2018
Antigen-Specific CD8 Lytic Phenotype Induced by Sipuleucel-T in Hormone-Sensitive or Castration-Resistant Prostate Cancer and Association with Overall Survival
Antonarakis ES, Small EJ, Petrylak D, Quinn DI, Kibel AS, Chang NN, Dearstyne E, Harmon M, Campogan D, Haynes H, Vu T, Sheikh NA, Drake CG. Antigen-Specific CD8 Lytic Phenotype Induced by Sipuleucel-T in Hormone-Sensitive or Castration-Resistant Prostate Cancer and Association with Overall Survival. Clinical Cancer Research 2018, 24: 4662-4671. PMID: 29858218, PMCID: PMC6481607, DOI: 10.1158/1078-0432.ccr-18-0638.Peer-Reviewed Original ResearchMeSH KeywordsAcid PhosphataseCD8-Positive T-LymphocytesCell Line, TumorCell ProliferationClinical Trials as TopicGene Expression Regulation, NeoplasticGranulocyte-Macrophage Colony-Stimulating FactorHumansLysosomal-Associated Membrane Protein 1MaleNeoplasm MetastasisNeoplasms, Hormone-DependentProstatic Neoplasms, Castration-ResistantRecombinant Fusion ProteinsT-Lymphocytes, CytotoxicTissue ExtractsConceptsSipuleucel-T treatmentMetastatic castration-resistant prostate cancerProstatic acid phosphataseOverall survivalCTL activityWeek 26Immune responseWeek 6Peripheral cellular immune responsesCytotoxic T lymphocyte activityCastration-resistant prostate cancerEfficacy of sipuleucelImproved overall survivalMedian overall survivalT lymphocyte activityT cell responsesCellular immune responsesT cell proliferationClin Cancer ResHealthy volunteer samplesCD107a expressionLonger OSLymphocyte activityCytolytic responsesTertile analysis
2015
Palbociclib
Mangini N, Wesolowski R, Ramaswamy B, Lustberg M, Berger M. Palbociclib. Annals Of Pharmacotherapy 2015, 49: 1252-1260. PMID: 26324355, PMCID: PMC7331461, DOI: 10.1177/1060028015602273.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Combined Chemotherapy ProtocolsBreast NeoplasmsClinical Trials, Phase I as TopicClinical Trials, Phase II as TopicClinical Trials, Phase III as TopicCyclin-Dependent KinasesDisease-Free SurvivalEstradiolFemaleFulvestrantHumansLetrozoleNeoplasms, Hormone-DependentNitrilesPiperazinesPyridinesRandomized Controlled Trials as TopicReceptor, ErbB-2TriazolesUnited StatesConceptsProgression-free survivalAdvanced breast cancerInvestigator-assessed median progression-free survivalMedian progression-free survivalPhase III trialsBreast cancerEndocrine therapyIII trialsOncology abstractsHER2-negative advanced breast cancerHuman epidermal growth factor receptor 2Epidermal growth factor receptor 2Negative advanced breast cancerConfirmatory phase III trialClinical Oncology abstractsMedical Oncology abstractsPALOMA-3 trialFirst-line settingPhase II trialGrowth factor receptor 2Drug Administration approvalFactor receptor 2Life-threatening diseaseCyclin-dependent kinase 4Novel small molecule inhibitor
2014
Emergence of Constitutively Active Estrogen Receptor-α Mutations in Pretreated Advanced Estrogen Receptor–Positive Breast Cancer
Jeselsohn R, Yelensky R, Buchwalter G, Frampton G, Meric-Bernstam F, Gonzalez-Angulo AM, Ferrer-Lozano J, Perez-Fidalgo JA, Cristofanilli M, Gómez H, Arteaga CL, Giltnane J, Balko JM, Cronin MT, Jarosz M, Sun J, Hawryluk M, Lipson D, Otto G, Ross JS, Dvir A, Soussan-Gutman L, Wolf I, Rubinek T, Gilmore L, Schnitt S, Come SE, Pusztai L, Stephens P, Brown M, Miller VA. Emergence of Constitutively Active Estrogen Receptor-α Mutations in Pretreated Advanced Estrogen Receptor–Positive Breast Cancer. Clinical Cancer Research 2014, 20: 1757-1767. PMID: 24398047, PMCID: PMC3998833, DOI: 10.1158/1078-0432.ccr-13-2332.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsEstrogen Receptor alphaFemaleHigh-Throughput Nucleotide SequencingHumansMCF-7 CellsMutationNeoplasm StagingNeoplasms, Hormone-DependentConceptsEstrogen receptor α mutationBreast cancerAdvanced estrogen receptor-positive breast cancerEstrogen receptor-positive breast cancerReceptor-positive breast cancerHormone-dependent breast cancerPrimary breast cancerSubgroup of patientsER-negative tumorsLine of treatmentCodon 537ER- diseaseEndocrine treatmentTreatment-naïveESR1 mutationsMetastatic diseaseCell line modelsEndocrine resistanceMetastatic tumorsReceptor constitutive activityEstrogen receptorMetastatic samplesTumor specimensCancer-related genesNatural historyA phase II study of preoperative capecitabine in women with operable hormone receptor positive breast cancer
