Search results for "triple negative"

showing 10 items of 68 documents

TEM8/ANTXR1-Specific CAR T Cells as a Targeted Therapy for Triple-Negative Breast Cancer.

2018

Abstract Triple-negative breast cancer (TNBC) is an aggressive disease lacking targeted therapy. In this study, we developed a CAR T cell–based immunotherapeutic strategy to target TEM8, a marker initially defined on endothelial cells in colon tumors that was discovered recently to be upregulated in TNBC. CAR T cells were developed that upon specific recognition of TEM8 secreted immunostimulatory cytokines and killed tumor endothelial cells as well as TEM8-positive TNBC cells. Notably, the TEM8 CAR T cells targeted breast cancer stem–like cells, offsetting the formation of mammospheres relative to nontransduced T cells. Adoptive transfer of TEM8 CAR T cells induced regression of established…

0301 basic medicineOncologyCancer ResearchAdoptive cell transfermedicine.medical_specialtyLung Neoplasmsmedicine.medical_treatmentT-LymphocytesCell- and Tissue-Based TherapyReceptors Antigen T-CellApoptosisReceptors Cell SurfaceTriple Negative Breast NeoplasmsTargeted therapy03 medical and health sciencesMice0302 clinical medicineBreast cancerAntigenInternal medicineBiomarkers TumorTumor Cells CulturedMedicineAnimalsHumansTriple-negative breast cancerCell Proliferationbusiness.industryMicrofilament ProteinsCancerImmunotherapyTriple Negative Breast Neoplasmsmedicine.diseasePrognosisXenograft Model Antitumor AssaysNeoplasm ProteinsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisCase-Control StudiesFemaleImmunotherapybusinessFollow-Up StudiesCancer research
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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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Analysis of miRNA expression profile induced by short term starvation in breast cancer cells treated with doxorubicin

2017

// Sergio Rizzo 1, * , Antonina Cangemi 1, * , Antonio Galvano 1, * , Daniele Fanale 1 , Silvio Buscemi 2 , Marcello Ciaccio 3 , Antonio Russo 1 , Sergio Castorina 4, 5, # and Viviana Bazan 1, # 1 Department of Surgical, Oncological and Oral Sciences, Section of Medical Oncology, University of Palermo, Palermo, Italy 2 Department of Internal and Specialistic Medicine (DIBIMIS), Laboratory of Clinical Nutrition, University of Palermo, Palermo, Italy 3 Section of Clinical Biochemistry and Clinical Molecular Medicine, Department of Biopathology and Medical Biotechnology, University of Palermo, U.O.C. Laboratory Medicine, Policlinico University Hospital, Palermo, Italy 4 Fondazione Mediterranea…

0301 basic medicineOncologymedicine.medical_specialtychemotherapy responseClinical nutritiondoxorubicin03 medical and health sciences0302 clinical medicineInternal medicinemicroRNAmedicineDoxorubicinTriple-negative breast cancershort term starvationtriple negative breast cancer cellsbusiness.industryCancerMicroRNAmedicine.diseaseMolecular medicinemicroRNAstriple negative breast cancer cell030104 developmental biologyOncologyTumor progression030220 oncology & carcinogenesisImmunologyBreast cancer cellsbusinessChemotherapy response; Doxorubicin; MicroRNAs; Short term starvation; triple negative breast cancer cells; Oncologymedicine.drugResearch PaperOncotarget
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BRCA1/2 pathogenic variants in triple-negative versus luminal-like breast cancers: genotype–phenotype correlation in a cohort of 531 patients

2020

Background: Several available data suggest the association between specific molecular subtypes and BRCA1/2 mutational status. Previous investigations showed the association between BRCA1/2 pathogenic variants (PVs) in specific genomic regions and phenotypic variations of cancer relative risk, while the role of PV type and location in determining the breast cancer (BC) phenotypic features remains still unclear. The aim of this research was to describe the germline BRCA1/2 PVs in triple-negative breast cancer (TNBC) versus luminal-like BC and their potential leverage on BC phenotype. Patients & methods: We retrospectively collected and analyzed all clinical information of 531 patients wit…

0301 basic medicineOncologymedicine.medical_specialtygenetic testingGenotype phenotypeCorrelation03 medical and health sciencesbreast cancer0302 clinical medicineBreast cancerInternal medicinemedicineMutational statusskin and connective tissue diseasesTriple negativeTriple-negative breast cancerOriginal ResearchGenetic testinggermline pathogenic variantmedicine.diagnostic_testbusiness.industryBRCA1medicine.diseaseBRCA2030104 developmental biologyluminal-like breast cancerOncology030220 oncology & carcinogenesisCohorttriple-negative breast cancergermline pathogenic variantsbusinessTherapeutic Advances in Medical Oncology
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Triple negative breast cancer subtypes and pathologic complete response rate to neoadjuvant chemotherapy.

2018

Triple negative breast cancer (TNBC) is a heterogeneous disease with distinct molecular subtypes that differentially respond to chemotherapy and targeted agents. The purpose of this study is to explore the clinical relevance of Lehmann TNBC subtypes by identifying any differences in response to neoadjuvant chemotherapy among them. We determined Lehmann subtypes by gene expression profiling in paraffined pre-treatment tumor biopsies from 125 TNBC patients treated with neoadjuvant anthracyclines and/or taxanes +/- carboplatin. We explored the clinicopathological characteristics of Lehmann subtypes and their association with the pathologic complete response (pCR) to different treatments. The g…

0301 basic medicineOncologymedicine.medical_specialtysubtypingmedicine.medical_treatmentCarboplatin03 medical and health scienceschemistry.chemical_compoundpathologic complete responseSubtyping0302 clinical medicineInternal medicinePathologic complete responsemedicineClinical significanceTriple negative breast cancerneoadjuvant therapyReceptorTriple-negative breast cancerNeoadjuvant therapyChemotherapybusiness.industryPhenotypeCarboplatinGene expression profiling030104 developmental biologyOncologychemistry030220 oncology & carcinogenesistriple negative breast cancercarboplatinNeoadjuvant therapybusinessResearch Paper
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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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