2025
Transcription elongation factor ELOF1 is required for efficient somatic hypermutation and class switch recombination
Wu L, Yadavalli A, Senigl F, Matos-Rodrigues G, Xu D, Pintado-Urbanc A, Simon M, Wu W, Nussenzweig A, Schatz D. Transcription elongation factor ELOF1 is required for efficient somatic hypermutation and class switch recombination. Molecular Cell 2025, 85: 1296-1310.e7. PMID: 40049160, PMCID: PMC11972161, DOI: 10.1016/j.molcel.2025.02.007.Peer-Reviewed Original ResearchRNA polymerase IITranscription-coupled nucleotide excision repairActivation-induced deaminaseClass switch recombinationSomatic hypermutationRNA polymerase II elongation complexDownstream of transcription start sitesRNA polymerase II transcriptionTranscription start siteSwitch recombinationMammalian B cellsImmunoglobulin (Ig) genesDNA cytidine deaminaseNucleotide excision repairPolymerase IISerine 5Transcribed genesTranscription elongationElongation complexStart siteGenetic screeningELOF1Excision repairTranscriptionProximity partners
2024
Strand-resolved mutagenicity of DNA damage and repair
Anderson C, Talmane L, Luft J, Connelly J, Nicholson M, Verburg J, Pich O, Campbell S, Giaisi M, Wei P, Sundaram V, Connor F, Ginno P, Sasaki T, Gilbert D, López-Bigas N, Semple C, Odom D, Aitken S, Taylor M. Strand-resolved mutagenicity of DNA damage and repair. Nature 2024, 630: 744-751. PMID: 38867042, PMCID: PMC11186772, DOI: 10.1038/s41586-024-07490-1.Peer-Reviewed Original ResearchConceptsDNA damageDNA damage-induced mutationsSingle-base resolutionCancer genome evolutionDamage-induced mutationsRepair of DNA damageNucleotide excision repairGenome evolutionMultiple distinct mutationsDNA accessibilityGenomic conditionsReplicative strandProcess genomesDNA base damageTranslesion polymerasesExcision repairDNAMutation patternsMutationsBase damageRepair efficiencyStrandsAlkyl adductsReplicationIdentity fidelityMutational signature-based identification of DNA repair deficient gastroesophageal adenocarcinomas for therapeutic targeting
Prosz A, Sahgal P, Huffman B, Sztupinszki Z, Morris C, Chen D, Börcsök J, Diossy M, Tisza V, Spisak S, Likasitwatanakul P, Rusz O, Csabai I, Cecchini M, Baca Y, Elliott A, Enzinger P, Singh H, Ubellaker J, Lazaro J, Cleary J, Szallasi Z, Sethi N. Mutational signature-based identification of DNA repair deficient gastroesophageal adenocarcinomas for therapeutic targeting. Npj Precision Oncology 2024, 8: 87. PMID: 38589664, PMCID: PMC11001913, DOI: 10.1038/s41698-024-00561-6.Peer-Reviewed Original ResearchNucleotide excision repairGastric cancer cell linesNucleotide excision repair-deficientPlatinum chemotherapyHR deficiencyCancer cell linesPARP inhibitorsHomologous recombinationGenome sequence dataSensitivity to platinum chemotherapySingle-cell RNA sequencingCell linesHR-deficient cancersDNA repair pathwaysSensitivity to cisplatinRad51 foci assaysMutational signature analysisSequence dataGenomic featuresWhole exomeInduce apoptosisRNA sequencingGastroesophageal adenocarcinomaRepair pathwaysHRD score
2022
Proteomic profiling reveals an association between ALDH and oxidative phosphorylation and DNA damage repair pathways in human colon adenocarcinoma stem cells
