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 reprogrammingCECR2 drives breast cancer metastasis by promoting NF-κB signaling and macrophage-mediated immune suppression
Zhang M, Liu ZZ, Aoshima K, Cai WL, Sun H, Xu T, Zhang Y, An Y, Chen JF, Chan LH, Aoshima A, Lang SM, Tang Z, Che X, Li Y, Rutter SJ, Bossuyt V, Chen X, Morrow JS, Pusztai L, Rimm DL, Yin M, Yan Q. CECR2 drives breast cancer metastasis by promoting NF-κB signaling and macrophage-mediated immune suppression. Science Translational Medicine 2022, 14: eabf5473. PMID: 35108062, PMCID: PMC9003667, DOI: 10.1126/scitranslmed.abf5473.Peer-Reviewed Original ResearchConceptsBreast cancer metastasisReticuloendotheliosis viral oncogene homolog ACancer metastasisImmune suppressionM2 macrophagesWorse metastasis-free survivalMetastatic breast cancerMetastasis-free survivalV-rel avian reticuloendotheliosis viral oncogene homolog ACancer-related deathPrimary breast tumorsMultiple mouse modelsNF-κB signalingImmunocompetent settingNuclear factor-κB family membersMetastasis-promoting genesDistant metastasisMetastatic sitesPrimary tumorEffective therapyBreast cancerMetastasis treatmentMouse modelBreast tumorsMetastasis
2020
PARP inhibition in homologous-recombination-deficient early-stage breast cancer
Pusztai L. PARP inhibition in homologous-recombination-deficient early-stage breast cancer. Annals Of Oncology 2020, 32: 4-5. PMID: 33181269, DOI: 10.1016/j.annonc.2020.11.001.Peer-Reviewed Original ResearchEarly Modulation of Circulating MicroRNAs Levels in HER2-Positive Breast Cancer Patients Treated with Trastuzumab-Based Neoadjuvant Therapy
Di Cosimo S, Appierto V, Pizzamiglio S, Silvestri M, Baselga J, Piccart M, Huober J, Izquierdo M, de la Pena L, Hilbers FS, de Azambuja E, Untch M, Pusztai L, Pritchard K, Nuciforo P, Vincent-Salomon A, Symmans F, Apolone G, de Braud FG, Iorio MV, Verderio P, Daidone MG. Early Modulation of Circulating MicroRNAs Levels in HER2-Positive Breast Cancer Patients Treated with Trastuzumab-Based Neoadjuvant Therapy. International Journal Of Molecular Sciences 2020, 21: 1386. PMID: 32085669, PMCID: PMC7073028, DOI: 10.3390/ijms21041386.Peer-Reviewed Original ResearchConceptsPathological complete responseNeoadjuvant therapyHER2-positive breast cancer patientsTrastuzumab-based neoadjuvant therapyAvailable predictive biomarkersBreast cancer patientsEstrogen receptor statusComplete responseReceptor statusCancer patientsPredictive biomarkersTreatment responseHCC progressionPatientsPredictive valueBivariate analysisMean differencePlasma pairsTherapyEarly modulationMicroRNA levelsTrastuzumabMAPK signalingMetabolism regulationKEGG analysis
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 increasesIdentification 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
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 cellsSystematic 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
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 ResearchMeSH KeywordsAnimalsCell Line, TumorFemaleHumansMiceMice, NudeMicroRNAsProto-Oncogene MasSrc-Family KinasesTriple Negative Breast NeoplasmsConceptsTriple-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
2015
The cell cycle regulator 14-3-3σ opposes and reverses cancer metabolic reprogramming
Phan L, Chou PC, Velazquez-Torres G, Samudio I, Parreno K, Huang Y, Tseng C, Vu T, Gully C, Su CH, Wang E, Chen J, Choi HH, Fuentes-Mattei E, Shin JH, Shiang C, Grabiner B, Blonska M, Skerl S, Shao Y, Cody D, Delacerda J, Kingsley C, Webb D, Carlock C, Zhou Z, Hsieh YC, Lee J, Elliott A, Ramirez M, Bankson J, Hazle J, Wang Y, Li L, Weng S, Rizk N, Wen YY, Lin X, Wang H, Wang H, Zhang A, Xia X, Wu Y, Habra M, Yang W, Pusztai L, Yeung SC, Lee MH. The cell cycle regulator 14-3-3σ opposes and reverses cancer metabolic reprogramming. Nature Communications 2015, 6: 7530. PMID: 26179207, PMCID: PMC4507299, DOI: 10.1038/ncomms8530.Peer-Reviewed Original ResearchMeSH Keywords14-3-3 