2019
Identification and Validation of a Novel Biologics Target in Triple Negative Breast Cancer
Wali VB, Patwardhan GA, Pelekanou V, Karn T, Cao J, Ocana A, Yan Q, Nelson B, Hatzis C, Pusztai L. Identification and Validation of a Novel Biologics Target in Triple Negative Breast Cancer. Scientific Reports 2019, 9: 14934. PMID: 31624295, PMCID: PMC6797726, DOI: 10.1038/s41598-019-51453-w.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic AgentsBreastCell Line, TumorCell MembraneCell ProliferationDatasets as TopicDrug DevelopmentFemaleGABA-A Receptor AntagonistsGene Expression ProfilingGene Knockdown TechniquesHumansImmunoconjugatesImmunoglobulin Fab FragmentsMaytansineMiceMolecular Targeted TherapyReceptors, GABA-ATriple Negative Breast NeoplasmsXenograft Model Antitumor AssaysConceptsTriple-negative breast cancerNegative breast cancerTNBC cell growthBreast cancerMDA-MB-468 xenograftsPotential novel therapeutic targetNovel biologic targetsNovel therapeutic targetBreast cancer tissuesReceptors/cellAntibody-drug conjugate (ADC) developmentMost normal tissuesTreatment optionsCell growthTherapeutic targetBiologic targetsNude miceCancer tissuesVivo functional assaysLow expressionNormal tissuesNovel targetCancerSignificant anticancer activityADC development
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 cancer
2011
P3-17-01: ApoE and Its Receptors (LRP8, VLDLR) Function as Growth Signals for Triple-Negative Breast Cancer and Represent a Novel Therapeutic Target.
Shiang C, Qi Y, Wang B, Broom B, Pusztai L. P3-17-01: ApoE and Its Receptors (LRP8, VLDLR) Function as Growth Signals for Triple-Negative Breast Cancer and Represent a Novel Therapeutic Target. Cancer Research 2011, 71: p3-17-01-p3-17-01. DOI: 10.1158/0008-5472.sabcs11-p3-17-01.Peer-Reviewed Original ResearchTriple-negative breast cancerER-negative cellsBreast cancerHuman epidermal growth factor 2 receptorReceptor systemAbstract Triple-negative breast cancerStimulatory effectCell linesEarly-onset breast cancerHuman triple-negative breast cancerER-negative cell linesExpression of estrogenReceptor-positive cancersER-positive cellsOnset breast cancerNovel therapeutic targetBreast cancer cell linesBreast cancer tissuesInflammatory signaling pathwaysMAPK/ERK pathwayPreferential growth inhibitionApoE4 expressionCancer cell linesTreatment optionsGrowth factor 2 receptorA clinically relevant gene signature in triple negative and basal-like breast cancer
Rody A, Karn T, Liedtke C, Pusztai L, Ruckhaeberle E, Hanker L, Gaetje R, Solbach C, Ahr A, Metzler D, Schmidt M, Müller V, Holtrich U, Kaufmann M. A clinically relevant gene signature in triple negative and basal-like breast cancer. Breast Cancer Research 2011, 13: r97. PMID: 21978456, PMCID: PMC3262210, DOI: 10.1186/bcr3035.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerBasal-like triple-negative breast cancerBreast cancerPrognostic markerMolecular subtypesMultivariate analysisBasal-like molecular subtypeClaudin-low molecular subtypeBasal-like breast cancerAttractive novel therapeutic targetB cell presenceHigh expressionER-positive cancersHigh histological gradeHigher B cellsIL-8 pathwayIL-8 activityNegative breast cancerNew prognostic markerNovel therapeutic targetBiology-based therapiesNon-neoplastic cell populationsRelevant gene signaturesRoutine clinicopathological variablesResultsSeventy-three percent