Wang Y, Chen Y, Garcia-Milian R, Golla JP, Charkoftaki G, Lam TT, Thompson DC, Vasiliou V. Proteomic profiling reveals an association between ALDH and oxidative phosphorylation and DNA damage repair pathways in human colon adenocarcinoma stem cells. Chemico-Biological Interactions 2022, 368: 110175. PMID: 36162455, PMCID: PMC9891852, DOI: 10.1016/j.cbi.2022.110175.Peer-Reviewed Original ResearchConceptsCancer stem cellsProteomic profilingOxidative phosphorylationLabel-free quantitative proteomic analysisDNA damage repair pathwaysQuantitative proteomic analysisAldehyde dehydrogenase familyColon cancer stem cellsCOLO320DM cellsStem cellsNucleotide excision repairDamage repair pathwaysIngenuity Pathway AnalysisCell populationsProteomic analysisProteomic datasetsDehydrogenase familyMetabolic switchProteomic studiesRepair pathwaysCellular pathwaysALDH enzymatic activityCellular survivalExcision repairALDH activityAn ELISA-based platform for rapid identification of structure-dependent nucleic acid–protein interactions detects novel DNA triplex interactors
Economos NG, Thapar U, Balasubramanian N, Karras GI, Glazer PM. An ELISA-based platform for rapid identification of structure-dependent nucleic acid–protein interactions detects novel DNA triplex interactors. Journal Of Biological Chemistry 2022, 298: 102398. PMID: 35988651, PMCID: PMC9493393, DOI: 10.1016/j.jbc.2022.102398.Peer-Reviewed Original ResearchConceptsNucleic acid structuresNucleic acid-protein interactionsNucleotide excision repairSingle-strand annealing repairDouble-strand break intermediatesUnusual nucleic acid structuresNovel interactorNucleic acid interactionsHigh-throughput platformCellular processesFactor localizationAcid structureExcision repairRelevant lociHuman cellsGene editingAcid interactionsInteractorsTherapeutic gene editingNucleic acidsDNA triplexesRapid identificationComparative approachGenomeTriplexes
2021
PARP inhibitors in head and neck cancer: Molecular mechanisms, preclinical and clinical data
Moutafi M, Economopoulou P, Rimm D, Psyrri A. PARP inhibitors in head and neck cancer: Molecular mechanisms, preclinical and clinical data. Oral Oncology 2021, 117: 105292. PMID: 33862558, DOI: 10.1016/j.oraloncology.2021.105292.Peer-Reviewed Original ResearchConceptsPoly (ADP-ribose) polymerase (PARP) inhibitorsCheckpoint inhibitorsCell death 1 (PD-1) checkpoint inhibitorsDeath-1 checkpoint inhibitorsDeath ligand 1 (PD-L1) expressionPARP inhibitorsPD-1 checkpoint inhibitorsNeck squamous cell carcinomaCornerstone of treatmentLigand 1 expressionImmune modulating effectsSquamous cell carcinomaSuccessful treatment outcomeDesign of trialsOutcome of therapyTreatment landscapeCell carcinomaNeck cancerTreatment outcomesClinical dataTherapeutic strategiesDNA damageRecent approvalImmune primingNucleotide excision repair
2020
EZH2 has a non-catalytic and PRC2-independent role in stabilizing DDB2 to promote nucleotide excision repair
Koyen A, Madden M, Park D, Minten E, Kapoor-Vazirani P, Werner E, Pfister N, Haji-Seyed-Javadi R, Zhang H, Xu J, Deng N, Duong D, Pecen T, Frazier Z, Nagel Z, Lazaro J, Mouw K, Seyfried N, Moreno C, Owonikoko T, Deng X, Yu D. EZH2 has a non-catalytic and PRC2-independent role in stabilizing DDB2 to promote nucleotide excision repair. Oncogene 2020, 39: 4798-4813. PMID: 32457468, PMCID: PMC7305988, DOI: 10.1038/s41388-020-1332-2.Peer-Reviewed Original ResearchConceptsSmall cell lung cancerCisplatin resistanceSCLC cellsCisplatin-based chemotherapyCell lung cancerImportant therapeutic targetZeste homolog 2Cellular cisplatinPoor outcomeAggressive malignancyNucleotide excision repairLung cancerClinical investigationTherapeutic targetEZH2 depletionPolycomb repressive complex 2Homolog 2DDB1-DDB2EZH2Important regulatorRepairExcision repairMethyltransferase activityPRC2-independent functionSynthetic lethality screen