ProteinsAdultAgedAged, 80 and overBiomarkers, TumorBreast NeoplasmsCell Line, TumorDisease-Free SurvivalEnergy MetabolismExoribonucleasesFemaleGene Expression Regulation, NeoplasticGene Knockout TechniquesGlutamineGlycolysisHCT116 CellsHumansMiddle AgedOrganelle BiogenesisPrognosisProteolysisProto-Oncogene Proteins c-mycUbiquitinationYoung AdultConceptsCancer metabolic reprogrammingMetabolic reprogrammingRecurrence-free survival ratesMetabolic gene expressionBreast cancer patientsCellular energy metabolismHallmarks of cancerMajor metabolic processesTumor glucose uptakeExtensive reprogrammingMetabolic programsMitochondrial biogenesisGene expressionTumorigenic transformationCancer glycolysisMolecular mechanismsReprogrammingCancer patientsMetabolic processesMetabolic shift
2014
In Situ Tumor PD-L1 mRNA Expression Is Associated with Increased TILs and Better Outcome in Breast Carcinomas
Schalper KA, Velcheti V, Carvajal D, Wimberly H, Brown J, Pusztai L, Rimm DL. In Situ Tumor PD-L1 mRNA Expression Is Associated with Increased TILs and Better Outcome in Breast Carcinomas. Clinical Cancer Research 2014, 20: 2773-2782. PMID: 24647569, DOI: 10.1158/1078-0432.ccr-13-2702.Peer-Reviewed Original ResearchB7-H1 AntigenBreast NeoplasmsCell Line, TumorFemaleFluorescent Antibody TechniqueGene Expression Regulation, NeoplasticHumansIn Situ HybridizationKaplan-Meier EstimateLymphatic MetastasisLymphocytes, Tumor-InfiltratingMiddle AgedMultivariate AnalysisNeoplasm Recurrence, LocalPrognosisReceptor, ErbB-2Receptors, EstrogenRNA, MessengerTissue Array AnalysisCombined analysis of gene expression, DNA copy number, and mutation profiling data to display biological process anomalies in individual breast cancers
Shi W, Balazs B, Györffy B, Jiang T, Symmans WF, Hatzis C, Pusztai L. Combined analysis of gene expression, DNA copy number, and mutation profiling data to display biological process anomalies in individual breast cancers. Breast Cancer Research And Treatment 2014, 144: 561-568. PMID: 24619174, DOI: 10.1007/s10549-014-2904-z.Peer-Reviewed Original ResearchConceptsDNA copy numberBiological processesIndividual molecular eventsCopy numberGene expressionMolecular eventsMulticellular organismal processGene Ontology databaseGO biological processesSignal transduction pathwaysOrganismal processesGO termsMolecular dataTransduction pathwaysSiRNA screenComplex genomic abnormalitiesIndividual cancersOntology databaseFunctional roleDriver eventsCell growthSequence abnormalitiesBreast cancer cell linesCancer cell linesGenomic abnormalitiesTP53 mutation‐correlated genes predict the risk of tumor relapse and identify MPS1 as a potential therapeutic kinase in TP53‐mutated breast cancers
Győrffy B, Bottai G, Lehmann-Che J, Kéri G, Őrfi L, Iwamoto T, Desmedt C, Bianchini G, Turner NC, de Thè H, André F, Sotiriou C, Hortobagyi GN, Di Leo A, Pusztai L, Santarpia L. TP53 mutation‐correlated genes predict the risk of tumor relapse and identify MPS1 as a potential therapeutic kinase in TP53‐mutated breast cancers. Molecular Oncology 2014, 8: 508-519. PMID: 24462521, PMCID: PMC5528634, DOI: 10.1016/j.molonc.2013.12.018.Peer-Reviewed Original ResearchConceptsBreast cancerTP53 mutation statusPrognostic valueBC cellsMutation statusER-negative breast cancerDifferent BC cell linesFuture clinical trialsSignificant prognostic markerPotential therapeutic targetBC cell linesType of treatmentNeoadjuvant chemotherapyBC patientsClinical behaviorPrognostic markerClinical trialsConventional chemotherapyEstrogen receptorPotent small molecule inhibitorsTumor relapseSmall molecule inhibitorsTherapeutic targetClinical relevanceTP53 statusMitochondrial 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
2012
A Systematic Evaluation of Multi-Gene Predictors for the Pathological Response of Breast Cancer Patients to Chemotherapy
