2022
Comprehensive Analysis of Metabolic Isozyme Targets in Cancer
Marczyk M, Gunasekharan V, Casadevall D, Qing T, Foldi J, Sehgal R, Shan NL, Blenman KRM, O'Meara TA, Umlauf S, Surovtseva YV, Muthusamy V, Rinehart J, Perry RJ, Kibbey R, Hatzis C, Pusztai L. Comprehensive Analysis of Metabolic Isozyme Targets in Cancer. Cancer Research 2022, 82: 1698-1711. PMID: 35247885, PMCID: PMC10883296, DOI: 10.1158/0008-5472.can-21-3983.Peer-Reviewed Original ResearchConceptsPotential therapeutic targetAcetyl-CoA carboxylase 1Therapeutic targetCancer typesCell linesBreast cancer viabilityPatient-derived xenograftsNovel metabolic targetsCorresponding cell linesExpression patternsDrug treatmentMatching normal tissuesRelated commentaryTumor growthMalignant transformationSmall molecule inhibitionCancer viabilityCancer Cell Line EncyclopediaNormal tissuesMetabolic vulnerabilitiesCarboxylase 1Anticancer therapyCellular changesCell proliferationMetabolic reprogramming
2016
miR-34a Silences c-SRC to Attenuate Tumor Growth in Triple-Negative Breast Cancer
Adams BD, Wali VB, Cheng CJ, Inukai S, Booth CJ, Agarwal S, Rimm DL, Győrffy B, Santarpia L, Pusztai L, Saltzman WM, Slack FJ. miR-34a Silences c-SRC to Attenuate Tumor Growth in Triple-Negative Breast Cancer. Cancer Research 2016, 76: 927-939. PMID: 26676753, PMCID: PMC4755913, DOI: 10.1158/0008-5472.can-15-2321.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerBreast cancerTumor growthMiR-34a replacement therapyTNBC cell linesDifferent TNBC subtypesPromising therapeutic strategyAttenuates tumor growthHuman clinical trialsMiRNA-profiling studiesMiR-34a levelsCell linesPotent antitumorigenic effectsMiR-34a targetsHuman tumor specimensC-SrcReplacement therapyTNBC subtypesAggressive subtypeTreatment optionsClinical trialsDisease progressionEffective therapyPatient outcomesC-Src inhibitor
2013
TIG1 Promotes the Development and Progression of Inflammatory Breast Cancer through Activation of Axl Kinase
Wang X, Saso H, Iwamoto T, Xia W, Gong Y, Pusztai L, Woodward WA, Reuben JM, Warner SL, Bearss DJ, Hortobagyi GN, Hung MC, Ueno NT. TIG1 Promotes the Development and Progression of Inflammatory Breast Cancer through Activation of Axl Kinase. Cancer Research 2013, 73: 6516-6525. PMID: 24014597, PMCID: PMC6135947, DOI: 10.1158/0008-5472.can-13-0967.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisAxl Receptor Tyrosine KinaseBlotting, WesternCell AdhesionCell CycleCell MovementCell ProliferationDisease ProgressionFemaleFluorescent Antibody TechniqueHumansImmunoprecipitationInflammatory Breast NeoplasmsMediator ComplexMiceNeoplasm InvasivenessProto-Oncogene ProteinsReal-Time Polymerase Chain ReactionReceptor Protein-Tyrosine KinasesReverse Transcriptase Polymerase Chain ReactionRNA, MessengerRNA, Small InterferingSignal TransductionTumor Cells, CulturedConceptsInflammatory breast cancerBreast cancerAxl expressionMalignant propertiesHigh tumoral expressionIBC cell proliferationMatrix metalloproteinase-9Inhibited tumor growthIBC specimensIBC cellsShorter survivalTumoral expressionProteasome-dependent degradationMetalloproteinase-9TIG1 expressionNF-κBTherapeutic targetTumor growthReceptor tyrosine kinasesAxl functionLethal formAxlIBC treatmentCancerAggressive properties
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 ResearchSeventeen-gene signature from enriched Her2/Neu mammary tumor-initiating cells predicts clinical outcome for human HER2+:ERα− breast cancer