Tolaney SM, Jeong J, Guo H, Brock J, Morganstern D, Come SE, Golshan M, Bellon J, Winer EP, Krop IE. A phase II study of preoperative capecitabine in women with operable hormone receptor positive breast cancer. Cancer Medicine 2014, 3: 293-299. PMID: 24464780, PMCID: PMC3987079, DOI: 10.1002/cam4.164.Peer-Reviewed Original ResearchConceptsHormone receptor-positive breast cancerReceptor-positive breast cancerPathological complete responsePositive breast cancerBreast cancerPreoperative capecitabineClinical responseHER2-negative operable breast cancerDihydropyrimidine dehydrogenaseOnly grade 3 toxicityOverall clinical response rateThymidine phosphorylaseGrade 3 responsePartial clinical responsePathological response assessmentsPreoperative chemotherapy regimensClinical response rateComplete clinical responseGrade 3 toxicityOperable breast cancerPhase II studyPalmar-plantar erythrodysesthesiaMetastatic breast cancerTime of surgeryMiller-Payne
2013
Enzalutamide for the treatment of castration-resistant prostate cancer.
Ha Y, Goodin S, DiPaola R, Kim I. Enzalutamide for the treatment of castration-resistant prostate cancer. Drugs Of Today 2013, 49: 7-13. PMID: 23362491, DOI: 10.1358/dot.2013.49.1.1910724.Peer-Reviewed Original ResearchConceptsCastration-resistant prostate cancerPhase III trialsAndrogen receptorIII trialsProstate cancerTreatment of CRPCMetastatic castration-resistant prostate cancerPhase I/II studyEffectiveness of enzalutamidePrior docetaxel chemotherapyBinding of AROptimal safety profileMajor clinical challengeSignificant antitumor activityPrior chemotherapyDocetaxel chemotherapyII studySafety profileClinical challengePreclinical studiesDrug AdministrationTumor growthChemotherapyU.S. FoodAntitumor activity
2012
Ki67 expression in the primary tumor predicts for clinical benefit and time to progression on first-line endocrine therapy in estrogen receptor-positive metastatic breast cancer
Delpech Y, Wu Y, Hess KR, Hsu L, Ayers M, Natowicz R, Coutant C, Rouzier R, Barranger E, Hortobagyi GN, Mauro D, Pusztai L. Ki67 expression in the primary tumor predicts for clinical benefit and time to progression on first-line endocrine therapy in estrogen receptor-positive metastatic breast cancer. Breast Cancer Research And Treatment 2012, 135: 619-627. PMID: 22890751, DOI: 10.1007/s10549-012-2194-2.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic Agents, HormonalBreast NeoplasmsBreast Neoplasms, MaleCarcinoma, Ductal, BreastDisease-Free SurvivalFemaleHumansKaplan-Meier EstimateKi-67 AntigenMaleMiddle AgedMultivariate AnalysisNeoplasm Recurrence, LocalNeoplasms, Hormone-DependentProportional Hazards ModelsReceptors, EstrogenRetrospective StudiesTreatment OutcomeConceptsFirst-line endocrine therapyEndocrine therapyMetastatic breast cancerMetastatic diseaseKi67 expressionClinical benefitPrimary tumorBreast cancerExpression groupEstrogen receptor-positive metastatic breast cancerIndependent adverse prognostic factorKaplan-Meier survival curvesClinical benefit rateKi67 expression levelsAdverse prognostic factorMedian survival timeLow Ki67 expressionBreast cancer correlatesHigh Ki67 expressionHigh clinical benefitPrognostic factorsMedian timeMetastatic recurrencePrimary cancerImmunohistochemical variablesAromatase Inhibition in Obese Women: How Much Is Enough?