Shen K, Song N, Kim Y, Tian C, Rice SD, Gabrin MJ, Symmans WF, Pusztai L, Lee JK. A Systematic Evaluation of Multi-Gene Predictors for the Pathological Response of Breast Cancer Patients to Chemotherapy. PLOS ONE 2012, 7: e49529. PMID: 23185353, PMCID: PMC3504014, DOI: 10.1371/journal.pone.0049529.Peer-Reviewed Original ResearchConceptsMulti-gene predictorsPatients' clinical outcomesClinical outcomesCancer patientsTherapeutic responseStandard combination chemotherapyBreast cancer patientsClinical outcome measurementsPatient's therapeutic responseBreast cancer cell linesCancer cell linesNegative patientsCombination chemotherapyPatient cohortPathological responseBreast cancerEstrogen receptorClinical utilityOutcome measurementsChemotherapyPatientsCell linesOutcomesPredictorsCOXENCell Line Derived Multi-Gene Predictor of Pathologic Response to Neoadjuvant Chemotherapy in Breast Cancer: A Validation Study on US Oncology 02-103 Clinical Trial
Shen K, Qi Y, Song N, Tian C, Rice SD, Gabrin MJ, Brower SL, Symmans WF, O’Shaughnessy J, Holmes FA, Asmar L, Pusztai L. Cell Line Derived Multi-Gene Predictor of Pathologic Response to Neoadjuvant Chemotherapy in Breast Cancer: A Validation Study on US Oncology 02-103 Clinical Trial. BMC Medical Genomics 2012, 5: 51. PMID: 23158478, PMCID: PMC3536618, DOI: 10.1186/1755-8794-5-51.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsArea Under CurveBreast NeoplasmsCell Line, TumorClinical Trials as TopicDemographyFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGenes, NeoplasmHumansMiddle AgedMultivariate AnalysisNeoadjuvant TherapyReproducibility of ResultsTreatment OutcomeUnited StatesConceptsMulti-gene predictorsBreast cancerNeoadjuvant chemotherapyCombination chemotherapyCyclophosphamide combination chemotherapyDocetaxel/capecitabineEpirubicin/cyclophosphamideER-negative patientsPathologic complete responseER-positive cancersReceiver-operating characteristic curveAU-ROCCell linesBlinded validation studyNeoadjuvant treatmentMost patientsComplete responseER statusPathologic responseClinical outcomesValidation studyResidual diseaseTx groupClinical trialsEstrogen receptorA network-based, integrative study to identify core biological pathways that drive breast cancer clinical subtypes
Dutta B, Pusztai L, Qi Y, André F, Lazar V, Bianchini G, Ueno N, Agarwal R, Wang B, Shiang CY, Hortobagyi GN, Mills GB, Symmans WF, Balázsi G. A network-based, integrative study to identify core biological pathways that drive breast cancer clinical subtypes. British Journal Of Cancer 2012, 106: 1107-1116. PMID: 22343619, PMCID: PMC3304402, DOI: 10.1038/bjc.2011.584.Peer-Reviewed Original ResearchMeSH KeywordsBreast NeoplasmsCell Line, TumorComputer SimulationDNA Copy Number VariationsEpithelial-Mesenchymal TransitionFemaleGene ExpressionGene Expression ProfilingGene Expression Regulation, NeoplasticGene Knockdown TechniquesGene Regulatory NetworksGenes, NeoplasmHumansModels, BiologicalProtein Interaction MapsReceptor, ErbB-2Receptors, EstrogenReceptors, ProgesteroneRNA InterferenceConceptsGenome-scale dataCore biological pathwaysTriple receptor-negative breast cancerProtein-protein interactionsCell line data setsGene knockdown experimentsGene copy number dataCopy number dataCopy number variation dataNumber variation dataMember genesGene networksTranscriptional disturbancesKnockdown experimentsBiological discoveryGene expressionFunctional specificityBiological pathwaysDifferential expressionIntegrative studyFunctional relevanceVariation dataLine data setsCell linesGenes
2010
PIK3CA mutations associated with gene signature of low mTORC1 signaling and better outcomes in estrogen receptor–positive breast cancer