Liu JC, Voisin V, Bader GD, Deng T, Pusztai L, Symmans WF, Esteva FJ, Egan SE, Zacksenhaus E. Seventeen-gene signature from enriched Her2/Neu mammary tumor-initiating cells predicts clinical outcome for human HER2+:ERα− breast cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2012, 109: 5832-5837. PMID: 22460789, PMCID: PMC3326451, DOI: 10.1073/pnas.1201105109.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, Monoclonal, HumanizedAntineoplastic AgentsBreast NeoplasmsCalcium-Binding ProteinsCD24 AntigenCell DifferentiationCell DivisionEstrogen Receptor alphaFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, NeoplasmHumansIntercellular Signaling Peptides and ProteinsJagged-1 ProteinMembrane ProteinsMiceNeoadjuvant TherapyNeoplastic Stem CellsPrognosisReceptor, ErbB-2Serrate-Jagged ProteinsSignal TransductionTrastuzumabTreatment OutcomeConceptsTumor-initiating cellsMammary tumor-initiating cellsBreast cancerClinical outcomesPrognostic signatureHuman epidermal growth factor receptorAnti-HER2 drugsAnti-HER2 therapyHigh-risk patientsHigh-risk subgroupsEpidermal growth factor receptorGrowth factor receptorBC cohortRisk patientsAggressive diseaseBC patientsRetrospective analysisImmune responsePrognostic powerTumor growthPatientsChemotherapyFactor receptorCancerFraction of cells
2011
P2-02-01: A Novel Inflammatory Breast Cancer-Specific Oncogene, Tazarotene-Induced Gene 1, Promotes Tumorigenicity and Invasiveness through the Receptor Tyrosine Kinase Axl.
Wang X, Saso H, Iwamoto T, Pusztai L, Gong Y, Woodward W, Reuben J, Hortobagyi G, Ueno N. P2-02-01: A Novel Inflammatory Breast Cancer-Specific Oncogene, Tazarotene-Induced Gene 1, Promotes Tumorigenicity and Invasiveness through the Receptor Tyrosine Kinase Axl. Cancer Research 2011, 71: p2-02-01-p2-02-01. DOI: 10.1158/0008-5472.sabcs11-p2-02-01.Peer-Reviewed Original ResearchInflammatory breast cancerReceptor tyrosine kinase AXLTIG1 expressionTyrosine kinase AXLBreast cancerSUM149 cellsTumor growthEffective standard therapyNon-IBC cell linesPrognosis of patientsTreatment of patientsMammary fat padMatrix metalloproteinase-9Athymic nude miceIBC cell linesCell linesIBC cellsStandard therapyGene 1 expressionMolecular mechanismsDownregulation of expressionAxl expressionClinical subtypesMetalloproteinase-9Malignant process
1998
Coexpression of the HER-2 Gene Product, pl85HER-2, and Epidermal Growth Factor Receptor, pl70EGF-R, on Epithelial Ovarian Cancers and Normal Tissues
Bast R, Pusztai L, Kerns B, MacDonald J, Jordan P, Daly L, Boyer C, Mendelsohn J, Berchuck A. Coexpression of the HER-2 Gene Product, pl85HER-2, and Epidermal Growth Factor Receptor, pl70EGF-R, on Epithelial Ovarian Cancers and Normal Tissues. Monoclonal Antibodies In Immunodiagnosis And Immunotherapy 1998, 17: 313-321. PMID: 9790065, DOI: 10.1089/hyb.1998.17.313.Peer-Reviewed Original ResearchConceptsOvarian cancerNormal ovarian epitheliumNormal tissuesOvarian epitheliumTumor cellsAdvanced ovarian cancerEpithelial ovarian cancerFavorable therapeutic indexCombination of antibodiesEpidermal growth factor receptorGrowth factor receptorEpithelial specimensHER-2Normal ovariesP170 expressionP185 expressionTherapeutic indexNeoplastic cellsTumor growthSynergistic cytotoxicityFrozen sectionsCancerTherapeutic activityDifferent antigensMonoclonal antibodies