Search results for "Neoplastic"

showing 10 items of 2901 documents

Red wine extract disrupts Th17 lymphocyte differentiation in a colorectal cancer context

2020

International audience; Scope: Scope: It is well established that immune response and inflammation promote tumoral progression. Immune cells communicate through direct contact or through cytokine secretion, and it is the pro-inflammatory status that will tip the balance toward tumor progression or anti-tumor immunity. It is demonstrated here that a red wine extract (RWE) can decrease inflammation through its action on the inflammasome complex. This study determines whether an RWE could impact other key actors of inflammation, including T helper 17 (Th17) immune cells in particular. Methods and results: Methods and results: Using an RWE containing 4.16 g of polyphenols/liter of wine, it is s…

0301 basic medicineCancers polyphenolsred wine extractPlateforme de Transfert en Biologie du Cancer (PTBC) ChalminWineCancers Lipids[SHS]Humanities and Social Scienceslymphocyte T Red wine extractchemopreventionLymphocytesEmericMice Inbred BALB CDominiqueInterleukin-17Lymphocyte differentiationVin rougeCell DifferentiationFlavieSanté humaineLipidscolon cancerFemaleInterleukin 17medicine.symptomCancers LimagneColorectal NeoplasmsCancersCancers DelmasBiotechnologyOEnologieInflammationBiology03 medical and health sciencesLymphocytes Tumor-InfiltratingImmune systemCell Line TumorCancers CourtautmedicineAnimalsHumanslymphocytes Th17Cell ProliferationNutrition030109 nutrition & dieteticsFannyPlant ExtractsInterleukinsPolyphenolsHCT116 CellsAntineoplastic Agents PhytogenicXenograft Model Antitumor AssaysMice Inbred C57BL030104 developmental biologyTumor progressionSTAT proteinCancer researchTh17 CellsCytokine secretionVirginieInflammasome complex[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyFood Science
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Integrative analysis of key candidate genes and signaling pathways in autoimmune thyroid dysfunction related to anti-CTLA-4 therapy by bioinformatics

2020

Summary Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4), the first immune checkpoint to be targeted clinically, has provided an effective treatment option for various malignancies. However, the clinical advantages associated with CTLA-4 inhibitors can be offset by the potentially severe immune-related adverse events (IRAEs), including autoimmune thyroid dysfunction. To investigate the candidate genes and signaling pathways involving in autoimmune thyroid dysfunction related to anti-CTLA-4 therapy, integrated differentially expressed genes (DEGs) were extracted from the intersection of genes from Gene Expression Omnibus (GEO) datasets and text mining. The functional enrichment was perfo…

0301 basic medicineCandidate geneCD74Signaling pathway.FCGR2BDifferentially expressed geneBiologyBioinformaticsHyperthyroidismAutoimmune Diseases03 medical and health sciencesMice0302 clinical medicineHypothyroidismmedicineAnimalsHumansPharmacology (medical)CTLA-4 AntigenProtein Interaction MapsKEGGGeneImmune Checkpoint InhibitorsPharmacologyPreclinical StudiesSignaling pathwayCancerComputational Biologymedicine.diseaseImmune checkpointGene Expression Regulation Neoplastic030104 developmental biologyGene OntologyAutoimmune thyroid dysfunctionOncologyCTLA-4030220 oncology & carcinogenesisDifferentially expressed genesCTLA-4BiomarkersImmune checkpoint blockadeSignal Transduction
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Identification of loci of functional relevance to Barrett's esophagus and esophageal adenocarcinoma: Cross-referencing of expression quantitative tra…

2019

Esophageal adenocarcinoma (EA) and its precancerous condition Barrett's esophagus (BE) are multifactorial diseases with rising prevalence rates in Western populations. A recent meta-analysis of genome-wide association studies (GWAS) data identified 14 BE/EA risk loci located in non-coding genomic regions. Knowledge about the impact of non-coding variation on disease pathology is incomplete and needs further investigation. The aim of the present study was (i) to identify candidate genes of functional relevance to BE/EA at known risk loci and (ii) to find novel risk loci among the suggestively associated variants through the integration of expression quantitative trait loci (eQTL) and genetic…

