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 survival
2000
High-frequency intrachromosomal gene conversion induced by triplex-forming oligonucleotides microinjected into mouse cells
Luo Z, Macris M, Faruqi A, Glazer P. High-frequency intrachromosomal gene conversion induced by triplex-forming oligonucleotides microinjected into mouse cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2000, 97: 9003-9008. PMID: 10900269, PMCID: PMC16811, DOI: 10.1073/pnas.160004997.Peer-Reviewed Original ResearchConceptsTriple helix-forming oligonucleotidesLtk- cell lineTK geneChromosomal lociIntrachromosomal gene conversionMouse Ltk- cell lineSingle chromosomal locusFunctional tk geneGene conversion eventsSite-specific recombinationSequence-specific mannerCell linesSimplex virus thymidine kinase geneVirus thymidine kinase geneHerpes simplex virus thymidine kinase geneThymidine kinase geneGene conversionIdentical base compositionMammalian cellsDownstream genesConversion eventsChromosomal sitesBase compositionKinase geneMutant copies
1999
Chromosomal 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
Role of DNA mismatch repair in the cytotoxicity of ionizing radiation.
Fritzell J, Narayanan L, Baker S, Bronner C, Andrew S, Prolla T, Bradley A, Jirik F, Liskay R, Glazer P. Role of DNA mismatch repair in the cytotoxicity of ionizing radiation. Cancer Research 1997, 57: 5143-7. PMID: 9371516.Peer-Reviewed Original ResearchConceptsMammalian cellsCellular responsesCell linesTranscription-coupled repairMMR systemWild-type cellsDNA-damaging agentsWild-type cell linesMMR-deficient cellsDNA mismatch repairDNA mismatch repair systemMismatch repair systemActive genesFutile repairMMR factorsAlkylation damageMismatch repairReplication errorsDNA damageRepair systemRelated miceCancer cellsClonogenic survivalMMR genesGenes
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 genep53 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 p53Mutagenesis by 8-methoxypsoralen and 5-methylangelicin photoadducts in mouse fibroblasts: mutations at cross-linkable sites induced by offoadducts as well as cross-links.
Gunther E, Yeasky T, Gasparro F, Glazer P. Mutagenesis by 8-methoxypsoralen and 5-methylangelicin photoadducts in mouse fibroblasts: mutations at cross-linkable sites induced by offoadducts as well as cross-links. Cancer Research 1995, 55: 1283-8. PMID: 7882323.Peer-Reviewed Original ResearchConceptsLambda phage shuttle vectorMutation reporter geneMammalian cellsCross-linkable sitesFibroblast cell lineMouse fibroblast cell lineReporter geneMolecular eventsShuttle vectorSpectrum of mutationsMouse fibroblastsPremutagenic lesionsSupF geneCross-link formationMutationsC transversionCell linesMutagenesisGenesApt sitePsoralen treatmentCellsSitesDNA
1985
Oncogene Expression in Isogenic, EBV-Positive and -Negative Burkitt Lymphoma Cell Lines
Glazer P, Summers W. Oncogene Expression in Isogenic, EBV-Positive and -Negative Burkitt Lymphoma Cell Lines. Intervirology 1985, 23: 82-89. PMID: 2984143, DOI: 10.1159/000149589.Peer-Reviewed Original ResearchConceptsEpstein-Barr virusNegative Burkitt lymphoma cell lineCell linesBJAB cellsOncogene expressionC-MycBurkitt's lymphoma cell linesMechanism of actionEBV infectionBL cell linesEBV-positiveC-myc expressionLymphoma cell linesLymphoid cellsOncogene c-mycBL cellsElevated expressionNormal karyotypeInitial reportMode of actionChromosomal translocationsBJABChromosome 8Ha-rasCellular oncogenes