2015
Multifaceted control of DNA repair pathways by the hypoxic tumor microenvironment
Scanlon SE, Glazer PM. Multifaceted control of DNA repair pathways by the hypoxic tumor microenvironment. DNA Repair 2015, 32: 180-189. PMID: 25956861, PMCID: PMC4522377, DOI: 10.1016/j.dnarep.2015.04.030.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsDNA repair pathwaysRepair pathwaysDNA repairCertain DNA repair genesMost DNA repair pathwaysDNA double-strand break repairDouble-strand break repairPost-translational modificationsNucleotide excision repairDNA repair genesTumor suppressor geneMultifaceted controlTranslational downregulationEpigenetic levelBreak repairMutator phenotypeCellular consequencesGenomic instabilityExcision repairHypoxic cancer cellsSuppressor geneIntra-tumor heterogeneityMismatch repairPersistent silencingDNA damage
2013
Early days of DNA repair: discovery of nucleotide excision repair and homology-dependent recombinational repair.
Rupp WD. Early days of DNA repair: discovery of nucleotide excision repair and homology-dependent recombinational repair. The Yale Journal Of Biology And Medicine 2013, 86: 499-505. PMID: 24348214, PMCID: PMC3848104.Peer-Reviewed Original ResearchConceptsHomology-dependent recombinational repairNucleotide excision repairRepairExcision repairFurther researchHypoxia and DNA repair.
Glazer PM, Hegan DC, Lu Y, Czochor J, Scanlon SE. Hypoxia and DNA repair. The Yale Journal Of Biology And Medicine 2013, 86: 443-51. PMID: 24348208, PMCID: PMC3848098.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsDNA repairHomology-dependent repairDNA repair pathwaysNucleotide excision repairDNA mismatch repairGenomic integrityDependent repairCell physiologyRepair pathwaysExcision repairHypoxic cancer cellsCell metabolismGenetic instabilityMismatch repairInduction of angiogenesisCancer progressionCell growthCancer cellsNeoplastic developmentRepairSolid tumorsKey componentHypoxiaProfound changesApoptosisGenetic Instability Induced by Hypoxic Stress
Scanlon S, Glazer P. Genetic Instability Induced by Hypoxic Stress. 2013, 151-181. DOI: 10.1007/978-1-4614-6280-4_8.ChaptersGenetic instabilityCell cycle checkpointsDNA repair pathwaysNucleotide excision repairHypoxic stress responseHomologous recombination repairGenomic integrityCellular machineryCycle checkpointsRepair pathwaysGenomic instabilityExcision repairRecombination repairStress responseApoptotic pathwayGenetic evolutionCellular responsesMismatch repairSignificant physiological stressCancer biologyDNA damageCancer progressionCell growthDNA damage rateHypoxic stress
2012
Rules of engagement for base excision repair in chromatin
Odell ID, Wallace SS, Pederson DS. Rules of engagement for base excision repair in chromatin. Journal Of Cellular Physiology 2012, 228: 258-266. PMID: 22718094, PMCID: PMC3468691, DOI: 10.1002/jcp.24134.Peer-Reviewed Original ResearchConceptsBase excision repairSingle-strand break repairNucleotide excision repairHomology-directed repairExcision repairCheckpoint activationCell cycle checkpoint activationStrand break repair pathwaysDouble-strand break repair pathwayStrand break repairBreak repair pathwayOxidative damage resultsNucleosome disruptionDNA replicationBreak repairRepair pathwaysDNA segmentsChromatinEfficient repairNumerous DNAOxidative DNA damageRegulatory factorsHuman cellsNucleosomesDNA damage
