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
2018
miR-221/222 activate the Wnt/β-catenin signaling to promote triple-negative breast cancer
Liu S, Wang Z, Liu Z, Shi S, Zhang Z, Zhang J, Lin H. miR-221/222 activate the Wnt/β-catenin signaling to promote triple-negative breast cancer. Journal Of Molecular Cell Biology 2018, 10: 302-315. PMID: 30053090, DOI: 10.1093/jmcb/mjy041.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerWnt/β-cateninMiR-221/222 expressionTNBC cell linesBreast cancerMiR-221/222Β-cateninHuman epidermal growth factor receptor 2Epidermal growth factor receptor 2Progression of TNBCGrowth factor receptor 2Limited treatment optionsWnt/β-catenin activationNegative breast cancerFactor receptor 2Primary tumor samplesWnt/β-catenin signalingCell linesWnt3a treatmentMultiple negative regulatorsΒ-catenin activationΒ-catenin signalingPatient survivalPoor prognosisTreatment options
2017
Systematic Drug Screening Identifies Tractable Targeted Combination Therapies in Triple-Negative Breast Cancer
Wali VB, Langdon CG, Held MA, Platt JT, Patwardhan GA, Safonov A, Aktas B, Pusztai L, Stern DF, Hatzis C. Systematic Drug Screening Identifies Tractable Targeted Combination Therapies in Triple-Negative Breast Cancer. Cancer Research 2017, 77: 566-578. PMID: 27872098, PMCID: PMC5582957, DOI: 10.1158/0008-5472.can-16-1901.Peer-Reviewed Original ResearchConceptsTriple-negative breast cancerTNBC cell linesPairwise drug combinationsClinical translationAggressive diseaseCombination therapyBreast cancerPreclinical proofDrug combinationsCombination treatmentInvestigational drugsSingle agentSensitivity patternCell sensitivityCell linesTherapyApoptotic activityAnticancer activityDownregulated genesMitogenic signalingCrizotinibBlockadeClinicAgentsCancer
2016
Minocycline, a putative neuroprotectant, co-administered with doxorubicin-cyclophosphamide chemotherapy in a xenograft model of triple-negative breast cancer
Himmel L, Lustberg M, DeVries A, Poi M, Chen C, Kulp S. Minocycline, a putative neuroprotectant, co-administered with doxorubicin-cyclophosphamide chemotherapy in a xenograft model of triple-negative breast cancer. Experimental And Toxicologic Pathology 2016, 68: 505-515. PMID: 27555377, PMCID: PMC5203928, DOI: 10.1016/j.etp.2016.08.001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisBlotting, WesternCell Line, TumorCell SurvivalCognition DisordersCyclophosphamideDNA DamageDoxorubicinFemaleHumansImmunohistochemistryMiceMice, NudeMinocyclineNeuroprotective AgentsTriple Negative Breast NeoplasmsXenograft Model Antitumor AssaysConceptsTriple-negative breast cancerChemotherapy-induced cognitive impairmentBreast cancer patientsNeural progenitor cellsPutative neuroprotectantCancer patientsBreast cancerXenograft modelDoublecortin-positive neural progenitor cellsFemale athymic nude miceDoxorubicin-cyclophosphamide chemotherapyProgenitor cellsEffects of minocyclineChemotherapeutic drug combinationsOrgan weight measurementsAbsence of minocyclineAthymic nude miceTNBC cell linesTumor-bearing miceAnti-oxidant pathwaysTumor-suppressive effectsBiomarkers of apoptosisTumor volume measurementsHuman neurologic diseasesMechanism of actionTriple-negative breast cancers with amplification of JAK2 at the 9p24 locus demonstrate JAK2-specific dependence
Balko JM, Schwarz LJ, Luo N, Estrada MV, Giltnane JM, Dávila-González D, Wang K, Sánchez V, Dean PT, Combs SE, Hicks D, Pinto JA, Landis MD, Doimi FD, Yelensky R, Miller VA, Stephens PJ, Rimm DL, Gómez H, Chang JC, Sanders ME, Cook RS, Arteaga CL. Triple-negative breast cancers with amplification of JAK2 at the 9p24 locus demonstrate JAK2-specific dependence. Science Translational Medicine 2016, 8: 334ra53. PMID: 27075627, PMCID: PMC5256931, DOI: 10.1126/scitranslmed.aad3001.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsCell Line, TumorCell ProliferationChromosomes, Human, Pair 9Cohort StudiesFemaleGene AmplificationGene Knockdown TechniquesGenetic LociHumansJanus Kinase 2Middle AgedSignal TransductionSpheroids, CellularSTAT3 Transcription FactorSTAT6 Transcription FactorTriple Negative Breast NeoplasmsConceptsTriple-negative breast cancerJAK2 amplificationBreast cancerUntreated triple-negative breast cancerEventual metastatic spreadBasal-like cancersBreast cancer subtypesTNBC cell linesAmplification of JAK2Janus kinase 2 (JAK2) geneNeoadjuvant chemotherapyOverall survivalTNBC xenograftsJAK1/2 inhibitorClinical trialsMetastatic spreadKinase 2 geneJAK2-specific inhibitorTumor growthCancer subtypesMammosphere formationPatientsPotential biomarkersTumor progressionJAK2 inhibitorsmiR-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
2009
Targeting of breast cancer with non-oncology drugs – possible novel therapeutic option for triple-negative breast cancer.
Liedtke C, Yan K, Wu Y, Hortobagyi G, Symmans W, Valero V, Goette M, Kiesel L, Pusztai L. Targeting of breast cancer with non-oncology drugs – possible novel therapeutic option for triple-negative breast cancer. Cancer Research 2009, 69: 2119. DOI: 10.1158/0008-5472.sabcs-2119.Peer-Reviewed Original ResearchTriple-negative breast cancerBreast cancerTherapeutic optionsCell linesEarly-stage breast cancerHuman triple-negative breast cancerCurrent chemotherapy agentsDrug targetsReceptor-positive cancersStage breast cancerBreast cancer cell line MCF-7Future therapeutic optionsNovel therapeutic optionsCancer cell line MCF-7TNBC cell linesBreast cancer cell linesGlutathione S-transferase piFine-needle biopsyDose-dependent inhibitionLack of ERCell line MCF-7Normal HER2 expressionCancer cell linesUnique drug targetsBiological presentation
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