Search results for "triple-negative"

showing 10 items of 70 documents

KDM5B and CBX5 as potential tumor-associated immunogenic antigens in triple-negative breast cancer (TNBC)

2021

Antigenbusiness.industryCancer researchMedicinebusinessTriple-negative breast cancerSenologie - Zeitschrift für Mammadiagnostik und -therapie
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miR-503-5p induces doxorubicin resistance in triple-negative breast cancer.

2021

1083 Background: Triple-negative breast cancer (TNBC) is an aggressive breast cancer (BC) subtype comprising approximately 15% of BC. Conventional cytotoxic chemotherapies continue to be the mainstay for treatment of this BC, which lacks targetable markers. In this context, microRNAs have been described to have an important role. The aim of this work was to elucidate the function of miR-503-5p in doxorubicin resistance in TNBC. Methods: miR-503-5p expression was evaluated in the TNBC cell line with acquired resistance to doxorubicin (MDA-MB-231R) and its parental cell line (MDA-MB-231), by qRT-PCR. Studies of gain/loss of function of miR-503-5p were carried out in MDA-MB-231 and MDA-MB-231…

Cancer ResearchBreast cancerOncologybusiness.industryCancer researchmedicineCytotoxic T cellDOXORUBICIN RESISTANCEmedicine.diseasebusinessTriple-negative breast cancerJournal of Clinical Oncology
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PDGFRβ and FGFR2 mediate endothelial cell differentiation capability of triple negative breast carcinoma cells

2014

Triple negative breast cancer (TNBC) is a very aggressive subgroup of breast carcinoma, still lacking specific markers for an effective targeted therapy and with a poorer prognosis compared to other breast cancer subtypes. In this study we investigated the possibility that TNBC cells contribute to the establishment of tumor vascular network by the process known as vasculogenic mimicry, through endothelial cell differentiation. Vascular-like functional properties of breast cancer cell lines were investigated in vitro by tube formation assay and in vivo by confocal microscopy, immunofluorescence or immunohistochemistry on frozen tumor sections. TNBCs express endothelial markers and acquire th…

Cancer ResearchPathologymedicine.medical_specialtyPDGFRmedicine.medical_treatmentTriple Negative Breast NeoplasmsMice SCIDBiologyEndothelial cell differentiationTargeted therapyReceptor Platelet-Derived Growth Factor betachemistry.chemical_compoundBreast cancerCell Line TumorGeneticsmedicineAnimalsHumansVasculogenic mimicryBreastRNA Small InterferingReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesTriple-negative breast cancerResearch ArticlesNeovascularization PathologicFGFREndothelial CellsCell DifferentiationGeneral MedicineTriple Negative Breast Neoplasmsmedicine.diseaseImmunohistochemistryVascular endothelial growth factorOncologychemistryVasculogenic mimicryCancer researchMolecular MedicineTNBC; Vasculogenic mimicry; PDGFR; FGFRTriple-Negative Breast CarcinomaFemaleRNA InterferenceTNBC
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Role of PD-L1 expression in triple-negative breast cancer stem cells.

2018

12081Background: Triple negative breast cancer (TNBC) is characterized by poor prognosis, lack of specific-targeted agents and is in need of new therapeutics. Immune checkpoint blockers have shown ...

Cancer ResearchPoor prognosisOncologybusiness.industryCancer researchMedicinePd l1 expressionStem cellbusinessTriple-negative breast cancerImmune checkpointJournal of Clinical Oncology
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Epigenetic changes and nuclear factor-κB activation, but not microRNA-224, downregulate Raf-1 kinase inhibitor protein in triple-negative breast canc…