2011
Reduced Level of Ribonucleotide Reductase R2 Subunits Increases Dependence on Homologous Recombination Repair of Cisplatin-Induced DNA Damage
Lin ZP, Lee Y, Lin F, Belcourt MF, Li P, Cory JG, Glazer PM, Sartorelli AC. Reduced Level of Ribonucleotide Reductase R2 Subunits Increases Dependence on Homologous Recombination Repair of Cisplatin-Induced DNA Damage. Molecular Pharmacology 2011, 80: 1000-1012. PMID: 21875941, PMCID: PMC3228527, DOI: 10.1124/mol.111.074708.Peer-Reviewed Original ResearchConceptsNucleotide excision repairHomologous recombination repairR2 subunitRibonucleotide reductaseRecombination repairCell cycleP53-deficient human colon cancer cellsDNA damageS phaseDepletion of BRCA1Mammalian ribonucleotide reductaseSubsequent S phaseDouble-strand breaksHuman colon cancer cellsP53-deficient cancer cellsSingle-strand gapsCancer cellsCisplatin-induced DNA damageColon cancer cellsCisplatin-DNA lesionsGap-filling synthesisHeteromeric enzymeReplication stressΓ-H2AX inductionDNA repair
2010
Variation Within DNA Repair Pathway Genes and Risk of Multiple Sclerosis
Briggs FB, Goldstein BA, McCauley JL, Zuvich RL, De Jager PL, Rioux JD, Ivinson AJ, Compston A, Hafler DA, Hauser SL, Oksenberg JR, Sawcer SJ, Pericak-Vance MA, Haines JL, Barcellos LF, Consortium F. Variation Within DNA Repair Pathway Genes and Risk of Multiple Sclerosis. American Journal Of Epidemiology 2010, 172: 217-224. PMID: 20522537, PMCID: PMC3658128, DOI: 10.1093/aje/kwq086.Peer-Reviewed Original ResearchConceptsDNA repair pathway genesPathway genesMultiple sclerosisExcision repairGeneral transcription factor IIHDouble-strand break repairTranscription factor IIHDNA repair pathwaysNucleotide excision repairRisk of MSBase excision repairPrimary genetic risk factorProminent genetic componentHuman leukocyte antigenComplex autoimmune diseaseSingle nucleotide polymorphism (SNP) variantsCentral nervous systemLogistic regression modelingGenetic risk factorsSingle nucleotide polymorphismsBreak repairRepair pathwaysCandidate genesAutoimmune diseasesGenesHuman Telomeres Are Hypersensitive to UV-Induced DNA Damage and Refractory to Repair
Rochette PJ, Brash DE. Human Telomeres Are Hypersensitive to UV-Induced DNA Damage and Refractory to Repair. PLOS Genetics 2010, 6: e1000926. PMID: 20442874, PMCID: PMC2861706, DOI: 10.1371/journal.pgen.1000926.Peer-Reviewed Original ResearchConceptsUV-induced DNA damageDNA damageTelomeric repeatsHuman telomeresExcision repairTelomeric repeat unitsNucleotide excision repairDouble-strand breaksUV-induced CPDGenome integrityGenomic integrityExcision repair sitesMitochondrial DNARegion of p53Opposite strandTelomeresCPD removalUnrepaired lesionsRepeatsPreeminent risk factorUV sensitivityPyrimidine dimersCancer developmentRepeat unitsCritical role
2004
Hypermutability in a Drosophila model for multiple endocrine neoplasia type 1
Busygina V, Suphapeetiporn K, Marek LR, Stowers RS, Xu T, Bale AE. Hypermutability in a Drosophila model for multiple endocrine neoplasia type 1. Human Molecular Genetics 2004, 13: 2399-2408. PMID: 15333582, DOI: 10.1093/hmg/ddh271.Peer-Reviewed Original ResearchConceptsDNA cross-linking agentsNucleotide excision repairDNA damage-induced mutationsTumor suppressor geneDamage-induced mutationsDrosophila homologGenomic integrityHuman meninMutant fliesBiochemical functionsTranscriptional modulationNuclear proteinsDrosophila modelProtein 50Novel memberExcision repairNull allelesMolecular mechanismsCancer genesHistone deacetylaseSuppressor geneHomozygous inactivationMnn1Normal fliesGenes