Ligibel JA, Winer EP. Aromatase Inhibition in Obese Women: How Much Is Enough? Journal Of Clinical Oncology 2012, 30: 2940-2942. PMID: 22802318, DOI: 10.1200/jco.2012.43.7244.Peer-Reviewed Original ResearchAdjuvant therapy in stage I carcinoma of the breast
Schwartz GF, Reis‐Fihlo J, Pusztai L, Fentiman IS, Holland R, Bartelink H, Rutgers EJ, Solin LJ, Palazzo J, Committee A. Adjuvant therapy in stage I carcinoma of the breast. Cancer 2012, 118: 2031-2038. PMID: 22392361, DOI: 10.1002/cncr.27431.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsChemotherapy, AdjuvantCombined Modality TherapyFemaleGene Expression ProfilingHumansNeoplasms, Hormone-DependentPractice Guidelines as TopicConceptsStage I breast cancerI breast cancerBreast cancerAdjuvant therapyConsensus conferenceStage ILymph node-negative breast cancerNode-negative breast cancerKimmel Cancer CenterAdjuvant chemotherapyAdjuvant hormonesAdjuvant treatmentCancer CenterClinical trialsThomas Jefferson UniversityTreatment criteriaTreatment decisionsIndividual tumorsCancerGenetic factorsChemotherapyMolecular phenotypingTherapyHormoneCurrent data
2011
Adjuvant chemotherapy in luminal breast cancers
Lim E, Winer EP. Adjuvant chemotherapy in luminal breast cancers. The Breast 2011, 20: s128-s131. PMID: 22015279, DOI: 10.1016/s0960-9776(11)70309-5.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntineoplastic AgentsAntineoplastic Agents, HormonalBiomarkersBreast NeoplasmsChemotherapy, AdjuvantDisease-Free SurvivalFemaleHumansMiddle AgedNeoplasm StagingNeoplasms, Hormone-DependentPrognosisRandomized Controlled Trials as TopicReceptor, ErbB-2Receptors, EstrogenReceptors, ProgesteroneRisk AssessmentSurvival AnalysisTreatment OutcomeConceptsAdjuvant endocrine therapyLuminal breast cancerEndocrine therapyBreast cancerEstrogen receptorAdjuvant chemotherapyProgesterone receptorHER2-negative breast cancerER-positive breast tumorsAddition of chemotherapyER-positive diseaseER-positive tumorsUse of chemotherapySubset of patientsSubgroup of patientsER-negative tumorsAdditional therapyCytotoxic chemotherapyEndocrine sensitivityClinicians' estimationTherapeutic responseFavorable outcomeCurrent biomarkersChemotherapyBreast tumorsPSA regulates androgen receptor expression in prostate cancer cells
Saxena P, Trerotola M, Wang T, Li J, Sayeed A, VanOudenhove J, Adams D, FitzGerald T, Altieri D, Languino L. PSA regulates androgen receptor expression in prostate cancer cells. The Prostate 2011, 72: 769-776. PMID: 21956655, PMCID: PMC3404455, DOI: 10.1002/pros.21482.Peer-Reviewed Original ResearchConceptsProstate-specific antigenAndrogen receptorC4-2B cellsShort hairpin RNAPrCa cellsAndrogen-independent cell linesAndrogen receptor expressionProtein levelsAR transcriptional activityAR protein levelsAR mRNA levelsProstate cancer progressionProstate cancer cellsTransient siRNA knockdownStable short hairpin RNAAR activatorsPSA levelsAR expressionEffect of downregulationPhosphorylation of SrcSerum biomarkersAR mRNAReceptor expressionAR levelsReal-time PCRHormonal Modulation in the Treatment of Breast Cancer
Adelson K, Germain D, Raptis G, Biran N. Hormonal Modulation in the Treatment of Breast Cancer. Endocrinology And Metabolism Clinics Of North America 2011, 40: 519-532. PMID: 21889718, DOI: 10.1016/j.ecl.2011.05.011.Peer-Reviewed Original ResearchSLCO2B1 and SLCO1B3 May Determine Time to Progression for Patients Receiving Androgen Deprivation Therapy for Prostate Cancer
