2014
Effects of Obesity on Transcriptomic Changes and Cancer Hallmarks in Estrogen Receptor–Positive Breast Cancer
Fuentes-Mattei E, Velazquez-Torres G, Phan L, Zhang F, Chou PC, Shin JH, Choi HH, Chen JS, Zhao R, Chen J, Gully C, Carlock C, Qi Y, Zhang Y, Wu Y, Esteva FJ, Luo Y, McKeehan WL, Ensor J, Hortobagyi GN, Pusztai L, Symmans W, Lee MH, Yeung SC. Effects of Obesity on Transcriptomic Changes and Cancer Hallmarks in Estrogen Receptor–Positive Breast Cancer. Journal Of The National Cancer Institute 2014, 106: dju158. PMID: 24957076, PMCID: PMC4110474, DOI: 10.1093/jnci/dju158.Peer-Reviewed Original ResearchMeSH KeywordsAdipocytesAdipokinesAgedAnimalsAntineoplastic AgentsBiomarkers, TumorBreast NeoplasmsCell ProliferationDisease Models, AnimalEverolimusFemaleHumansKaplan-Meier EstimateMetforminMiceMice, TransgenicMiddle AgedObesityPostmenopauseProspective StudiesProto-Oncogene Proteins c-aktReceptors, EstrogenSignal TransductionSirolimusTOR Serine-Threonine KinasesTranscriptomeConceptsEstrogen receptor-positive breast cancerReceptor-positive breast cancerBreast cancer cell proliferationEffect of obesityBreast cancer patientsObese mouse modelAdipocyte-secreted adipokineCancer cell proliferationCancer patientsBreast cancerMouse modelCell proliferationAssociation of obesityAkt/mTOR activationMammary tumor growthEpithelial-mesenchymal transition genesAKT/mTOR pathwayBreast cancer aggressivenessBreast tumor formationCancer hallmarksPostmenopausal womenPretreatment biopsiesProspective cohortAdipokine secretionCancer death
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 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 number
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 ResearchMeSH KeywordsBreast NeoplasmsCell DivisionClass I Phosphatidylinositol 3-KinasesFemaleGenomicsHumansMutationPhosphatidylinositol 3-KinasesProteomicsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseConceptsPIK3CA 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
2007
Expression patterns and predictive value of phosphorylated AKT in early-stage breast cancer
Andre F, Nahta R, Conforti R, Boulet T, Aziz M, Yuan LX, Meslin F, Spielmann M, Tomasic G, Pusztai L, Hortobagyi GN, Michiels S, Delaloge S, Esteva FJ. Expression patterns and predictive value of phosphorylated AKT in early-stage breast cancer. Annals Of Oncology 2007, 19: 315-320. PMID: 17804473, DOI: 10.1093/annonc/mdm429.Peer-Reviewed Original ResearchMeSH KeywordsAdultAge FactorsAgedBiomarkers, TumorBreast NeoplasmsChi-Square DistributionCohort StudiesCombined Modality TherapyDisease-Free SurvivalErbB ReceptorsFemaleFollow-Up StudiesGene Expression Regulation, NeoplasticHumansImmunohistochemistryMiddle AgedNeoplasm StagingPredictive Value of TestsProbabilityProportional Hazards ModelsProto-Oncogene Proteins c-aktRandomized Controlled Trials as TopicReceptor, ErbB-2Risk AssessmentSurvival AnalysisTime FactorsTreatment OutcomeConceptsEarly breast cancerBreast cancerPredictive valuePhosphorylated AktAdjuvant chemotherapyPAkt expressionAnthracycline-based adjuvant chemotherapyEarly-stage breast cancerEpidermal growth factor receptor expressionGrowth factor receptor expressionAkt phosphorylationBreast cancer tissuesFactor receptor expressionGrowth factor receptorHER2 tumorsRandomized trialsAssessable tumorsHER2 expressionReceptor expressionPositive stainingCancer tissuesEGFR expressionHER2Tumor resistancePatients