Loi S, Haibe-Kains B, Majjaj S, Lallemand F, Durbecq V, Larsimont D, Gonzalez-Angulo AM, Pusztai L, Symmans WF, Bardelli A, Ellis P, Tutt AN, Gillett CE, Hennessy BT, Mills GB, Phillips WA, Piccart MJ, Speed TP, McArthur GA, Sotiriou C. PIK3CA mutations associated with gene signature of low mTORC1 signaling and better outcomes in estrogen receptor–positive breast cancer. Proceedings Of The National Academy Of Sciences Of The United States Of America 2010, 107: 10208-10213. PMID: 20479250, PMCID: PMC2890442, DOI: 10.1073/pnas.0907011107.Peer-Reviewed Original ResearchMeSH KeywordsAntibiotics, AntineoplasticAntineoplastic Agents, HormonalBase SequenceBreast NeoplasmsCell Line, TumorClass I Phosphatidylinositol 3-KinasesDNA PrimersFemaleGene Expression ProfilingHumansMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesMutationNeoplasms, Hormone-DependentOligonucleotide Array Sequence AnalysisPhosphatidylinositol 3-KinasesPrognosisProteinsProto-Oncogene Proteins c-aktReceptor, ErbB-2Receptors, EstrogenSignal TransductionSirolimusTamoxifenTOR Serine-Threonine KinasesTranscription FactorsConceptsBreast cancerPIK3CA mutationsClinical outcomesEstrogen receptor-positive breast cancerReceptor-positive breast cancerGene signaturePIK3CA mutation statusPI3K/mTOR inhibitorBetter clinical outcomesPI3K/mTOR inhibitionHuman breast cancerBC cell linesPIK3CA mutant breast cancersCommon genetic aberrationsTamoxifen monotherapyBetter prognosisMTOR inhibitorsBetter outcomesMutation statusMTOR inhibitionPathway activationExperimental modelGenetic aberrationsPrognosisCell linesDevelopment of Candidate Genomic Markers to Select Breast Cancer Patients for Dasatinib Therapy
Moulder S, Yan K, Huang F, Hess KR, Liedtke C, Lin F, Hatzis C, Hortobagyi GN, Symmans WF, Pusztai L. Development of Candidate Genomic Markers to Select Breast Cancer Patients for Dasatinib Therapy. Molecular Cancer Therapeutics 2010, 9: 1120-1127. PMID: 20423993, DOI: 10.1158/1535-7163.mct-09-1117.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic AgentsBiomarkers, PharmacologicalBiomarkers, TumorBreast NeoplasmsCarcinomaCell Line, TumorDasatinibDrug Resistance, NeoplasmFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticGenetic Association StudiesGenome, HumanHumansMatched-Pair AnalysisOligonucleotide Array Sequence AnalysisPatient SelectionPrognosisPyrimidinesThiazolesConceptsClinical trialsCell linesPhase I/II trialIndependent breast cancer cell linesEarly phase clinical trialsDasatinib-resistant cellsPrimary breast cancerBreast cancer patientsDasatinib-resistant cell linesDifferent patient subsetsBreast cancer cell linesGenomic predictorsCancer cell linesDasatinib therapyDifferent potential predictorsII trialPatient subsetsPatient selectionCancer patientsBreast cancerDasatinib sensitivityMammary epithelial cellsDasatinib responseActivity indexPatient samples
2009
Amplification of fibroblast growth factor receptor-1 in breast cancer and the effects of brivanib alaninate
Shiang CY, Qi Y, Wang B, Lazar V, Wang J, Fraser Symmans W, Hortobagyi GN, Andre F, Pusztai L. Amplification of fibroblast growth factor receptor-1 in breast cancer and the effects of brivanib alaninate. Breast Cancer Research And Treatment 2009, 123: 747-755. PMID: 20024612, DOI: 10.1007/s10549-009-0677-6.Peer-Reviewed Original ResearchMeSH KeywordsAlanineAntineoplastic AgentsBreast NeoplasmsCell Line, TumorCell ProliferationComparative Genomic HybridizationDose-Response Relationship, DrugFemaleFibroblast Growth Factor 2Gene AmplificationGene DosageGene Expression ProfilingGene Expression Regulation, NeoplasticHumansInhibitory Concentration 50Mitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3PhosphorylationProto-Oncogene Proteins c-aktReceptor, Fibroblast Growth Factor, Type 1RNA, MessengerSignal TransductionTriazinesConceptsFibroblast growth factor receptor 1Growth factor receptor 1Breast cancer cell linesBreast cancerFactor receptor 1Cancer cell linesKinase activityProtein overexpressionReceptor 1Cell linesCopy numberDirect anti-proliferative effectsGene expression profilingHuman breast cancerTyrosine kinase activityAnti-angiogenic effectsMDA-MB-361Small molecule inhibitorsAnti-proliferative effectsGrowth inhibitionDNA copy numberProtein expression levelsBrivanib treatmentFGFR-1 mRNANormal copy number