2018
Ataxia Telangiectasia Mutated Protein Loss and Benefit From Oxaliplatin-based Chemotherapy in Colorectal Cancer
Sundar R, Miranda S, Rodrigues D, Chénard-Poirier M, Dolling D, Clarke M, Figueiredo I, Bertan C, Yuan W, Ferreira A, Chistova R, Boysen G, Perez D, Tunariu N, Mateo J, Wotherspoon A, Chau I, Cunningham D, Valeri N, Carreira S, de Bono J. Ataxia Telangiectasia Mutated Protein Loss and Benefit From Oxaliplatin-based Chemotherapy in Colorectal Cancer. Clinical Colorectal Cancer 2018, 17: 280-284. PMID: 30042009, DOI: 10.1016/j.clcc.2018.05.011.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic Combined Chemotherapy ProtocolsAtaxia Telangiectasia Mutated ProteinsBiomarkers, TumorColorectal NeoplasmsDNA RepairFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansLiver NeoplasmsMaleMiddle AgedOxaliplatinPrognosisRetrospective StudiesSurvival RateYoung AdultConceptsATM lossColorectal cancerAssociated with superior overall survivalDNA repair targeting agentsMetastatic colorectal cancer patientsAtaxia telangiectasiaIrinotecan-based therapySuperior overall survivalOxaliplatin-based therapyOxaliplatin-based chemotherapyTreatment of colorectal cancerATM protein expressionClinical outcome dataNuclear staining intensityColorectal cancer patientsDrug Development UnitColorectal cancer samplesOverall survivalMutation statusH-scoreTargeted agentsClinical outcomesDNA repair signalingTumor samplesCancer patients
2013
Radio-sensitization of human leukaemic MOLT-4 cells by DNA-dependent protein kinase inhibitor, NU7441
Tichy A, Durisova K, Salovska B, Pejchal J, Zarybnicka L, Vavrova J, Dye N, Sinkorova Z. Radio-sensitization of human leukaemic MOLT-4 cells by DNA-dependent protein kinase inhibitor, NU7441. Radiation And Environmental Biophysics 2013, 53: 83-92. PMID: 24100951, DOI: 10.1007/s00411-013-0494-5.Peer-Reviewed Original ResearchConceptsDNA-dependent protein kinasePhosphorylation of H2A.XMOLT-4 cellsDNA-dependent protein kinase inhibitorDNA repair signalingProtein kinase inhibitorsAnti-apoptotic Mcl-1Cleavage of PARPHistone H2A.X.Cdc25A phosphataseProtein kinaseRepair signalingMolecular mechanismsNU7441Mcl-1Detection of IRDNA damageSpecific inhibitorPhosphorylationDetection of proteinsH2A.XSubsequent inductionKinase inhibitorsWestern blottingApoptosisInhibition of Hsp27 Radiosensitizes Head-and-Neck Cancer by Modulating Deoxyribonucleic Acid Repair
Guttmann DM, Hart L, Du K, Seletsky A, Koumenis C. Inhibition of Hsp27 Radiosensitizes Head-and-Neck Cancer by Modulating Deoxyribonucleic Acid Repair. International Journal Of Radiation Oncology • Biology • Physics 2013, 87: 168-175. PMID: 23849696, DOI: 10.1016/j.ijrobp.2013.05.028.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsCell Line, TumorDNA RepairDNA-Binding ProteinsDNA, NeoplasmGene Knockdown TechniquesHead and Neck NeoplasmsHistonesHSP27 Heat-Shock ProteinsHumansMiceMice, NudeOligonucleotidesProtein Serine-Threonine KinasesRadiation ToleranceRNA, Small InterferingTumor Suppressor ProteinsConceptsShort hairpin RNANeck cancer cell linesCancer cell linesNeck cancerNude miceTumor growthHsp27 knockdownRadiotherapy of headFractionated radiation therapyFaDu human headEffect of Hsp27Cell linesEffective clinical agentRole of HSP27LNA treatmentFlank tumorsRadiation therapyTumor xenograftsDeoxyribonucleic acid repairTumor radiosensitizationClonogenic survivalClinical agentsHairpin RNAHSP27DNA repair signaling
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