2022
Randomized Trial of Olaparib With or Without Cediranib for Metastatic Castration-Resistant Prostate Cancer: The Results From National Cancer Institute 9984
Kim JW, McKay RR, Radke MR, Zhao S, Taplin ME, Davis NB, Monk P, Appleman LJ, Lara PN, Vaishampayan UN, Zhang J, Paul AK, Bubley G, Van Allen EM, Unlu S, Huang Y, Loda M, Shapiro GI, Glazer PM, LoRusso PM, Ivy SP, Shyr Y, Swisher EM, Petrylak DP. Randomized Trial of Olaparib With or Without Cediranib for Metastatic Castration-Resistant Prostate Cancer: The Results From National Cancer Institute 9984. Journal Of Clinical Oncology 2022, 41: 871-880. PMID: 36256912, PMCID: PMC9901975, DOI: 10.1200/jco.21.02947.Peer-Reviewed Original ResearchConceptsMetastatic castration-resistant prostate cancerRadiographic progression-free survivalMedian radiographic progression-free survivalCastration-resistant prostate cancerArm AProstate cancerAdverse eventsGrade 3Progressive metastatic castration-resistant prostate cancerEndothelial growth factor receptor inhibitorEnd pointHomologous recombination repair genesGrowth factor receptor inhibitorsPrimary end pointSecondary end pointsProgression-free survivalRecombination repair genesPoly (ADP-ribose) polymerase inhibitionTreat setTreat patientsClinical outcomesRandomized trialsPreclinical modelsReceptor inhibitorsCediranib
2021
Cooperation between oncogenic Ras and wild-type p53 stimulates STAT non-cell autonomously to promote tumor radioresistance
Dong YL, Vadla GP, Lu J, Ahmad V, Klein TJ, Liu LF, Glazer PM, Xu T, Chabu CY. Cooperation between oncogenic Ras and wild-type p53 stimulates STAT non-cell autonomously to promote tumor radioresistance. Communications Biology 2021, 4: 374. PMID: 33742110, PMCID: PMC7979758, DOI: 10.1038/s42003-021-01898-5.Peer-Reviewed Original ResearchMeSH KeywordsA549 CellsAnimalsAnimals, Genetically ModifiedCell ProliferationCytokinesDrosophila melanogasterDrosophila ProteinsFemaleGene Expression Regulation, NeoplasticGenes, rasHumansJanus KinasesLung NeoplasmsMaleMice, NudeMice, TransgenicParacrine CommunicationRadiation ToleranceSignal TransductionSTAT Transcription FactorsTumor BurdenTumor Suppressor Protein p53Xenograft Model Antitumor AssaysConceptsTumor microenvironmentTumor radioresistanceRas clonesOncogenic Ras mutationsClinical outcomesRA tissuesCancer patientsJAK/STATRadiation therapyRobust tumorOncogenic RasTherapy outcomeTumor resistanceTumor tissueRas mutationsTumor cellsJAK/OutcomesRadioresistanceCellular responsesTissueCell-cell interactionsPatientsCytokinesRadiotherapyClinical 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
2014
MicroRNA silencing for cancer therapy targeted to the tumour microenvironment
Cheng CJ, Bahal R, Babar IA, Pincus Z, Barrera F, Liu C, Svoronos A, Braddock DT, Glazer PM, Engelman DM, Saltzman WM, Slack FJ. MicroRNA silencing for cancer therapy targeted to the tumour microenvironment. Nature 2014, 518: 107-110. PMID: 25409146, PMCID: PMC4367962, DOI: 10.1038/nature13905.Peer-Reviewed Original Research
2000
Mutagenesis 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 mutationsPrognostic significance of cyclin D1 protein levels in early‐stage larynx cancer treated with primary radiation
Yoo S, Carter D, Turner B, Sasaki C, Son Y, Wilson L, Glazer P, Haffty B. Prognostic significance of cyclin D1 protein levels in early‐stage larynx cancer treated with primary radiation. International Journal Of Cancer 2000, 90: 22-28. PMID: 10725854, DOI: 10.1002/(sici)1097-0215(20000220)90:1<22::aid-ijc3>3.0.co;2-t.Peer-Reviewed Original ResearchConceptsEarly-stage larynx cancerLocal relapsePrognostic significanceLarynx cancerTotal median dosePrimary radiation therapySquamous cell carcinomaCell nuclear antigen levelsParaffin-embedded specimensSignificant clinical implicationsCase-control designPercent distributionLarynx cancer patientsCyclin D1 protein levelsCyclin D1 levelsMedian doseControl patientsLocal recurrenceAntigen levelsCancer patientsCell carcinomaDaily fractionsRadiation therapyIndex caseClinical information
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