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
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
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
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
Development and validation of a clinical cancer genomic profiling test based on massively parallel DNA sequencing
Frampton GM, Fichtenholtz A, Otto GA, Wang K, Downing SR, He J, Schnall-Levin M, White J, Sanford EM, An P, Sun J, Juhn F, Brennan K, Iwanik K, Maillet A, Buell J, White E, Zhao M, Balasubramanian S, Terzic S, Richards T, Banning V, Garcia L, Mahoney K, Zwirko Z, Donahue A, Beltran H, Mosquera JM, Rubin MA, Dogan S, Hedvat CV, Berger MF, Pusztai L, Lechner M, Boshoff C, Jarosz M, Vietz C, Parker A, Miller VA, Ross JS, Curran J, Cronin MT, Stephens PJ, Lipson D, Yelensky R. Development and validation of a clinical cancer genomic profiling test based on massively parallel DNA sequencing. Nature Biotechnology 2013, 31: 1023-1031. PMID: 24142049, PMCID: PMC5710001, DOI: 10.1038/nbt.2696.Peer-Reviewed Original Research
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
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 processP3-17-01: 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 receptor
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 samplesAssessment of an RNA interference screen-derived mitotic and ceramide pathway metagene as a predictor of response to neoadjuvant paclitaxel for primary triple-negative breast cancer: a retrospective analysis of five clinical trials
Juul N, Szallasi Z, Eklund AC, Li Q, Burrell RA, Gerlinger M, Valero V, Andreopoulou E, Esteva FJ, Symmans WF, Desmedt C, Haibe-Kains B, Sotiriou C, Pusztai L, Swanton C. Assessment of an RNA interference screen-derived mitotic and ceramide pathway metagene as a predictor of response to neoadjuvant paclitaxel for primary triple-negative breast cancer: a retrospective analysis of five clinical trials. The Lancet Oncology 2010, 11: 358-365. PMID: 20189874, DOI: 10.1016/s1470-2045(10)70018-8.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAntineoplastic Combined Chemotherapy ProtocolsArea Under CurveBreast NeoplasmsCeramidesDrug Screening Assays, AntitumorFemaleHumansLogistic ModelsMetagenomicsMiddle AgedMitosisModels, GeneticMultivariate AnalysisNeoadjuvant TherapyPaclitaxelPredictive Value of TestsRetrospective StudiesRNA InterferenceConceptsTriple-negative breast cancerPathological complete responseMultivariate logistic regressionBreast cancerClinical trialsPrimary triple-negative breast cancerEpidermal growth factor receptor 2Logistic regressionBreast Cancer Research FoundationAddition of taxanesPaclitaxel-containing chemotherapyClinical trial cohortProportion of patientsCohort of patientsGrowth factor receptor 2Paclitaxel combination chemotherapyUK Medical Research CouncilAlternative treatment regimensPredictors of responseCancer Research UKBreast cancer cell linesTriple-negative breast cancer cell linesFactor receptor 2Cancer Research FoundationCell lines
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 numberThe Molecular Anatomy of Breast Cancer Stroma; Independent Prognostic Role in ER-Positive and ER-Negative Cancers.
Bianchini G, Bianchini G, Alvarez R, Qi Y, Hatzis C, Iwamoto T, Shiang C, Coutant C, Hortobagyi G, Symmans W, Pusztai L. The Molecular Anatomy of Breast Cancer Stroma; Independent Prognostic Role in ER-Positive and ER-Negative Cancers. Cancer Research 2009, 69: 105-105. DOI: 10.1158/0008-5472.sabcs-09-105.Peer-Reviewed Original ResearchDistant metastasis-free survivalCore needle biopsyFine-needle aspirationER- cancersPrognostic valueCancer cell linesER- tumorsB cells/plasma cellsStromal signaturesStromal genesBreast cancer stromaConsistent prognostic valueER- breast cancer cell linesReproducible prognostic markerTamoxifen-treated patientsIndependent prognostic roleER-negative cancersMetastasis-free survivalStromal gene signatureBreast cancer cell linesVariable prognostic valueCell linesFree survivalPreoperative chemotherapyUntreated patientsFrom the Lab to the Clinic: Gene-Expression Profiles That Are Associated with Mek-Inhibitor Sensitivity In Vitro Are Coordinately Co-Expressed in Breast Cancer Biopsy Samples from the I-SPY Trial (CALGB 150007/150012, ACRIN 6657).