0301 basic medicineCandidate geneEsophageal MucosaEsophageal NeoplasmsMedizinGene ExpressionGenome-wide association study0302 clinical medicineMathematical and Statistical TechniquesGeneticsMultidisciplinarySodium-Hydrogen Exchanger 3QStatisticsRGenomicsMetaanalysisGene Expression Regulation NeoplasticResearch Design030220 oncology & carcinogenesisPhysical SciencesMedicineResearch Articlemedicine.medical_specialtyScienceQuantitative Trait LociReplication StudiesContext (language use)BiologyAdenocarcinomaResearch and Analysis MethodsPolymorphism Single NucleotideMolecular Genetics03 medical and health sciencesBarrett EsophagusMolecular geneticsmedicineGeneticsGenome-Wide Association StudiesHumansGenetic Predisposition to DiseaseGene RegulationStatistical MethodsGeneMolecular BiologyGenetic associationProteinsBiology and Life SciencesComputational BiologyHuman Geneticsmedicine.diseaseGenome AnalysisRepressor Proteins030104 developmental biologyGenetic LociBarrett's esophagusExpression quantitative trait lociGenetics of DiseaseMathematicsGenome-Wide Association StudyPloS one
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c-Fos induces chondrogenic tumor formation in immortalized human mesenchymal progenitor cells

2018

Mesenchymal progenitor cells (MPCs) have been hypothesized as cells of origin for sarcomas, and c-Fos transcription factor has been showed to act as an oncogene in bone tumors. In this study, we show c-Fos is present in most sarcomas with chondral phenotype, while multiple other genes are related to c-Fos expression pattern. To further define the role of c-Fos in sarcomagenesis, we expressed it in primary human MPCs (hMPCs), immortalized hMPCs and transformed murine MPCs (mMPCs). In immortalized hMPCs, c-Fos expression generated morphological changes, reduced mobility capacity and impaired adipogenic- and osteogenic-differentiation potentials. Remarkably, immortalized hMPCs or mMPCs express…

0301 basic medicineCarcinogenesisCelllcsh:MedicineMice SCIDArticleCell Line03 medical and health sciencesMice0302 clinical medicineMice Inbred NODmedicineAnimalsHumansProgenitor celllcsh:ScienceRegulation of gene expressionMultidisciplinaryOncogeneChemistryMesenchymal stem celllcsh:RGenes fosMesenchymal Stem CellsSarcomaChondrogenesisPhenotypeCell biologyGene Expression Regulation Neoplastic030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticCell culture030220 oncology & carcinogenesislcsh:QProto-Oncogene Proteins c-fos
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Mcl-1 targeting could be an intriguing perspective to cure cancer

2018

The Bcl-2 family, which plays important roles in controlling cancer development, is divided into antiapoptotic and proapoptotic members. The change in the balance between these members governs the life and death of the cells. Mcl-1 is an antiapoptotic member of this family and its distribution in normal and cancerous tissues strongly differs from that of Bcl-2. In human cancers, where upregulation of antiapoptotic proteins is common, Mcl-1 expression is regulated independent of Bcl-2 and its inhibition promotes senescence, a major barrier to tumorigenesis. Cancer chemotherapy determines various kinds of responses, such as senescence and autophagy; however, the ideal response to chemotherapy…