2015

Raf-1 kinase inhibitor protein (RKIP) is a tumor suppressor and metastasis inhibitor, which enhances drug-induced apoptosis of cancer cells. Downregulation of RKIP may be significant in the biology of highly aggressive and drug-resistant tumors, for example triple-negative breast cancers (TNBCs). Potential causes for the low levels of RKIP expressed by SUM 159 TNBC cells were investigated in the present study. Bisulphite modification, methylation specific-polymerase chain reaction (PCR) and a TransAM NF-κB assay were performed and the results suggested that various mechanisms, including methylation of the gene promoter, histone deacetylation and nuclear factor-κB (NF-κB) activation, but not…

Cancer Researchmedicine.drug_classCell growthtriple-negative breast cancer Raf-1 kinase inhibitor protein epigenetic changes microRNA-224 nuclear factor-κBHistone deacetylase inhibitorArticlesCell cycleBiologyMolecular biologyDemethylating agentchemistry.chemical_compoundTrichostatin AOncologychemistryCancer cellmedicineCancer researchGrowth inhibitionTranscription factormedicine.drug
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Abstract 1855: Role of mTOR inhibition in triple-negative breast cancer

2016

Abstract BACKGROUND: Triple-negative breast cancers (TNBC) represent the 10-17% of all diagnosed breast cancers (BC) and are characterized by the absence of ER/PgR expression, HER2 amplification and often show a basal-like phenotype. TNBC are often diagnosed in patients with BRCA1 germline mutation and unfortunately treatment options are still limited. The mTOR (Mammalian Target Of Rapamycin) pathway seems to play an important role in BC pathogenesis and it is possible to target this pathway by inhibitors such as rapamycin. In human BC cross talk between ER/PgR receptors signaling and the mTOR pathway is believed to be responsible for resistance to hormone therapy probably due to a down reg…

Cancer Researchmedicine.medical_specialtyCell growthmedicine.drug_classCancerBiologymedicine.diseaseEndocrinologyOncologyHormone receptorEstrogenInternal medicinemedicineCancer researchViability assayReceptorPI3K/AKT/mTOR pathwayTriple-negative breast cancerCancer Research
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PO-344 miR-302b as adjuvant therapeutic tool to improve chemotherapy efficacy in human triple negative breast cancer

2018

Introduction MiRNAs are a class of non-coding regulatory RNAs playing key roles in different biological processes including cancer. Triple-negative breast cancer (TNBC) accounts for 15%–20% of all breast cancer cases, with the worst outcome of all subtypes. For TNBC, still lacking targeted therapies, the only therapeutic option is chemotherapy. MiRNAs can modulate chemotherapy response by affecting DNA repair, cell cycle progression, apoptosis and also tumour microenvironment. Macrophages constitute a major component of the immune microenvironment of cancer and pro-tumour M2 macrophages have been associated with response to chemotherapeutic treatments. Here, we investigated the potential of…

CisplatinCancer Researchbusiness.industryCancermedicine.diseaseBreast cancerOncologymicroRNACancer researchGene silencingMedicinebusinessITGA6Triple-negative breast cancermedicine.drugIRF4ESMO Open
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A loop involving NRF2, miR‐29b‐1‐5p and AKT, regulates cell fate of MDA‐MB‐231 triple‐negative breast cancer cells

2019

The present study shows that nuclear factor erythroid 2-related factor 2 (NRF2) and miR-29b-1-5p are two opposite forces which could regulate the fate of MDA-MB-231 cells, the most studied triple-negative breast cancer (TNBC) cell line. We show that NRF2 activation stimulates cell growth and markedly reduces reactive oxygen species (ROS) generation, whereas miR-29b-1-5p overexpression increases ROS generation and reduces cell proliferation. Moreover, NRF2 downregulates miR-29b-1-5p expression, whereas miR-29b-1-5p overexpression decreases p-AKT and p-NRF2. Furthermore, miR-29b-1-5p overexpression induces both inhibition of DNA N-methyltransferases (DNMT1, DNMT3A, and DNMT3B) expression and …

