2020
Multi-Omics Investigation of Innate Navitoclax Resistance in Triple-Negative Breast Cancer Cells
Marczyk M, Patwardhan GA, Zhao J, Qu R, Li X, Wali VB, Gupta AK, Pillai MM, Kluger Y, Yan Q, Hatzis C, Pusztai L, Gunasekharan V. Multi-Omics Investigation of Innate Navitoclax Resistance in Triple-Negative Breast Cancer Cells. Cancers 2020, 12: 2551. PMID: 32911681, PMCID: PMC7563413, DOI: 10.3390/cancers12092551.Peer-Reviewed Original ResearchTriple-negative breast cancer cellsCancer cellsBreast cancer cellsStress response genesMulti-omics landscapeCell population compositionDrug-induced cell deathMulti-omics investigationsCell linesBCL2 family inhibitorsSingle-cell analysisChromatin accessibilityGenome structureMDA-MB-231 triple-negative breast cancer cellsChromatin structureMethylation stateResponse genesFamily inhibitorsCell deathTNBC cell linesNumber variationsDefense mechanismsResistance mechanismsNew therapeutic strategiesGenes
2019
CD36-Mediated Metabolic Rewiring of Breast Cancer Cells Promotes Resistance to HER2-Targeted Therapies
Feng WW, Wilkins O, Bang S, Ung M, Li J, An J, del Genio C, Canfield K, DiRenzo J, Wells W, Gaur A, Robey RB, Guo JY, Powles RL, Sotiriou C, Pusztai L, Febbraio M, Cheng C, Kinlaw WB, Kurokawa M. CD36-Mediated Metabolic Rewiring of Breast Cancer Cells Promotes Resistance to HER2-Targeted Therapies. Cell Reports 2019, 29: 3405-3420.e5. PMID: 31825825, PMCID: PMC6938262, DOI: 10.1016/j.celrep.2019.11.008.Peer-Reviewed Original ResearchConceptsFA uptakeHER2-positive breast cancerFA transporter CD36Anti-HER2 therapyBreast cancer patientsMetabolic rewiringHER2 inhibitor lapatinibMMTV-neu miceDeletion of CD36Breast cancer cellsAcquisition of resistancePoor prognosisCancer patientsHER2 inhibitionBreast cancerInhibitor lapatinibCDNA microarray analysisPharmacological inhibitionMammary tissueDe novo FA synthesisCD36Promotes ResistanceResistant cellsCancer cellsExpression increases
2017
Integrated MicroRNA–mRNA Profiling Identifies Oncostatin M as a Marker of Mesenchymal-Like ER-Negative/HER2-Negative Breast Cancer
Bottai G, Diao L, Baggerly KA, Paladini L, Győrffy B, Raschioni C, Pusztai L, Calin GA, Santarpia L. Integrated MicroRNA–mRNA Profiling Identifies Oncostatin M as a Marker of Mesenchymal-Like ER-Negative/HER2-Negative Breast Cancer. International Journal Of Molecular Sciences 2017, 18: 194. PMID: 28106823, PMCID: PMC5297825, DOI: 10.3390/ijms18010194.Peer-Reviewed Original ResearchConceptsEpidermal growth factorExpression profilesMessenger RNA (mRNA) expression profilesMiRNA-regulated pathwaysAvailable gene expression profilesOncostatin M signalingMesenchymal-like breast cancer cellsGene expression profilesRNA expression profilesImmune-related pathwaysPathway regulationGlobal miRNAOncogenic networksGene expressionSpecific miRNAsPathway analysisBreast cancer cellsHuman estrogen receptorTriple-negative breast cancerEMT pathwayMesenchymal transitionMiRNAMRNA dataOncostatin MCancer cells
2014
Open-label randomized clinical trial of standard neoadjuvant chemotherapy with paclitaxel followed by FEC versus the combination of paclitaxel and everolimus followed by FEC in women with triple receptor-negative breast cancer †
Gonzalez-Angulo AM, Akcakanat A, Liu S, Green MC, Murray JL, Chen H, Palla SL, Koenig KB, Brewster AM, Valero V, Ibrahim NK, Moulder-Thompson S, Litton JK, Tarco E, Moore J, Flores P, Crawford D, Dryden MJ, Symmans WF, Sahin A, Giordano SH, Pusztai L, Do K, Mills GB, Hortobagyi GN, Meric-Bernstam F. Open-label randomized clinical trial of standard neoadjuvant chemotherapy with paclitaxel followed by FEC versus the combination of paclitaxel and everolimus followed by FEC in women with triple receptor-negative breast cancer †. Annals Of Oncology 2014, 25: 1122-1127. PMID: 24669015, PMCID: PMC4037860, DOI: 10.1093/annonc/mdu124.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerPathological complete responseStandard neoadjuvant chemotherapyNeoadjuvant chemotherapyReverse phase protein arrayBreast cancerPrimary triple-negative breast cancerMTOR pathwayReceptor-negative breast cancerTriple receptor-negative breast cancerAddition of everolimusGrade 3 pneumonitisGrade 3/4 stomatitisPI3K/AKT/mTOR pathwayRash/desquamationClinical response rateGrade 3/4 toxicitiesPhase II studyClinical end pointsCombination of paclitaxelAKT/mTOR pathwayDirect antiproliferative activityBreast cancer cellsDownregulation of mTORII studyMitochondrial dysfunction in some triple-negative breast cancer cell lines: role of mTOR pathway and therapeutic potential