0301 basic medicineCarcinogenesisPhysiologyClinical BiochemistryApoptosisBiologymedicine.disease_causecancer care03 medical and health sciencesMcl-1 in cancer0302 clinical medicineBcl-2 familyimmune system diseasesCancer stem cellhemic and lymphatic diseasesNeoplasmsmedicinecancer-stem-cellHumansPost-translational regulationMolecular Targeted TherapyneoplasmsCellular SenescenceOncogeneBcl-2 familyAutophagyCancerCell Biologymedicine.diseaseMcl-1 isoformGene Expression Regulation Neoplastic030104 developmental biologyUSP9XProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCancer researchtargeting Mcl-1Myeloid Cell Leukemia Sequence 1 ProteinCarcinogenesisProtein Processing Post-Translational
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MYC-driven epigenetic reprogramming favors the onset of tumorigenesis by inducing a stem cell-like state

2018

Breast cancer consists of highly heterogeneous tumors, whose cell of origin and driver oncogenes are difficult to be uniquely defined. Here we report that MYC acts as tumor reprogramming factor in mammary epithelial cells by inducing an alternative epigenetic program, which triggers loss of cell identity and activation of oncogenic pathways. Overexpression of MYC induces transcriptional repression of lineage-specifying transcription factors, causing decommissioning of luminal-specific enhancers. MYC-driven dedifferentiation supports the onset of a stem cell-like state by inducing the activation of de novo enhancers, which drive the transcriptional activation of oncogenic pathways. Furthermo…

0301 basic medicineCarcinogenesisScienceGeneral Physics and AstronomyBreast NeoplasmsMice SCIDTumor initiationBiologyBreast cancer MYC Tumorigenesismedicine.disease_causeArticleGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticProto-Oncogene Proteins c-mycMice03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpigeneticslcsh:ScienceEnhancerTranscription factorRegulation of gene expressionMultidisciplinaryQGeneral ChemistryCellular ReprogrammingCell biologyGene Expression Regulation NeoplasticEnhancer Elements Genetic030104 developmental biologyNeoplastic Stem CellsFemalelcsh:QStem cellCarcinogenesisReprogramming
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Induction of cancer cell stemness by depletion of macrohistone H2A1 in hepatocellular carcinoma.

2017

Hepatocellular carcinomas (HCC) contain a subpopulation of cancer stem cells (CSCs), which exhibit stem cell–like features and are responsible for tumor relapse, metastasis, and chemoresistance. The development of effective treatments for HCC will depend on a molecular-level understanding of the specific pathways driving CSC emergence and stemness. MacroH2A1 is a variant of the histone H2A and an epigenetic regulator of stem-cell function, where it promotes differentiation and, conversely, acts as a barrier to somatic-cell reprogramming. Here, we focused on the role played by the histone variant macroH2A1 as a potential epigenetic factor promoting CSC differentiation. In human HCC section…

0301 basic medicineCarcinoma HepatocellularBiologyMetastasisHistones03 medical and health sciencesCancer stem cellHistone H2AmedicineHumansEpigeneticsPhosphorylationCell ProliferationHepatologyCell growthGene Expression ProfilingLiver NeoplasmsTranscription Factor RelAHep G2 Cellsmedicine.disease030104 developmental biologyHistoneCancer cellCancer researchbiology.proteinNeoplastic Stem CellsReprogrammingHepatology (Baltimore, Md.)
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Study of novel anticancer 4-thiazolidinone derivatives

2016

Abstract 4-Thiazolidinones are a known class of prospective drug-like molecules, especially in the design of new anticancer agents. Two of the most prominent subtypes of these compounds are 5-ene-2-amino(amino)-4-thiazolidinones and thiopyrano[2,3-d]thiazoles. The latter are considered to be cyclic mimetics of biologically active 5-ene-4-thiazolidinones with similar pharmacological profiles. Therefore, the aim of this study was to evaluate the impact of 4-thiazolidinone-based compounds on cytotoxicity, the apoptotic process, and metabolism in the human squamous carcinoma (SCC-15) cell line. The SCC-15 cells were cultured in phenol red-free DMEM/F12 medium supplemented with 10% FBS, hydrocor…