DNA (Cytosine-5-)-Methyltransferase 10301 basic medicineNF-E2-Related Factor 2PhysiologyClinical BiochemistryTriple Negative Breast NeoplasmsAKT DNMTs miR‐29b‐1‐5p NRF2 parthenolide tumor suppressor genesCell fate determinationenvironment and public healthDNA Methyltransferase 3A03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaCell Line TumorCyclin D2HumansParthenolideDNA (Cytosine-5-)-MethyltransferasesProtein kinase BTriple-negative breast cancerCell Proliferationchemistry.chemical_classificationReactive oxygen speciesCell growthTumor Suppressor ProteinsCell BiologyDNA Methylationrespiratory systemCell biologyGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologychemistryCell culture030220 oncology & carcinogenesisDNMT1FemaleReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSesquiterpenesSignal TransductionJournal of Cellular Physiology
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Can NF-κB Be Considered a Valid Drug Target in Neoplastic Diseases? Our Point of View

2020

Multidrug resistance (MDR), of the innate and acquired types, is one of major problems in treating tumor diseases with a good chance of success. In this review, we examine the key role of nuclear factor-kappa B (NF-κB) to induce MDR in three tumor models characterized precisely by innate or acquired MDR, in particular triple negative breast cancer (TNBC), hepatocellular carcinoma (HCC), and acute myeloid leukemia (AML). We also present different pharmacological approaches that our group have employed to reduce the expression/activation of this transcriptional factor and thus to restore chemo-sensitivity. Finally, we examine the latest scientific evidence found by other groups, the most sign…

Drug targetAntineoplastic AgentsReviewCatalysisNF-κBdrug targetlcsh:ChemistryInorganic Chemistrychemistry.chemical_compoundNeoplasmsMDRmedicineBiomarkers TumorcancerAnimalsHumansMolecular Targeted TherapyPhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyTriple-negative breast cancerbusiness.industryOrganic ChemistryNF-kappa BCancerMyeloid leukemiaNF-κBGeneral Medicinemedicine.diseaseComputer Science ApplicationsMultiple drug resistanceClinical trialCell Transformation Neoplasticlcsh:Biology (General)lcsh:QD1-999chemistryDrug Resistance NeoplasmHepatocellular carcinomaCancer researchSettore BIO/14 - FarmacologiaDisease SusceptibilitybusinessInternational Journal of Molecular Sciences
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Eribulin Mesylate for the Treatment of Metastatic Hormone-refractory and Triple-negative Breast Cancer: A Multi-institutional Real-world Report on Ef…

2021

Objective Eribulin mesylate (EM) is a fully synthetic macrocyclic ketone analogue of the marine natural product halichondrin. EM has been reported to be active in metastatic breast cancer. In this paper, we report efficacy and safety of data of EM in a retrospective, real-world series of patients with poor prognosis, hormone-refractory, or triple-negative metastatic breast cancer. Materials and methods The analysis was carried out at 4 interrelated oncology centers. EM was delivered at the dose of 1.4 mg/m2 in 100 mL of normal saline over 2 to 5 minutes on days 1 and 8 every 21 days. EM was continued until disease progression or unacceptable toxicity. Side effects were reported every cycle …

Eribulin MesylateOncologyAdultCancer Researchmedicine.medical_specialtyNeoplasms Hormone-Dependenteribulin mesylateSettore MED/06 - Oncologia Medicamedicine.medical_treatmentAntineoplastic AgentsTriple Negative Breast Neoplasmstriple negative03 medical and health sciences0302 clinical medicineStable DiseaseBreast cancerbreast cancerInternal medicineAntineoplastic Combined Chemotherapy Protocolshormonal refractorymedicineHumans030212 general & internal medicineFuransSalineTriple-negative breast cancerAgedRetrospective StudiesChemotherapybusiness.industryKetonesMiddle Agedmedicine.diseaseMetastatic breast cancerSettore MED/18 - Chirurgia GeneraleTreatment OutcomeOncology030220 oncology & carcinogenesisToxicityFemalebusiness
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