Wolf D, Das D, Lenburg M, Paquette J, Spellman P, Gray J, Gray J, Pusztai L, Symmans F, Hatzis C, Esserman L, van 't Veer L, I-SPY Investigators .. From the Lab to the Clinic: Gene-Expression Profiles That Are Associated with Mek-Inhibitor Sensitivity In Vitro Are Coordinately Co-Expressed in Breast Cancer Biopsy Samples from the I-SPY Trial (CALGB 150007/150012, ACRIN 6657). Cancer Research 2009, 69: 2042-2042. DOI: 10.1158/0008-5472.sabcs-09-2042.Peer-Reviewed Original ResearchSensitive cell linesCancer cell linesOutcome dataCell linesI-SPY 2 TRIALI-SPY 1 TRIALInitial tumor responseNeo-adjuvant chemotherapyPre-treatment biopsiesThird of patientsBreast cancer biopsy samplesDrug response predictorsBreast cancer therapyBreast cancer cell linesMEK inhibitor sensitivityExpression of genesTumor responseTherapeutic responseResponse predictorsPatientsBiopsy samplesTumor samplesPatient samplesCancer ResDrug sensitivitySecreted Frizzled Receptor Protein 1 (sFRP-1) as Both a Potential Novel Biomarker of Triple Negative Breast Cancer (TNBC), and Its Sensitivity Against Taxane/Anthracycline Containing Neoadjuvant Chemotherapy.
Liedtke C, Ruckert C, Goette M, von Wahlde M, Kiesel L, Symmans W, Pusztai L. Secreted Frizzled Receptor Protein 1 (sFRP-1) as Both a Potential Novel Biomarker of Triple Negative Breast Cancer (TNBC), and Its Sensitivity Against Taxane/Anthracycline Containing Neoadjuvant Chemotherapy. Cancer Research 2009, 69: 4047-4047. DOI: 10.1158/0008-5472.sabcs-09-4047.Peer-Reviewed Original ResearchTriple-negative breast cancerRelapse-free survivalNegative breast cancerNeoadjuvant chemotherapyBreast cancerKi67 expressionTriple-negative breast cancer (TNBC) phenotypeNovel markerProtein 1Breast cancer phenotypeExpression of Ki67Breast cancer subtypesSFRP-1Breast cancer cell linesMDA-MB-468 breast cancer cell linePotential novel biomarkersCell linesSFRP-1 expressionNegative cell linesAnthracycline chemotherapyCancer cell linesFree survivalSystemic therapyUnfavorable prognosisNovel biomarkersClinical evaluation of chemotherapy response predictors developed from breast cancer cell lines
Liedtke C, Wang J, Tordai A, Symmans WF, Hortobagyi GN, Kiesel L, Hess K, Baggerly KA, Coombes KR, Pusztai L. Clinical evaluation of chemotherapy response predictors developed from breast cancer cell lines. Breast Cancer Research And Treatment 2009, 121: 301-309. PMID: 19603265, DOI: 10.1007/s10549-009-0445-7.Peer-Reviewed Original ResearchMeSH KeywordsAntineoplastic Combined Chemotherapy ProtocolsBiomarkers, TumorBreast NeoplasmsCell Line, TumorCyclophosphamideDoxorubicinDrug Resistance, NeoplasmFemaleFluorouracilGene Expression ProfilingHumansNeoplasm StagingOligonucleotide Array Sequence AnalysisPaclitaxelPredictive Value of TestsTreatment OutcomeConceptsBreast cancer cell linesCancer cell linesResponse predictorsBaseline gene expression dataCell linesChemotherapy drugsHuman breast cancer cell linesStandard chemotherapy drugsFine-needle aspiration specimensNeedle aspiration specimensPathologic responseAffymetrix U133A gene chipsClinical evaluationBreast cancerPharmacogenomic predictorsSame drugStage IPredictive valueAspiration specimensMultigene predictorsTumor samplesPatientsResistant cellsPatient dataDrugsTargeting 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
2008
An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer
Stemke-Hale K, Gonzalez-Angulo AM, Lluch A, Neve RM, Kuo WL, Davies M, Carey M, Hu Z, Guan Y, Sahin A, Symmans WF, Pusztai L, Nolden LK, Horlings H, Berns K, Hung MC, van de Vijver MJ, Valero V, Gray JW, Bernards R, Mills GB, Hennessy BT. An Integrative Genomic and Proteomic Analysis of PIK3CA, PTEN, and AKT Mutations in Breast Cancer. Cancer Research 2008, 68: 6084-6091. PMID: 18676830, PMCID: PMC2680495, DOI: 10.1158/0008-5472.can-07-6854.Peer-Reviewed Original ResearchConceptsPIK3CA mutationsBreast cancerAKT1 mutationsPTEN lossPathway aberrationsHormone receptor-positive breast cancer patientsHormone receptor-positive breast cancerPTEN mutationsReceptor-positive breast cancer patientsHormone receptor-positive cancersPI3K pathway aberrationsCell linesReceptor-positive breast cancerAdjuvant tamoxifen therapyReceptor-positive cancersBreast cancer patientsDifferent breast cancer subtypesDownstream PI3K/AktBasal-like tumorsBreast cancer subtypesHuman breast cancerPI3K inhibitor LY294002PI3K/AktK inhibitor LY294002PI3K inhibition