0301 basic medicineCell SurvivalCytotoxicityAntineoplastic AgentsApoptosisToxicology01 natural sciencesAnticancer activity03 medical and health sciencesCell Line TumormedicineHumansViability assayCytotoxicitychemistry.chemical_classificationReactive oxygen speciesL-Lactate Dehydrogenase010405 organic chemistryChemistryCaspase 3ThiazolothiopyranesBiological activityGeneral MedicineMetabolism0104 chemical sciencesSquamous carcinomaThiazoles030104 developmental biologyMechanism of actionBiochemistryMicroscopy FluorescenceCell cultureThiazolidinonemedicine.symptomReactive Oxygen SpeciesChemico-Biological Interactions
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Indomethacin Disrupts Autophagic Flux by Inducing Lysosomal Dysfunction in Gastric Cancer Cells and Increases Their Sensitivity to Cytotoxic Drugs

2018

AbstractNSAIDs inhibit tumorigenesis in gastrointestinal tissues and have been proposed as coadjuvant agents to chemotherapy. The ability of cancer epithelial cells to adapt to the tumour environment and to resist cytotoxic agents seems to depend on rescue mechanisms such as autophagy. In the present study we aimed to determine whether an NSAID with sensitizing properties such as indomethacin modulates autophagy in gastric cancer epithelial cells. We observed that indomethacin causes lysosomal dysfunction in AGS cells and promotes the accumulation of autophagy substrates without altering mTOR activity. Indomethacin enhanced the inhibitory effects of the lysosomotropic agent chloroquine on l…

0301 basic medicineCell SurvivalIndomethacinlcsh:MedicineAntineoplastic AgentsAdenocarcinomaArticle03 medical and health sciencesStomach NeoplasmsCell Line TumorLysosomeAutophagymedicineHumansCytotoxic T cellViability assayCytotoxicitylcsh:SciencePI3K/AKT/mTOR pathwayAnalysis of VarianceMultidisciplinaryCell DeathChemistryAnti-Inflammatory Agents Non-SteroidalAutophagylcsh:RChloroquineDrug SynergismOxaliplatin030104 developmental biologymedicine.anatomical_structureDrug Resistance NeoplasmApoptosisCancer cellCancer researchlcsh:QMacrolidesLysosomesScientific Reports
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Chemopreventive Property of Sencha Tea Extracts towards Sensitive and Multidrug-Resistant Leukemia and Multiple Myeloma Cells

2020

The popular beverage green tea possesses chemopreventive activity against various types of tumors. However, the effects of its chemopreventive effect on hematological malignancies have not been defined. In the present study, we evaluated antitumor efficacies of a specific green tea, sencha tea, on sensitive and multidrug-resistant leukemia and a panel of nine multiple myelomas (MM) cell lines. We found that sencha extracts induced cytotoxicity in leukemic cells and MM cells to different extents, yet its effect on normal cells was limited. Furthermore, sencha extracts caused G2/M and G0/G1 phase arrest during cell cycle progression in CCRF/CEM and KMS-12-BM cells, respectively. Specifically,…

0301 basic medicineCell Survivalnatural productsgreen tealcsh:QR1-502Cell morphologychemotherapyBiochemistryArticlelcsh:Microbiologyfunctional foodPhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCell Line TumorHumansCytotoxicityMolecular BiologyProtein kinase BcatechinsPI3K/AKT/mTOR pathwaypolyphenolsCell ProliferationMembrane Potential MitochondrialLeukemiadrug resistanceTeaPlant ExtractsChemistryCell growthCell CycleNF-kappa BCell cycleAntineoplastic Agents PhytogenicDrug Resistance MultipleGene Expression Regulation Neoplastic030104 developmental biologyDrug Resistance NeoplasmApoptosisCell culture030220 oncology & carcinogenesisflavonoidsCancer researchmicroarray analysisMultiple MyelomaReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSignal TransductionBiomolecules
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