Yang M, Xie W, Mostaghel E, Nakabayashi M, Werner L, Sun T, Pomerantz M, Freedman M, Ross R, Regan M, Sharifi N, Figg W, Balk S, Brown M, Taplin M, Oh W, Lee G, Kantoff P. SLCO2B1 and SLCO1B3 May Determine Time to Progression for Patients Receiving Androgen Deprivation Therapy for Prostate Cancer. Journal Of Clinical Oncology 2011, 29: 2565-2573. PMID: 21606417, PMCID: PMC3138634, DOI: 10.1200/jco.2010.31.2405.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAdultAgedAged, 80 and overAndrogen AntagonistsAndrogensAntineoplastic Agents, HormonalBiological TransportDehydroepiandrosterone SulfateDisease ProgressionDisease-Free SurvivalDNA Mutational AnalysisDrug Resistance, NeoplasmGenotypeGonadotropin-Releasing HormoneHumansKaplan-Meier EstimateMaleMiddle AgedNeoplasms, Hormone-DependentOrchiectomyOrganic Anion TransportersOrganic Anion Transporters, Sodium-IndependentPolymorphism, Single NucleotideProstatic NeoplasmsSolute Carrier Organic Anion Transporter Family Member 1B3TestosteroneConceptsAndrogen deprivation therapyTime to progressionShorter time to progressionProstate cancerDeprivation therapyProstate cancer treated with androgen deprivation therapyResistance to androgen deprivation therapyGenetic variantsAssociated with time to progressionMedian time to progressionAdvanced prostate cancerGene-gene interactionsSingle nucleotide polymorphismsPharmacogenomic determinantsSLCO2B1 genotypeEnhanced cell growthTransports androgensSLCO1B3 genotypesEfficient importNucleotide polymorphismsSLCO2B1Biological functionsAndrogenCell growthProstatePC3 is a cell line characteristic of prostatic small cell carcinoma
Tai S, Sun Y, Squires J, Zhang H, Oh W, Liang C, Huang J. PC3 is a cell line characteristic of prostatic small cell carcinoma. The Prostate 2011, 71: 1668-1679. PMID: 21432867, PMCID: PMC3426349, DOI: 10.1002/pros.21383.Peer-Reviewed Original ResearchMeSH KeywordsAdenocarcinomaAnimalsBlotting, WesternCarcinoma, NeuroendocrineCarcinoma, Small CellCell Line, TumorHumansImmunohistochemistryMaleMiceMice, SCIDNeoplasm TransplantationNeoplasms, Hormone-DependentProstate-Specific AntigenProstatic NeoplasmsReceptors, AndrogenReverse Transcriptase Polymerase Chain ReactionRNA, NeoplasmTransplantation, HeterologousConceptsSmall cell neuroendocrine carcinomaProstate-specific antigenHuman prostate adenocarcinomaLNCaP cellsAndrogen receptorProstatic adenocarcinomaProstate cancerPC3 cellsHormone therapyProstatic small cell neuroendocrine carcinomaProstatic small cell carcinomaInhibit AR signalingCell neuroendocrine carcinomaSmall cell carcinomaPC cell linesAndrogen withdrawalMetastatic adenocarcinomaNeuroendocrine carcinomaCell carcinomaNeuroendocrine markersAndrogen-dependentAR signalingWestern blot analysisGlandular formationTumor cellsGefitinib or Placebo in Combination with Tamoxifen in Patients with Hormone Receptor–Positive Metastatic Breast Cancer: A Randomized Phase II Study
Osborne CK, Neven P, Dirix LY, Mackey JR, Robert J, Underhill C, Schiff R, Gutierrez C, Migliaccio I, Anagnostou VK, Rimm DL, Magill P, Sellers M. Gefitinib or Placebo in Combination with Tamoxifen in Patients with Hormone Receptor–Positive Metastatic Breast Cancer: A Randomized Phase II Study. Clinical Cancer Research 2011, 17: 1147-1159. PMID: 21220480, PMCID: PMC3074404, DOI: 10.1158/1078-0432.ccr-10-1869.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAntineoplastic Agents, HormonalAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorBreast NeoplasmsDrug-Related Side Effects and Adverse ReactionsErbB ReceptorsFemaleGefitinibHumansMiddle AgedNeoplasms, Hormone-DependentPlacebosQuinazolinesReceptor, ErbB-2Receptors, EstrogenSignal TransductionTamoxifenTreatment OutcomeConceptsAdjuvant aromatase inhibitorsMetastatic breast cancerBreast cancerHormone receptor-positive metastatic breast cancerPositive metastatic breast cancerRandomized phase II studyRandomized phase II trialClinical benefit ratePhase II studyPhase II trialProgression-free survivalStratum 1Epidermal growth factor receptor inhibitor gefitinibFurther investigationAdjuvant tamoxifenImproved PFSPFS HRAI therapyII studyII trialMetastatic diseaseAppropriate patientsPredictive biomarkersPrimary tumorTamoxifen resistance
