2021
Treatment scheduling effects on the evolution of drug resistance in heterogeneous cancer cell populations
Patwardhan GA, Marczyk M, Wali VB, Stern DF, Pusztai L, Hatzis C. Treatment scheduling effects on the evolution of drug resistance in heterogeneous cancer cell populations. Npj Breast Cancer 2021, 7: 60. PMID: 34040000, PMCID: PMC8154902, DOI: 10.1038/s41523-021-00270-4.Peer-Reviewed Original ResearchHeterogeneous cancer cell populationsCancer cell populationsTriple-negative breast cancerSingle-cell RNA sequencingCell populationsFitness advantageRNA sequencingMDA-MB-231 TNBC cellsDrug resistanceMechanisms of resistanceVitro screening assaysClonal dynamicsTNBC cellsScreening assaysResistant clonesPatterns of resistanceConcomitant treatmentTherapy combinationsBreast cancerClinical studiesTreatment doseTreatment scheduleBarcodesSequencingTreatment
2015
Predictive and Prognostic Value of the TauProtein in Breast Cancer.
Bonneau C, Gurard-Levin ZA, Andre F, Pusztai L, Rouzier R. Predictive and Prognostic Value of the TauProtein in Breast Cancer. Anticancer Research 2015, 35: 5179-84. PMID: 26408675.Peer-Reviewed Original ResearchConceptsBreast cancerTau protein expressionTau proteinPrognostic valueTau expressionHuman epidermal growth factor receptor 2 (HER2) expressionEpidermal growth factor receptor 2 expressionLow tau expressionProtein expressionSubset of patientsReceptor 2 expressionIncreased response rateEffects of taxanesNodal statusBetter prognosisPredictive markerTaxane resistanceChemotherapy sensitivityPredictive valueResponse ratePubMed databaseDrug resistanceCancerHormone receptorsTaxanes
2012
Intratumor Heterogeneity: Seeing the Wood for the Trees
Yap TA, Gerlinger M, Futreal PA, Pusztai L, Swanton C. Intratumor Heterogeneity: Seeing the Wood for the Trees. Science Translational Medicine 2012, 4: 127ps10. PMID: 22461637, DOI: 10.1126/scitranslmed.3003854.Peer-Reviewed Original Research
2010
The role of tumor initiating cells in drug resistance of breast cancer: Implications for future therapeutic approaches
Lacerda L, Pusztai L, Woodward WA. The role of tumor initiating cells in drug resistance of breast cancer: Implications for future therapeutic approaches. Drug Resistance Updates 2010, 13: 99-108. PMID: 20739212, DOI: 10.1016/j.drup.2010.08.001.Peer-Reviewed Original ResearchConceptsTumor initiating cellsInitiating cellsCancer cellsLong-term outcomesBreast cancer recurrenceFuture therapeutic approachesTumor-stromal interactionsBreast cancer cellsHedgehog inhibitor cyclopamineNeoadjuvant chemotherapyResidual diseaseEffective therapyCancer recurrenceBreast cancerTherapeutic approachesInhibitor lapatinibInhibitor cyclopamineTherapy resistanceRegulation of tumorChemical library screenDrug resistanceChemotherapy-resistant subpopulationMultidrug resistanceNovel targetResistant subpopulations
1999
Chemo-signal therapy, an emerging new approach to modify drug resistance in breast cancer
Pusztai L, Esteva F, Cristofanilli M, Hung M, Hortobagyi G. Chemo-signal therapy, an emerging new approach to modify drug resistance in breast cancer. Cancer Treatment Reviews 1999, 25: 271-277. PMID: 10544071, DOI: 10.1053/ctrv.1999.0132.Peer-Reviewed Original ResearchConceptsBreast cancerResponse modifiersPromising new treatment modalityNew treatment modalitiesCombination of chemotherapyNon-cytotoxic agentsCurrent clinical researchClinical drug developmentTreatment modalitiesClinical trialsClinical experienceChemotherapyCytotoxic drugsDrug resistanceClinical researchCancerOncogene expressionGrowth factor signalingDrug developmentSelect groupTherapyDevelopment of novelEarly phaseDrugsFactor signaling
1998
High-dose chemotherapy: how resistant is breast cancer?
Pusztai L, Hortobagyi G. High-dose chemotherapy: how resistant is breast cancer? Drug Resistance Updates 1998, 1: 62-72. PMID: 17092798, DOI: 10.1016/s1368-7646(98)80216-1.Peer-Reviewed Original ResearchHigh-dose chemotherapyClinical drug resistanceBreast cancerDrug resistancePartial responseClinical patternResponse rateComplete response rateHigh-dose therapyInitial complete responseObjective response rateStandard-dose chemotherapyDifferent clinical patternsMajority of patientsPrimary drug resistanceStem cell supportHigh cure ratesDrug-resistant clonesInduction therapyInitial chemosensitivityPathologic resistanceStable diseaseCancer dieOverall survivalComplete responsePhysiologic 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 ResearchConceptsEarly-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