Search results for "Triple Negative Breast Neoplasms"

showing 10 items of 48 documents

PTTG1-interacting protein (PTTG1IP/PBF) predicts breast cancer survival.

2017

Background: PTTG1-interacting protein (PTTG1IP) is an oncogenic protein, which participates in metaphase-anaphase transition of the cell cycle through activation of securin (PTTG1). PTTG1IP promotes the shift of securin from the cell cytoplasm to the nucleus, allowing the interaction between separase and securin. PTTG1IP overexpression has been previously observed in malignant disease, e.g. in breast carcinoma. However, the prognostic value of PTTG1IP in breast carcinoma patients has not previously been revealed. Methods: A total of 497 breast carcinoma patients with up to 22-year follow-up were analysed for PTTG1IP and securin immunoexpression. The results were evaluated for correlations w…

0301 basic medicineOncologyCancer ResearchTriple Negative Breast NeoplasmsKaplan-Meier EstimatePBF0302 clinical medicineBreast cancerSurgical oncologyRisk FactorsAged 80 and overrintasyöpäPTTG1 interacting proteinIntracellular Signaling Peptides and ProteinsCell cycleMiddle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisImmunohistochemistrySecurinsyöpägeenitOncologySecurin030220 oncology & carcinogenesisImmunohistochemistryFemaleSeparaseBreast carcinomaResearch ArticleAdultmedicine.medical_specialtyPTTG1IPBreast Neoplasmslcsh:RC254-282immunohistokemia03 medical and health sciencesBreast cancerInternal medicineGeneticsmedicineBiomarkers TumorHumansAgedbusiness.industryMembrane Proteinsmedicine.disease030104 developmental biologyMultivariate AnalysisCancer researchprognosisproteiinitbusinessBMC cancer
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Neoadjuvant eribulin mesylate following anthracycline and taxane in triple negative breast cancer: Results from the HOPE study

2019

BackgroundEribulin mesylate (E) is indicated for metastatic breast cancer patients previously treated with anthracycline and taxane. We argued that E could also benefit patients eligible for neoadjuvant chemotherapy.MethodsPatients with primary triple negative breast cancer ≥2 cm received doxorubicin 60 mg/m2 and paclitaxel 200 mg/m2 x 4 cycles (AT) followed by E 1.4 mg/m2 x 4 cycles. Primary endpoint was pathological complete response (pCR) rate; secondary and explorative endpoints included clinical/metabolic response rates and safety, and biomarker analysis, respectively. Using a two-stage Simon design, 43 patients were to be included provided that 4 of 13 patients had achieved pCR in the…

0301 basic medicineOncologyCancer TreatmentTriple Negative Breast NeoplasmsImmunostainingToxicologyPathology and Laboratory MedicineBiochemistryMetastasis0302 clinical medicineBreast TumorsClinical endpointMedicine and Health Sciencesmetastatic breast cancer Eribulin mesylate epithelial–mesenchymal transition.AnthracyclinesTriple-negative breast cancerStainingMultidisciplinaryPharmaceuticsQRKetonesMetastatic breast cancerNeoadjuvant TherapyTreatment OutcomeSurgical OncologyOncology030220 oncology & carcinogenesisMedicineFemaleTaxoidsResearch ArticleAdultBridged-Ring CompoundsClinical Oncologymedicine.medical_specialtyAnthracyclineScienceSurgical and Invasive Medical ProceduresNeutropeniaResearch and Analysis Methods03 medical and health sciencesCancer ChemotherapyBreast cancerbreast cancerDrug TherapyInternal medicinemedicineHumansChemotherapyFuransTaxaneToxicitybusiness.industryCancers and NeoplasmsBiology and Life Sciencesmedicine.disease030104 developmental biologySpecimen Preparation and TreatmentMED/06 - ONCOLOGIA MEDICAClinical MedicinebusinessBiomarkers
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A multicentre analytical comparison study of inter-reader and inter-assay agreement of four programmed death-ligand 1 immunohistochemistry assays for…

2020

AIMS Studies in various cancer types have demonstrated discordance between results from different programmed death-ligand 1 (PD-L1) assays. Here, we compare the reproducibility and analytical concordance of four clinically developed assays for assessing PD-L1-positivity in tumour-infiltrating immune cells in the tumour area (PD-L1-IC-positivity) in triple-negative breast cancer (TNBC). METHODS AND RESULTS Primary TNBC resection specimens (n = 30) were selected based on their PD-L1-IC-positivity per VENTANA SP142 ( 5%: eight cases). Serial histological sections were stained for PD-L1 using VENTANA SP142, VENTANA SP263, DAKO 22C3 and DAKO 28-8. PD-L1-IC-positivity and tumour cell expression (…

