Search results for "TRIP"

showing 10 items of 2134 documents

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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Voyage d’étude autour de la pratique officinale suisse

2017

International audience; Twenty-seven students from the Dijon health sciences training and research unit in the 6th year of their course and specialising in the community setting had the opportunity to undertake a study trip to meet Swiss colleagues. They discovered an innovative vision of pharmacy practice. The results of a feedback questionnaire highlighted the benefit of this pedagogical approach for the construction of the professional identity of these future community pharmacists.; L’intégration d’un voyage d’étude dans le cursus pharmaceutique parcours “officine” a permis à 27 étudiants de 6e année de l’unité de formation et de recherche des sciences de santé de Dijon d’aller à la ren…

0301 basic medicinePharmacologymedia_common.quotation_subject030106 microbiologyArt historyArtvaccinationstudy trip03 medical and health sciences[ SDV.SP ] Life Sciences [q-bio]/Pharmaceutical sciencesCommunity settingPharmacology (medical)Cercles de qualitépolypharmacy interviewentretien de polymédicationSuisseHumanitiesvoyage d’étudeSwitzerlandnetCare®media_common
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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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Metabolic Imaging in Multicellular Spheroids of Oncogene-transfected Fibroblasts

2000

Four rat embryo fibroblast (REF) cell lines with defined oncogenic transformation were used to study the relationship between tumorigenic conversion, metabolism, and development of cell death in a 3D spheroid system. Rat1 (spontaneously immortalized) and M1 ( myc-transfected) fibroblasts represent early nontumorigenic transformation stages, whereas Rat1-T1 (T24Ha- ras-transfected Rat1) and MR1 ( myc/T24Ha- ras-co-transfected REF) cells express a highly tumorigenic phenotype. Localized ATP, glucose, and lactate concentrations in spheroid median sections were determined by imaging bioluminescence. ATP concentrations were low in the nonproliferating Rat1 aggregates despite sufficient oxygen an…

0301 basic medicineProgrammed cell deathHistologyGenes mycApoptosisBiology030218 nuclear medicine & medical imaging03 medical and health sciencesAdenosine Triphosphate0302 clinical medicineSpheroids CellularImage Processing Computer-AssistedmedicineAnimalsFrozen SectionsLactic AcidFibroblastCell Line Transformed030102 biochemistry & molecular biologyOncogeneSpheroidEmbryoTransfectionMetabolismMolecular biologyRats Inbred F344RatsCell biologyGenes rasGlucosemedicine.anatomical_structureCell cultureLuminescent Measurementsembryonic structuresAnatomyCell DivisionJournal of Histochemistry & Cytochemistry
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SERCA and P-glycoprotein inhibition and ATP depletion are necessary for celastrol-induced autophagic cell death and collateral sensitivity in multidr…

2019

Multidrug resistance (MDR) represents an obstacle in anti-cancer therapy. MDR is caused by multiple mechanisms, involving ATP-binding cassette (ABC) transporters such as P-glycoprotein (P-gp), which reduces intracellular drug levels to sub-therapeutic concentrations. Therefore, sensitizing agents retaining effectiveness against apoptosis- or drug-resistant cancers are desired for the treatment of MDR cancers. The sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA) pump is an emerging target to overcome MDR, because of its continuous expression and because the calcium transport function is crucial to the survival of tumor cells. Previous studies showed that SERCA inhibitors exhibit anti-c…

0301 basic medicineProgrammed cell deathSERCALung NeoplasmsCell SurvivalAntineoplastic AgentsAutophagy-Related Protein 7Sarcoplasmic Reticulum Calcium-Transporting ATPases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAdenosine TriphosphateCell Line TumorAutophagyAnimalsHumansATP Binding Cassette Transporter Subfamily B Member 1P-glycoproteinPharmacologybiologyDose-Response Relationship DrugChemistryAutophagyXenograft Model Antitumor AssaysDrug Resistance MultipleTriterpenesMultiple drug resistanceMice Inbred C57BL030104 developmental biologyCelastrolApoptosisDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchHepatocytesPentacyclic TriterpenesPharmacological research
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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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Down-Regulation of CD62L Shedding in T Cells by CD39+ Regulatory T Cells Leads to Defective Sensitization in Contact Hypersensitivity Reactions

2016

Injection of regulatory T cells (Tregs) followed by sensitization with 2,4,6-trinitrochlorobenzene induced a transient increase in size and cellularity of skin-draining lymph nodes (LNs) in mice. This led us to hypothesize that Tregs may affect the trafficking of T cells from and to peripheral LNs. Two to three hours after sensitization, we found fewer CD8+ T cells expressing CD62L in LNs compared with untreated controls. Injection of wild-type Tregs prevented this down-regulation of CD62L. In contrast, Tregs devoid of the adenosine triphosphate (ATP)-degrading ecto-enzyme CD39 were unable to do so. As for the mechanism of CD62L regulation, we found that ATP, which is released in skin upon …

0301 basic medicineRegulatory T cellBlotting WesternMedizinDown-Regulationchemical and pharmacologic phenomenaDermatologyT-Lymphocytes RegulatoryBiochemistryArticleMice03 medical and health scienceschemistry.chemical_compoundAdenosine Triphosphate0302 clinical medicineImmune systemDownregulation and upregulationAntigenAntigens CDReference ValuesmedicineAnimalsImmunologic FactorsL-SelectinMolecular BiologyCells CulturedSensitizationintegumentary systemChemistryApyrasehemic and immune systemsCell BiologyDendritic cellFlow CytometryCell biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureEpidermal CellsDermatitis Allergic ContactImmunologyImmunizationLymph NodesEpidermisAdenosine triphosphateCD8030215 immunologyJournal of Investigative Dermatology
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