2010
Utility of oncotype DX risk estimates in clinically intermediate risk hormone receptor‐positive, HER2‐normal, grade II, lymph node‐negative breast cancers
Kelly CM, Krishnamurthy S, Bianchini G, Litton JK, Gonzalez‐Angulo A, Hortobagyi GN, Pusztai L. Utility of oncotype DX risk estimates in clinically intermediate risk hormone receptor‐positive, HER2‐normal, grade II, lymph node‐negative breast cancers. Cancer 2010, 116: 5161-5167. PMID: 20665886, DOI: 10.1002/cncr.25269.Peer-Reviewed Original ResearchConceptsTrial Assigning Individualized OptionsRisk of recurrenceOncotype DXRecurrence scoreBreast cancerIntermediate riskGrade I/II tumorsLymph node-negative breast cancerNode-negative breast cancerStage I/IID. Anderson Cancer CenterOncotype DX breast cancerRisk estimatesIntermediate-risk populationEarly breast cancerRoutine clinical variablesHigh-risk groupOncotype DX testingAnderson Cancer CenterAdjuvant chemotherapyDistant recurrenceConsecutive patientsII tumorsClinicopathological variablesLobular carcinomaAssociation Between Patient and Tumor Characteristics With Clinical Outcomes in Women With Ductal Carcinoma In Situ
Shamliyan T, Wang SY, Virnig BA, Tuttle TM, Kane RL. Association Between Patient and Tumor Characteristics With Clinical Outcomes in Women With Ductal Carcinoma In Situ. JNCI Monographs 2010, 2010: 121-129. PMID: 20956815, PMCID: PMC5161074, DOI: 10.1093/jncimonographs/lgq034.Peer-Reviewed Original ResearchMeSH KeywordsAdultAge FactorsAgedBody Mass IndexBreast NeoplasmsCarcinoma, Intraductal, NoninfiltratingFemaleGonadal Steroid HormonesHumansMammographyMenopauseNeoplasm Recurrence, LocalNeoplasms, Hormone-DependentPrognosisRacial GroupsRandomized Controlled Trials as TopicReceptor, ErbB-2Receptors, EstrogenReceptors, ProgesteroneRiskSocioeconomic FactorsTreatment OutcomeTumor BurdenConceptsDuctal carcinomaClinical outcomesRecurrent cancerTumor characteristicsWorse outcomesNegative estrogen receptor statusAdvanced recurrent cancerPositive surgical marginsEstrogen receptor statusLarger tumor sizeHigh-risk categoryComposite prognostic indicesReceptor statusSurgical marginsPrognostic indexTumor sizeComedo necrosisPathological gradingClinical trialsObservational studyHigh riskHER2 receptorSynthesis of evidenceHigh mortalityYoung womenHigher parity and shorter breastfeeding duration
Shinde SS, Forman MR, Kuerer HM, Yan K, Peintinger F, Hunt KK, Hortobagyi GN, Pusztai L, Symmans WF. Higher parity and shorter breastfeeding duration. Cancer 2010, 116: 4933-4943. PMID: 20665494, DOI: 10.1002/cncr.25443.Peer-Reviewed Original ResearchMeSH KeywordsAdultAge FactorsAgedAged, 80 and overBreast FeedingBreast NeoplasmsFemaleHumansMenarcheMiddle AgedNeoplasms, Hormone-DependentParityPhenotypePregnancyRisk FactorsTime FactorsConceptsTriple-negative BCInvasive breast cancerDuration of breastfeedingBreast cancer phenotypeHigher parityOdds ratioBreast cancerTriple-negative breast cancer (TNBC) phenotypeConsecutive case seriesMultivariate logistic regressionConfidence intervalsAfrican American ethnicityCancer phenotypeShort durationCase seriesFamily historyNegative BCProgenitor cell populationsYounger ageLogistic regressionBreastfeedingAmerican ethnicityDemographic informationCell populationsAgePIK3CA mutations associated with gene signature of low mTORC1 signaling and better outcomes in estrogen receptor–positive breast cancer