0301 basic medicineOncologyMalemedicine.medical_specialtyHistologyConcordanceTriple Negative Breast NeoplasmsB7-H1 AntigenPathology and Forensic MedicineCohort Studies03 medical and health sciences0302 clinical medicineBreast cancerLymphocytes Tumor-InfiltratingInternal medicinemedicineBiomarkers TumorHumansTriple-negative breast cancerAgedReproducibilityWhole Genome Sequencingbusiness.industryCancerHigh-Throughput Nucleotide SequencingReproducibility of ResultsGeneral MedicineMiddle Agedmedicine.diseaseImmunohistochemistryddc:030104 developmental biology030220 oncology & carcinogenesisMutationComparison studyImmunohistochemistryFemaleNeoplasm GradingbusinessProgrammed deathHistopathologyReferences
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Suppressive role exerted by microRNA-29b-1-5p in triple negative breast cancer through SPIN1 regulation

2017

MiR-29 family dysregulation occurs in various cancers including breast cancers. We investigated miR-29b-1 functional role in human triple negative breast cancer (TNBC) the most aggressive breast cancer subtype. We found that miR-29b-1-5p was downregulated in human TNBC tissues and cell lines. To assess whether miR- 29b-1-5p correlated with TNBC regenerative potential, we evaluated cancer stem cell enrichment in our TNBC cell lines, and found that only MDA-MB-231 and BT-20 produced primary, secondary and tertiary mammospheres, which were progressively enriched in OCT4, NANOG and SOX2 stemness genes. MiR-29b-1-5p expression inversely correlated with mammosphere stemness potential, and miR-29b…

0301 basic medicineOncologycancer stem cellsCarcinogenesisCell Cycle ProteinsTriple Negative Breast NeoplasmsMicroRNA 29b0302 clinical medicineCell MovementSettore BIO/10 - BiochimicaCancer stem cells; MiR-29b-1; SPIN1; Triple-negative breast cancer; Wnt/β-catenin and Akt signaling pathwaysMedicineBreastBreast -- CancerTriple-negative breast cancerWnt signaling pathwayMicroRNANanog Homeobox ProteinGene Expression Regulation NeoplasticOncologyWnt/β-catenin and Akt signaling pathway030220 oncology & carcinogenesisMiR-29b-1Wnt/β-catenin and Akt signaling pathwaysNeoplastic Stem Cellstriple-negative breast cancerFemaleMicrotubule-Associated ProteinsSignal TransductionResearch Papermedicine.medical_specialtycancer stem cellPaclitaxelDown-Regulation03 medical and health sciencesBreast cancerSOX2Cancer stem cellInternal medicineCell Line TumormicroRNAHumansNeoplasm InvasivenessCell ProliferationSPIN1business.industrySOXB1 Transcription Factorsmedicine.diseasePhosphoproteinsMolecular medicineAntineoplastic Agents PhytogenicMicroRNAs030104 developmental biologyDrug Resistance NeoplasmbusinessOctamer Transcription Factor-3
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A two-gene epigenetic signature for the prediction of response to neoadjuvant chemotherapy in triple-negative breast cancer patients

2019

Background Pathological complete response (pCR) after neoadjuvant chemotherapy (NAC) in triple-negative breast cancer (TNBC) varies between 30 and 40% approximately. To provide further insight into the prediction of pCR, we evaluated the role of an epigenetic methylation-based signature. Methods Epigenetic assessment of DNA extracted from biopsy archived samples previous to NAC from TNBC patients was performed. Patients included were categorized according to previous response to NAC in responder (pCR or residual cancer burden, RCB = 0) or non-responder (non-pCR or RCB > 0) patients. A methyloma study was performed in a discovery cohort by the Infinium HumanMethylation450 BeadChip (450K arra…

0301 basic medicineOncologymedicine.medical_treatmentADNlcsh:MedicineTriple Negative Breast NeoplasmsEpigenesis Genetic0302 clinical medicineGenetics (clinical)Triple-negative breast cancermedicine.diagnostic_testHigh-Throughput Nucleotide SequencingNuclear ProteinsMethylationMiddle AgedNeoadjuvant TherapyGene Expression Regulation NeoplasticTreatment OutcomeMyogenic Regulatory FactorsEfectes secundaris dels medicaments030220 oncology & carcinogenesisCohortFemaleTaxoidsMetilacióMicrotubule-Associated ProteinsAdultmedicine.medical_specialtylcsh:QH426-470MethylationMinor Histocompatibility Antigens03 medical and health sciencesBreast cancerTriple-negative breast cancerInternal medicineCell Line TumorBiopsyGeneticsmedicineHumansEpigeneticsMolecular BiologyEpigenetic signatureAgedChemotherapybusiness.industryGene Expression ProfilingResearchlcsh:RSequence Analysis DNADNADNA Methylationmedicine.diseaseHuman geneticsRepressor Proteinslcsh:Genetics030104 developmental biologyDrug side effectsbusinessPredictionDevelopmental Biology
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miR-9 and miR-200 regulate PDGFRβ-mediated endothelial differentiation of tumor cells in triple-negative breast cancer

