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 interactionsPatientsCytokinesRadiotherapy
2000
Ionizing radiation-induced apoptosis via separate Pms2- and p53-dependent pathways.
Zeng M, Narayanan L, Xu X, Prolla T, Liskay R, Glazer P. Ionizing radiation-induced apoptosis via separate Pms2- and p53-dependent pathways. Cancer Research 2000, 60: 4889-93. PMID: 10987303.Peer-Reviewed Original ResearchMutant p53 protein overexpression in women with ipsilateral breast tumor recurrence following lumpectomy and radiation therapy
Turner B, Gumbs A, Carbone C, Carter D, Glazer P, Haffty B. Mutant p53 protein overexpression in women with ipsilateral breast tumor recurrence following lumpectomy and radiation therapy. Cancer 2000, 88: 1091-1098. PMID: 10699900, DOI: 10.1002/(sici)1097-0142(20000301)88:5<1091::aid-cncr21>3.0.co;2-y.Peer-Reviewed Original ResearchConceptsIpsilateral breast tumor recurrenceMutant p53 protein overexpressionBreast carcinoma patientsP53 protein overexpressionBreast tumor recurrenceDistant disease-free survivalDisease-free survivalCase-control studyPrimary breast tumorsCarcinoma patientsMutant p53 proteinBreast tumor relapseRadiation therapyTumor recurrenceBreast tumorsFree survivalProtein overexpressionPrognostic significanceP53 proteinEstrogen receptorTumor relapseIndex caseP53 mutationsControl casesP53 protein immunoreactivity
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 p53