1999
Targeted Correction of an Episomal Gene in Mammalian Cells by a Short DNA Fragment Tethered to a Triplex-forming Oligonucleotide*
Chan P, Lin M, Faruqi A, Powell J, Seidman M, Glazer P. Targeted Correction of an Episomal Gene in Mammalian Cells by a Short DNA Fragment Tethered to a Triplex-forming Oligonucleotide*. Journal Of Biological Chemistry 1999, 274: 11541-11548. PMID: 10206960, DOI: 10.1074/jbc.274.17.11541.Peer-Reviewed Original ResearchConceptsMammalian cellsGene correctionSV40 shuttle vectorTriplex motifNucleotide excision repairSequence-specific mannerEpisomal geneSupF reporter geneXPA cDNASpecific target sitesGene conversionShort DNA fragmentsDNA repairGene targetingTarget genesDNA segmentsReporter geneExcision repairDNA fragmentsBifunctional oligonucleotidesShuttle vectorSequence conversionGenesSV40 vectorsFlexible linker
1995
Induction of p53 in mouse cells decreases mutagenesis by UV radiation
Yuan J, Yeasky T, Havre P, Glazer P. Induction of p53 in mouse cells decreases mutagenesis by UV radiation. Carcinogenesis 1995, 16: 2295-2300. PMID: 7586125, DOI: 10.1093/carcin/16.10.2295.Peer-Reviewed Original ResearchConceptsInduction of p53Cell cycle blockCell linesCycle blockRole of p53Cell cycle analysisInvolvement of p53Lambda phage shuttle vectorWestern blotChromosomal damageClonogenic survivalNucleotide excision repairUV-induced mutationsCellular DNA damageP53 alleleRecent evidenceP53Recoverable lambda phage shuttle vectorFibroblast cell lineMutation reporter geneUV-induced lesionsG1 phaseP53 activityMouse fibroblast cell lineReporter geneAltered Repair of Targeted Psoralen Photoadducts in the Context of an Oligonucleotide-mediated Triple Helix (∗)
Wang G, Glazer P. Altered Repair of Targeted Psoralen Photoadducts in the Context of an Oligonucleotide-mediated Triple Helix (∗). Journal Of Biological Chemistry 1995, 270: 22595-22601. PMID: 7673252, DOI: 10.1074/jbc.270.38.22595.Peer-Reviewed Original ResearchConceptsTriplex-forming oligonucleotidesMammalian cellsPattern of mutationsSV40 shuttle vectorHeLa whole cell extractsMonkey COS cellsDNA repair pathwaysNucleotide excision repairSequence-specific mannerWhole cell extractsExcision repair patchesTriple helixPsoralen adductsSite-specific modificationThird strandGenetic manipulationSame target siteRepair pathwaysCOS cellsExcision repairAltered repairShuttle vectorCell extractsIncision stepTarget site
1991
Requirement for the replication protein SSB in human DMA excision repair
Coverley D, Kenny M, Munn M, Rupp W, Lane D, Wood R. Requirement for the replication protein SSB in human DMA excision repair. Nature 1991, 349: 538-541. PMID: 1992355, DOI: 10.1038/349538a0.Peer-Reviewed Original ResearchConceptsHuman SSBReplication proteinsExcision repairDNA excision repairEukaryotic replication proteinsSimian virus 40 DNA replicationDNA replication proteinsDNA-binding proteinsNucleotide excision repairCell-free systemRelative molecular massProtein SSBDNA replicationDNA repairRepair eventsPolymerase αSemiconservative replicationSV40 DNAGenetic materialMolecular massPlasmid moleculesMultienzyme processT antigenEssential processProtein
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