2016

Abstract Organization of cancer cells into endothelial-like cell-lined structures to support neovascularization and to fuel solid tumors is a hallmark of progression and poor outcome. In triple-negative breast cancer (TNBC), PDGFRβ has been identified as a key player of this process and is considered a promising target for breast cancer therapy. Thus, we aimed at investigating the role of miRNAs as a therapeutic approach to inhibit PDGFRβ-mediated vasculogenic properties of TNBC, focusing on miR-9 and miR-200. In MDA-MB-231 and MDA-MB-157 TNBC cell lines, miR-9 and miR-200 promoted and inhibited, respectively, the formation of vascular-like structures in vitro. Induction of endogenous miR-9…

0301 basic medicinePathologymedicine.medical_specialtyCancer ResearchCellular differentiationBlotting WesternFluorescent Antibody TechniqueTriple Negative Breast NeoplasmsMice SCIDBiologySettore MED/08 - Anatomia PatologicaPolymerase Chain ReactionNeovascularizationReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesMice0302 clinical medicinemicroRNAmedicineAnimalsHumansTriple-negative breast cancerIn Situ HybridizationRegulation of gene expressionNeovascularization PathologicCancerEndothelial CellsCell Differentiationmedicine.diseaseImmunohistochemistryGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyOncologyOncology; Cancer Research030220 oncology & carcinogenesisGene Knockdown TechniquesCancer cellCancer researchHeterograftsEctopic expressionFemalemedicine.symptom
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MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation

2017

Summary Most patients with advanced triple-negative breast cancer (TNBC) develop drug resistance. MYC and MCL1 are frequently co-amplified in drug-resistant TNBC after neoadjuvant chemotherapy. Herein, we demonstrate that MYC and MCL1 cooperate in the maintenance of chemotherapy-resistant cancer stem cells (CSCs) in TNBC. MYC and MCL1 increased mitochondrial oxidative phosphorylation (mtOXPHOS) and the generation of reactive oxygen species (ROS), processes involved in maintenance of CSCs. A mutant of MCL1 that cannot localize in mitochondria reduced mtOXPHOS, ROS levels, and drug-resistant CSCs without affecting the anti-apoptotic function of MCL1. Increased levels of ROS, a by-product of a…

0301 basic medicinePhysiologyMice NudeTriple Negative Breast NeoplasmsOxidative phosphorylationTumor initiationMitochondrionBiologyOxidative PhosphorylationArticleProto-Oncogene Proteins c-myc03 medical and health sciencesCancer stem cellCell Line TumorAnimalsHumansMCL1Molecular BiologyTriple-negative breast cancerchemistry.chemical_classificationReactive oxygen speciesCell BiologyMitochondria030104 developmental biologychemistryDrug Resistance NeoplasmNeoplastic Stem CellsCancer researchMyeloid Cell Leukemia Sequence 1 ProteinFemaleStem cellReactive Oxygen SpeciesCell Metabolism
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Cytotoxic activity of the histone deacetylase 3-Selective inhibitor Pojamide on MDA-MB-231 triple-negative breast cancer cells

2019

We examined the effects of the ferrocene-based histone deacetylase-3 inhibitor Pojamide (N1-(2-aminophenyl)-N8-ferrocenyloctanediamide) and its two derivatives N1-(2-aminophenyl)-N6-ferrocenyladipamide and N1-(2-aminophenyl)-N8-ferroceniumoctanediamide tetrafluoroborate on triple-negative MDA-MB-231 breast cancer cells. Viability/growth assays indicated that only the first two compounds at 70 &mu

0301 basic medicineQD0901Triple Negative Breast Neoplasmslcsh:Chemistry0302 clinical medicinebreast cancer cellmitochondrial transmembrane potentialCytotoxic T cellQDSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopyTriple-negative breast cancerreactive oxygen speciesCell DeathChemistryHistone deacetylase inhibitorQapoptosisGeneral MedicineCell cycle3. Good healthComputer Science Applications030220 oncology & carcinogenesisFemalecell cycleProgrammed cell deathautophagymedicine.drug_classCell SurvivalCatalysisArticleHistone DeacetylasesInorganic Chemistry03 medical and health sciencesCell Line TumormedicineBiomarkers TumorHumansViability assayPhysical and Theoretical ChemistryMolecular Biologyhistone deacetylase inhibitorcell viabilityOrganic ChemistryAutophagyapoptosiMatrix MetalloproteinasesHistone Deacetylase InhibitorsSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999ApoptosisCancer researchQD0146breast cancer cells
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Biological Effect of a Hybrid Anticancer Agent Based on Kinase and Histone Deacetylase Inhibitors on Triple-Negative (MDA-MB231) Breast Cancer Cells

