. Mutagenesis induced by the tumor microenvironment. Mutation Research/Fundamental And Molecular Mechanisms Of Mutagenesis 1998, 400: 439-446. PMID: 9685702, DOI: 10.1016/s0027-5107(98)00042-6.Peer-Reviewed Original Research
1995
p53 inactivation by HPV16 E6 results in increased mutagenesis in human cells.
Havre P, Yuan J, Hedrick L, Cho K, Glazer P. p53 inactivation by HPV16 E6 results in increased mutagenesis in human cells. Cancer Research 1995, 55: 4420-4. PMID: 7671255.Peer-Reviewed Original ResearchConceptsHigh-risk E6P53 inactivationHPV16 E6Low-risk E6Human papillomavirus proteinsG1 arrestCell linesHPV16 E6 geneHPV11 E6Carcinoma cell linesColon carcinoma cell linePapillomavirus proteinsLow dosesHPV16 E7E6 geneClonal cell linesE7 bindsNormal p53RKO cellsTumor suppressor protein p53P53 degradationSuppressor protein p53P53E6Protein p53