Loi S, Haibe-Kains B, Majjaj S, Lallemand F, Durbecq V, Larsimont D, Gonzalez-Angulo AM, Pusztai L, Symmans WF, Bardelli A, Ellis P, Tutt AN, Gillett CE, Hennessy BT, Mills GB, Phillips WA, Piccart MJ, Speed TP, McArthur GA, Sotiriou C. PIK3CA mutations associated with gene signature of low mTORC1 signaling and better outcomes in estrogen receptor–positive breast cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 10208-10213. PMID: 20479250, PMCID: PMC2890442, DOI: 10.1073/pnas.0907011107.Peer-Reviewed Original ResearchMeSH KeywordsAntibiotics, AntineoplasticAntineoplastic Agents, HormonalBase SequenceBreast NeoplasmsCell Line, TumorClass I Phosphatidylinositol 3-KinasesDNA PrimersFemaleGene Expression ProfilingHumansMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesMutationNeoplasms, Hormone-DependentOligonucleotide Array Sequence AnalysisPhosphatidylinositol 3-KinasesPrognosisProteinsProto-Oncogene Proteins c-aktReceptor, ErbB-2Receptors, EstrogenSignal TransductionSirolimusTamoxifenTOR Serine-Threonine KinasesTranscription FactorsConceptsBreast cancerPIK3CA mutationsClinical outcomesEstrogen receptor-positive breast cancerReceptor-positive breast cancerGene signaturePIK3CA mutation statusPI3K/mTOR inhibitorBetter clinical outcomesPI3K/mTOR inhibitionHuman breast cancerBC cell linesPIK3CA mutant breast cancersCommon genetic aberrationsTamoxifen monotherapyBetter prognosisMTOR inhibitorsBetter outcomesMutation statusMTOR inhibitionPathway activationExperimental modelGenetic aberrationsPrognosisCell lines
2009
Breast cancer. Clinical practice guidelines in oncology.
Carlson RW, Allred DC, Anderson BO, Burstein HJ, Carter WB, Edge SB, Erban JK, Farrar WB, Goldstein LJ, Gradishar WJ, Hayes DF, Hudis CA, Jahanzeb M, Kiel K, Ljung BM, Marcom PK, Mayer IA, McCormick B, Nabell LM, Pierce LJ, Reed EC, Smith ML, Somlo G, Theriault RL, Topham NS, Ward JH, Winer EP, Wolff AC. Breast cancer. Clinical practice guidelines in oncology. Journal Of The National Comprehensive Cancer Network 2009, 7: 122-92. PMID: 19200416, DOI: 10.6004/jnccn.2009.0012.Peer-Reviewed Original ResearchAlgorithmsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAromatase InhibitorsBreastBreast NeoplasmsCombined Modality TherapyFemaleHumansLymphatic MetastasisMastectomyNeoadjuvant TherapyNeoplasm InvasivenessNeoplasm Recurrence, LocalNeoplasm StagingNeoplasms, Hormone-DependentPostmenopausePremenopauseRandomized Controlled Trials as TopicReceptor, ErbB-2Selective Estrogen Receptor ModulatorsSentinel Lymph Node BiopsyTamoxifenTrastuzumabTime to prostate‐specific antigen nadir independently predicts overall survival in patients who have metastatic hormone‐sensitive prostate cancer treated with androgen‐deprivation therapy
Choueiri T, Xie W, D'Amico A, Ross R, Hu J, Pomerantz M, Regan M, Taplin M, Kantoff P, Sartor O, Oh W. Time to prostate‐specific antigen nadir independently predicts overall survival in patients who have metastatic hormone‐sensitive prostate cancer treated with androgen‐deprivation therapy. Cancer 2009, 115: 981-987. PMID: 19152438, PMCID: PMC2931827, DOI: 10.1002/cncr.24064.Peer-Reviewed Original ResearchConceptsAndrogen deprivation therapy initiationProstate-specific antigen nadirHormone-sensitive prostate cancerMetastatic hormone-sensitive prostate cancerAndrogen deprivation therapyProstate-specific antigenInitiation of androgen deprivation therapyTreated with androgen deprivation therapyGleason score >7Overall survivalPSA declineShorter OSProstate cancerKinetics of prostate-specific antigenResponse to ADTNadir prostate-specific antigenProstate-specific antigen declineAssociated with shorter OSAssociated with shorter survival durationMedian PSA levelSerum PSA valuesSerum PSA determinationMedian follow-upAuthors' institutional databaseShorter survival duration
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