2016

We examined the effects of the histone deacetylase inhibitor (HDACi) suberoylanilide\ud hydroxamic acid (SAHA) combined with the vascular endothelial growth factor receptor-1/2 inhibitor\ud (3Z)-5-hydroxy-3-(1H-pyrrol-2-ylmethylidene)-2,3-dihydro-1H-indol-2-one on MDA-MB-231 breast\ud cancer cells (triple-negative) in the form of both a cocktail of the separate compounds and a chemically\ud synthesized hybrid (N-hydroxy-N'-[(3Z)-2-oxo-3-(1H-pyrrol-2-ylmethylidene)-2,3-dihydro-1H-indol-\ud 5-yl]octanediamide). Comparative flow cytometric and Western blot analyses were performed on\ud cocktail- and hybrid-treated cells to evaluate cell cycle distribution, autophagy/apoptosis modulation,\ud an…

0301 basic medicineVascular Endothelial Growth Factor AIndolesCytotoxicityTriple Negative Breast Neoplasmsbreast cancer; MDA-MB231 cells; histone deacetylase inhibitor; vascular endothelial growth factor receptor-2 inhibitor; cytotoxicity; cell cycle; apoptosis; autophagy; mitochondrial metabolismHydroxamic AcidsCatalysi0302 clinical medicineBreast cancerTumor Cells CulturedCytotoxic T cellSettore BIO/06 - Anatomia Comparata E CitologiaSpectroscopyVorinostatVascular endothelial growth factor receptor-2 inhibitorApoptosis; Autophagy; Breast cancer; Cell cycle; Cytotoxicity; Histone deacetylase inhibitor; MDA-MB231 cells; Mitochondrial metabolism; Vascular endothelial growth factor receptor-2 inhibitor; Catalysis; Molecular Biology; Spectroscopy; Computer Science Applications1707 Computer Vision and Pattern Recognition; Physical and Theoretical Chemistry; Organic Chemistry; Inorganic ChemistryKinaseHistone deacetylase inhibitorapoptosisComputer Science Applications1707 Computer Vision and Pattern RecognitionGeneral MedicineCell cycleFlow CytometryComputer Science ApplicationsCell biologyMDA-MB231 cell030220 oncology & carcinogenesisFemaleQD0241Programmed cell deathmedicine.drug_classCell SurvivalBlotting WesternAntineoplastic AgentsBiologyCell cycleCatalysisArticleInorganic Chemistry03 medical and health sciencesmedicineAutophagyHumansPhysical and Theoretical ChemistryProtein Kinase InhibitorsMolecular BiologyQD0415Histone deacetylase inhibitorAutophagyOrganic ChemistryApoptosiHistone Deacetylase Inhibitors030104 developmental biologyApoptosisMitochondrial metabolismMDA-MB231 cellsHistone deacetylaseInternational Journal of Molecular Sciences; Volume 17; Issue 8; Pages: 1235
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Aberrantly Expressed Embryonic Protein NODAL Alters Breast Cancer Cell Susceptibility to γδ T Cell Cytotoxicity

2020

Gamma delta (γδ) T cells kill transformed cells, and increased circulating γδ T cells levels correlate with improved outcome in cancer patients; however, their function within the breast tumor microenvironment (TME) remains controversial. As tumors progress, they begin to express stem-cell associated proteins, concomitant with the emergence of therapy resistant metastatic disease. For example, invasive breast cancers often secrete the embryonic morphogen, NODAL. NODAL has been shown to promote angiogenesis, therapy resistance and metastasis in breast cancers. However, to date, little is known about how this secreted protein may interact with cells in the TME. Herein we explore how NODAL in …

0301 basic medicinelcsh:Immunologic diseases. AllergyNodal ProteinAngiogenesisT cellImmunologytumor evasionTriple Negative Breast NeoplasmsBiologyMetastasis03 medical and health sciences0302 clinical medicineTumor Microenvironmentmedicineinvasive ductal carcinomaHumansImmunology and Allergygamma delta T cellsIntraepithelial LymphocytesTriple-negative breast cancerOriginal ResearchAgedAged 80 and overT-cell receptorCancerReceptors Antigen T-Cell gamma-deltaMiddle Agedmedicine.diseasegammadelta030104 developmental biologymedicine.anatomical_structureCell culturetriple negative breast cancerMICACancer researchFemaleTumor EscapeNODALNODALlcsh:RC581-607030215 immunologyFrontiers in Immunology
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