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
Metabolic isoenzyme shifts in cancer as potential novel therapeutic targets
Ononye SN, Shi W, Wali VB, Aktas B, Jiang T, Hatzis C, Pusztai L. Metabolic isoenzyme shifts in cancer as potential novel therapeutic targets. Breast Cancer Research And Treatment 2014, 148: 477-488. PMID: 25395317, DOI: 10.1007/s10549-014-3194-1.Peer-Reviewed Original ResearchConceptsIsoform-specific inhibitorsMetabolic isoenzymesCancer cellsNeoplastic transformationMetabolic enzyme expressionFunctional redundancyEnzymatic functionIsoenzyme diversityAdditional isoformsCancer metabolismMetabolic enzymesSingle isoformMetabolic pathwaysPotential novel therapeutic targetNovel therapeutic targetMetabolic precursorsEnzyme expressionNormal cellsNew therapeutic strategiesStages of developmentIsoformsTherapeutic targetExpressionIsoenzyme expressionTreatment of cancerMitochondrial 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
2011
Plasma microRNA 210 levels correlate with sensitivity to trastuzumab and tumor presence in breast cancer patients
Jung E, Santarpia L, Kim J, Esteva FJ, Moretti E, Buzdar AU, Di Leo A, Le X, Bast RC, Park S, Pusztai L, Calin GA. Plasma microRNA 210 levels correlate with sensitivity to trastuzumab and tumor presence in breast cancer patients. Cancer 2011, 118: 2603-2614. PMID: 22370716, PMCID: PMC3864019, DOI: 10.1002/cncr.26565.Peer-Reviewed Original ResearchConceptsBreast cancer patientsPositive breast cancerMiR-210 levelsBreast cancerMiR-210Cancer patientsMicroRNA expression levelsTumor presenceExpression levelsPlasma samplesBT474 cellsNeoadjuvant trastuzumab-based chemotherapyHuman epidermal growth factor receptor 2Epidermal growth factor receptor 2Trastuzumab-resistant breast cancer cellsMiR expression levelsTrastuzumab-based chemotherapyPathologic complete responseGrowth factor receptor 2Cancer cellsPostoperative plasma samplesPreoperative plasma samplesReverse transcriptase-polymerase chain reactionQuantitative reverse transcriptase-polymerase chain reactionMiR-210 expression
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
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
1998
Cell surface density of p185(c-erbB-2) determines susceptibility to anti-p185(c-erbB-2)-ricin A chain (RTA) immunotoxin therapy alone and in combination with anti-p170(EGFR)-RTA in ovarian cancer cells.
Dean G, Pusztai L, Xu F, O'Briant K, DeSombre K, Conaway M, Boyer C, Mendelsohn J, Bast R. Cell surface density of p185(c-erbB-2) determines susceptibility to anti-p185(c-erbB-2)-ricin A chain (RTA) immunotoxin therapy alone and in combination with anti-p170(EGFR)-RTA in ovarian cancer cells. Clinical Cancer Research 1998, 4: 2545-50. PMID: 9796989.Peer-Reviewed Original ResearchConceptsOvarian cancer cellsReceptors/cellCancer cellsC-erbBSynergistic cytotoxicityCopies/cellTumor cellsSKOV3 human ovarian cancer cellsHuman ovarian cancer cellsClonogenic tumor cellsCell surface densityBreast cancerRTA immunotoxinsNude miceSame immunotoxinFirst treatmentAnchorage-independent growthAnchorage-dependent growthVivo growthClonogenic cellsImmunotoxinExpression levelsSignificant correlationCell linesNormal cells