Pelicano H, Zhang W, Liu J, Hammoudi N, Dai J, Xu RH, Pusztai L, Huang P. Mitochondrial dysfunction in some triple-negative breast cancer cell lines: role of mTOR pathway and therapeutic potential. Breast Cancer Research 2014, 16: 434. PMID: 25209360, PMCID: PMC4303115, DOI: 10.1186/s13058-014-0434-6.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateCell Line, TumorElectron Transport Chain Complex ProteinsEnergy MetabolismFemaleGlucoseGlutathioneHumansHydrocarbons, BrominatedLactic AcidMitochondriaNADPOxidation-ReductionOxygen ConsumptionPropionatesReactive Oxygen SpeciesReceptor, ErbB-2Receptors, EstrogenReceptors, ProgesteroneSignal TransductionTOR Serine-Threonine KinasesTriple Negative Breast NeoplasmsConceptsTNBC cellsBreast cancer cellsBreast cancerCancer cellsPositive cellsMetabolic alterationsIntroductionTriple-negative breast cancerMTOR pathwayEstrogen receptor-positive cellsER-positive cellsEffective therapeutic approachReceptor-positive cellsBreast cancer subtypesBreast cancer cell linesEffective therapeutic strategyTriple-negative breast cancer cell linesCurrent chemotherapeutic agentsMalignant breast cancerProfound metabolic alterationsHigher glucose uptakeInhibition of glycolysisCancer cell linesPoor prognosisLower mitochondrial respirationMitochondrial respiration
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
2009
Inhibition of Lipocalin 2 Impairs Breast Tumorigenesis and Metastasis
Leng X, Ding T, Lin H, Wang Y, Hu L, Hu J, Feig B, Zhang W, Pusztai L, Symmans WF, Wu Y, Arlinghaus RB. Inhibition of Lipocalin 2 Impairs Breast Tumorigenesis and Metastasis. Cancer Research 2009, 69: 8579-8584. PMID: 19887608, DOI: 10.1158/0008-5472.can-09-1934.Peer-Reviewed Original ResearchMeSH KeywordsAcute-Phase ProteinsAnimalsBlotting, WesternBreast NeoplasmsCell Line, TumorFemaleFlow CytometryGene Expression Regulation, NeoplasticHumansImmunohistochemistryLipocalin-2LipocalinsMatrix Metalloproteinase 9MiceMice, KnockoutNeoplasm InvasivenessNF-kappa BOncogene ProteinsReceptor, ErbB-2Reverse Transcriptase Polymerase Chain ReactionSignal TransductionConceptsLCN2 expressionBreast cancerBreast tumorigenesisMatrix metalloproteinase-9 activityTumor formationMammary tumor mouse modelMammary tumor formationMetalloproteinase-9 activityMatrix metalloproteinase-9Breast cancer therapyTumor mouse modelBreast tumor formationAkt/NFBreast cancer cellsMurine breast tumorsInhibitory monoclonal antibodiesLCN2 functionsLung metastasesLipocalin-2Metalloproteinase-9Mouse modelAggressive typeBreast tumorsKappaB pathwayMetastasisEpstein-Barr virus (EBV) in fine needle aspirates containing inflammatory breast cancer cells.
Li C, Pusztai L, Cohen E, Symmans F, Wang B, Lee B, Hortobagyi G, Cristofanilli M, Reuben J. Epstein-Barr virus (EBV) in fine needle aspirates containing inflammatory breast cancer cells. Cancer Research 2009, 69: 3084. DOI: 10.1158/0008-5472.sabcs-3084.Peer-Reviewed Original ResearchInflammatory breast cancerEpstein-Barr virusFine needle aspiratesEBV DNABreast cancerEBV genomeQuantitative polymerase chain reactionLABC patientsNeedle aspiratesFNA samplesHuman herpes virus 8Findings warrants further investigationPotential viral oncogenesAdvanced breast cancerLatent EBV infectionHerpes virus 8Primary breast cancerBreast cancer patientsPossible viral etiologyEBV DNA sequencesQ-PCRInflammatory breast cancer cellsMouse mammary tumorsBreast cancer cellsWarrants further investigation
2005
Microtubule-associated protein tau: A marker of paclitaxel sensitivity in breast cancer
Rouzier R, Rajan R, Wagner P, Hess KR, Gold DL, Stec J, Ayers M, Ross JS, Zhang P, Buchholz TA, Kuerer H, Green M, Arun B, Hortobagyi GN, Symmans WF, Pusztai L. Microtubule-associated protein tau: A marker of paclitaxel sensitivity in breast cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2005, 102: 8315-8320. PMID: 15914550, PMCID: PMC1149405, DOI: 10.1073/pnas.0408974102.Peer-Reviewed Original ResearchConceptsPathologic complete responseBreast cancerBreast cancer cellsLow tau expressionPaclitaxel-containing chemotherapyCancer cellsLower mRNA expressionRegulation of tauPaclitaxel therapyComplete responseIndependent predictorsNuclear gradePaclitaxel sensitivityTau expressionTherapeutic strategiesStage IMultivariate analysisProtein tauTau proteinMRNA expressionTissue arraysDiagnostic testsPaclitaxelCancerChemotherapy