2019
Impact of hypoxia on DNA repair and genome integrity
Kaplan AR, Glazer PM. Impact of hypoxia on DNA repair and genome integrity. Mutagenesis 2019, 35: 61-68. PMID: 31282537, PMCID: PMC7317153, DOI: 10.1093/mutage/gez019.Peer-Reviewed Original ResearchConceptsDNA repairDNA repair pathwaysHomology-directed repairBase excision repairGenome integrityRepair pathwaysGenomic instabilityExcision repairHypoxia mimeticMismatch repairDiverse mechanismsImpact of hypoxiaCancer progressionMutation frequencyTumor biologyTumor microenvironmentDevelopment of metastasesPotential clinical relevanceProfound effectRepairBiologyHypoxiaPathwayHallmarkMicroenvironment
2001
Hypermutability to ionizing radiation in mismatch repair-deficient, Pms2 knockout mice.
Xu X, Narayanan L, Dunklee B, Liskay R, Glazer P. Hypermutability to ionizing radiation in mismatch repair-deficient, Pms2 knockout mice. Cancer Research 2001, 61: 3775-80. PMID: 11325851.Peer-Reviewed Original ResearchConceptsMismatch repairSimple sequence repeatsWild-type transgenic miceCell linesLambda cII geneMutation frequencyDNA mismatch repairHigher clonogenic survivalMMR-deficient miceLambda shuttle vectorTolerance phenotypeSequence repeatsPatterns of IRReporter geneRepeat sequencesMononucleotide repeat sequencesShuttle vectorSingle bp deletionCII geneNullizygous animalsNullizygous miceHypermutabilityBp deletionWild-type miceClonogenic survivalGenomic Instability in Cancer
Rockwell S, Yuan J, Peretz S, Glazer P. Genomic Instability in Cancer. Novartis Foundation Symposia 2001, 240: 133-151. PMID: 11727926, DOI: 10.1002/0470868716.ch9.Peer-Reviewed Original ResearchConceptsGenomic instabilityChromosomal fragile sitesExposure of cellsNutrient deprivationDNA repairGenomic rearrangementsSelection pressureDNA overreplicationGene expressionGenetic changesFragile sitesGenetic heterogeneityCell proliferationGene amplificationCell populationsBenign cell populationsMutation frequencyHypoxic environmentAggressive phenotypeSolid tumorsExpressionOverreplicationCellsAdverse microenvironmentCytogenetic changes
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 detectionMutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts
Andrew S, Xu X, Baross-Francis A, Narayanan L, Milhausen K, Liskay R, Jirik F, Glazer P. Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts. Carcinogenesis 2000, 21: 1291-1296. PMID: 10874005, DOI: 10.1093/carcin/21.7.1291.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphatasesAnimalsBase Pair MismatchCrosses, GeneticDNA RepairDNA Repair EnzymesDNA-Binding ProteinsFemaleFrameshift MutationGenes, ReporterGenotypeGerm-Line MutationMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicMismatch Repair Endonuclease PMS2MutagenesisMutS Homolog 2 ProteinPoint MutationProteinsProto-Oncogene ProteinsConceptsPms2-deficient miceMsh2-deficient miceHereditary non-polyposis colorectal cancer patientsCII target geneDNA mismatch repair deficiencyColorectal cancer patientsPMS2 germline mutationsMismatch repair deficiencyReporter transgenic miceMutation frequencyLacI target geneCancer patientsTarget genesMouse modelKnockout miceTumor spectrumTransgenic miceFrameshift mutationGermline mutationsMiceRepair deficiencyPMS2 deficiencySupF target geneMSH2Predominant mutationsMutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts
Andrew S, Xu X, Baross-Francis A, Narayanan L, Milhausen K, Liskay R, Jirik F, Glazer P. Mutagenesis in PMS2- and MSH2-deficient mice indicates differential protection from transversions and frameshifts. Carcinogenesis 2000, 21: 1291-1296. DOI: 10.1093/carcin/21.5.291.Peer-Reviewed Original ResearchPms2-deficient miceMouse modelMsh2-deficient miceHereditary non-polyposis colorectal cancer patientsCII target geneDNA mismatch repair deficiencyColorectal cancer patientsPMS2 germline mutationsMismatch repair deficiencyReporter transgenic miceMsh2-/- miceKnockout mouse modelMutation frequencyLacI target geneCancer patientsTarget genesKnockout miceTumor spectrumTransgenic miceFrameshift mutationGermline mutationsMiceRepair deficiencyPMS2 deficiencySupF target gene
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 genesChromosomal mutations induced by triplex-forming oligonucleotides in mammalian cells
Vasquez K, Wang G, Havre P, Glazer P. Chromosomal mutations induced by triplex-forming oligonucleotides in mammalian cells. Nucleic Acids Research 1999, 27: 1176-1181. PMID: 9927753, PMCID: PMC148300, DOI: 10.1093/nar/27.4.1176.Peer-Reviewed Original ResearchConceptsTriplex-forming oligonucleotidesMutation reporter geneMultiple chromosomal copiesMutation frequencyMammalian chromosomesTriplex binding siteMammalian cellsChromosomal copyFibroblast cell lineChromosomal lociGenetic manipulationMouse fibroblast cell lineSequencing dataChromosomal mutationsDuplex DNAUntreated control cellsBinding sitesCell linesControl cellsSpecific recognitionMutagenesisMutationsT transversionSpecific sitesCells
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 micePotassium-Resistant Triple Helix Formation and Improved Intracellular Gene Targeting by Oligodeoxyribonucleotides Containing 7-Deazaxanthine
Faruqi A, Krawczyk S, Matteucci M, Glazer P. Potassium-Resistant Triple Helix Formation and Improved Intracellular Gene Targeting by Oligodeoxyribonucleotides Containing 7-Deazaxanthine. Nucleic Acids Research 1997, 25: 633-640. PMID: 9016606, PMCID: PMC146453, DOI: 10.1093/nar/25.3.633.Peer-Reviewed Original ResearchConceptsTriple helix-forming oligonucleotidesTriple helix formationGel mobility shift assaysHelix formationMutation reporter geneMobility shift assaysMammalian cellsAnti-gene strategyHigh mutation frequencyShift assaysGene targetingReporter geneGenesPhosphodiester backboneMutation frequencyPsoralen adductsVivo geneTriplex formationPhysiological concentrationsNucleotide chemistry