2009
Amplification of fibroblast growth factor receptor-1 in breast cancer and the effects of brivanib alaninate
Shiang CY, Qi Y, Wang B, Lazar V, Wang J, Fraser Symmans W, Hortobagyi GN, Andre F, Pusztai L. Amplification of fibroblast growth factor receptor-1 in breast cancer and the effects of brivanib alaninate. Breast Cancer Research And Treatment 2009, 123: 747-755. PMID: 20024612, DOI: 10.1007/s10549-009-0677-6.Peer-Reviewed Original ResearchMeSH KeywordsAlanineAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell ProliferationComparative Genomic HybridizationDose-Response Relationship, DrugFemaleFibroblast Growth Factor 2Gene AmplificationGene DosageGene Expression ProfilingGene Expression Regulation, NeoplasticHumansInhibitory Concentration 50Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 1RNA, MessengerSignal TransductionTriazinesConceptsFibroblast growth factor receptor 1Growth factor receptor 1Breast cancer cell linesBreast cancerFactor receptor 1Cancer cell linesKinase activityProtein overexpressionReceptor 1Cell linesCopy numberDirect anti-proliferative effectsGene expression profilingHuman breast cancerTyrosine kinase activityAnti-angiogenic effectsMDA-MB-361Small molecule inhibitorsAnti-proliferative effectsGrowth inhibitionDNA copy numberProtein expression levelsBrivanib treatmentFGFR-1 mRNANormal copy number
2003
Phase II study of pegylated liposomal doxorubicin in combination with gemcitabine in patients with metastatic breast cancer.
Rivera E, Valero V, Arun B, Royce M, Adinin R, Hoelzer K, Walters R, Wade JL, Pusztai L, Hortobagyi GN. Phase II study of pegylated liposomal doxorubicin in combination with gemcitabine in patients with metastatic breast cancer. Journal Of Clinical Oncology 2003, 21: 3249-54. PMID: 12947059, DOI: 10.1200/jco.2003.03.111.Peer-Reviewed Original ResearchConceptsMetastatic breast cancerLiposomal doxorubicinBreast cancerOverall survivalDay 1Median cumulative anthracycline doseLeft ventricular ejection fractionPhase II clinical trialCommon grade 3Cumulative anthracycline doseFrequent nonhematologic toxicitiesPrevious anthracycline exposureHand-foot syndromeMedian overall survivalMedian response durationPhase II studyFront-line therapyVentricular ejection fractionOverall response rateAdjuvant chemotherapyAnthracycline doseAssessable patientsMeasurable diseaseNeutropenic complicationsNonhematologic toxicity
2000
Novel marine-derived anticancer agents: a phase I clinical, pharmacological, and pharmacodynamic study of dolastatin 10 (NSC 376128) in patients with advanced solid tumors.
Madden T, Tran H, Beck D, Huie R, Newman R, Pusztai L, Wright J, Abbruzzese J. Novel marine-derived anticancer agents: a phase I clinical, pharmacological, and pharmacodynamic study of dolastatin 10 (NSC 376128) in patients with advanced solid tumors. Clinical Cancer Research 2000, 6: 1293-301. PMID: 10778954.Peer-Reviewed Original ResearchConceptsConcentration-time curveDose levelsPhase IMajor nonhematological toxicityAntitumor activityAdvanced solid tumorsDose-limiting toxicityPlasma concentration-time dataEpisodes of thrombocytopeniaRapid distribution phaseParent drug concentrationsConcentration-time dataPercentage of declineVivo tumor modelsNonhematological toxicitiesObjective responseTwo-compartment modelSevere anemiaClinical PharmacokineticsCytokine supportPlasma levelsIntrapatient variabilityClinical dataNovel agentsPharmacodynamic studies
1999
Phase II study of mitoxantrone by 14-day continuous infusion with granulocyte colony-stimulating factor (GCSF) support in patients with metastatic breast cancer and limited prior therapy
Pusztai L, Holmes F, Fraschini G, Hortobagyi G. Phase II study of mitoxantrone by 14-day continuous infusion with granulocyte colony-stimulating factor (GCSF) support in patients with metastatic breast cancer and limited prior therapy. Cancer Chemotherapy And Pharmacology 1999, 43: 86-91. PMID: 9923546, DOI: 10.1007/s002800050867.Peer-Reviewed Original ResearchConceptsMetastatic breast cancerGranulocyte colony-stimulating factor supportColony-stimulating factor supportObjective response ratePhase II studyContinuous infusionBreast cancerII studyFactor supportSide effectsResponse rateMajor dose-limiting side effectDose-limiting side effectDiscontinuation of therapySecond-line chemotherapySecond-line regimensPhase II evaluationComplete tumor responseContinuous intravenous infusionMaximal cytotoxic effectLimited antitumor activityAsymptomatic cardiotoxicityPrevious therapyStable diseaseMetastatic disease
1998
Physiologic and Pathologic Drug Resistance in Ovarian Carcinoma: A Hypothesis Based on a Clonal Progression Model
Pusztai L, Siddik Z, Mills G, Bast R. Physiologic and Pathologic Drug Resistance in Ovarian Carcinoma: A Hypothesis Based on a Clonal Progression Model. Acta Oncologica 1998, 37: 629-640. PMID: 10050979, DOI: 10.1080/028418698429964.Peer-Reviewed Original ResearchMeSH KeywordsApoptosisDNA DamageDose-Response Relationship, DrugDrug Resistance, NeoplasmFemaleHumansNeoplasm Recurrence, LocalOvarian NeoplasmsRandomized Controlled Trials as TopicTreatment FailureConceptsEarly-stage ovarian cancerDrug-resistant cellsDrug resistanceDrug sensitivityOvarian cancerTumor progressionDisease-free survivalHigh-dose chemotherapyNumerous clinical studiesDifferent treatment strategiesCell populationsHigh response rateCorresponding normal tissuesInsufficient chemotherapyAdjuvant chemotherapyIntensive chemotherapyAdvanced diseaseClinical responseCombination chemotherapyConventional dosesMolecular biological observationsOvarian carcinomaPhysiological drug resistanceClinical failureClinical studies