Search results for " Tumor necrosis factor"

showing 10 items of 110 documents

A 2-year comparative open label randomized study of efficacy and safety of etanercept and infliximab in patients with ankylosing spondylitis

2010

The signs and symptoms of ankylosing spondylitis (AS) respond inadequately to nonsteroidal antiinflammatory drugs, corticosteroids, and disease modifying antirheumatic drugs in quite a number of patients. Tumor necrosis factor inhibitors have demonstrated to be of value in reducing AS disease activity in clinical trials. The efficacy and safety of both etanercept and infliximab in patients with ankylosing spondylitis were compared in a 2-year open label randomised study. Our results are consistent with a significant more rapid clinical improvement in the infliximab treated group. Treatment with both etanercept and infliximab at the end of the study was effective, safe, and well tolerated. ©…

MaleAntibodieReceptors Tumor Necrosis FactorEtanerceptlaw.inventionEtanerceptRandomized controlled triallawimmune system diseasesOutcome Assessment Health CareMonoclonalImmunology and Allergyskin and connective tissue diseasesAntirheumatic AgentAntibodies MonoclonalAntirheumatic AgentsTreatment OutcomeAntirheumatic AgentsFemalemedicine.drugHumanReceptormusculoskeletal diseasesAdultAnkylosingmedicine.medical_specialtyImmunologyDrug Administration ScheduleOutcome Assessment (Health Care)RheumatologyInternal medicinemedicineHumansSpondylitis AnkylosingSpondylitisSpondylitiAnkylosing spondylitisbusiness.industryTumor Necrosis Factor-alphaAnkylosing spondylitis; Etanercept; Infliximab; Adult; Antibodies Monoclonal; Antirheumatic Agents; Drug Administration Schedule; Etanercept; Female; Humans; Immunoglobulin G; Infliximab; Male; Outcome Assessment (Health Care); Receptors Tumor Necrosis Factor; Spondylitis Ankylosing; Treatment Outcome; Tumor Necrosis Factor-alpha; Rheumatology; Immunology; Immunology and Allergymedicine.diseaseInfliximabRheumatologyInfliximabClinical trialAnkylosing spondylitistomatognathic diseasesImmunoglobulin GPhysical therapybusinessTumor Necrosis Factor
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TNF-alpha gene promoter polymorphisms and risk of venous thromboembolism in gastrointestinal cancer patients undergoing chemotherapy

2013

Abstract Background TNF-α has been proposed as a predictive factor for venous thromboembolism (VTE). Genetic polymorphisms could regulate TNF-α production. However, the relationship between TNFA gene variants and VTE is not clarified. This study aims to investigate the predictive role of five different TNFA gene promoter SNPs, or their haplotype combination(s), for a first VTE episode in gastrointestinal cancer out-patients treated with chemotherapy. Patients and methods Serum TNF-α levels and TNFA -863C/A, -857C/T, -376G/A, -308G/A and -238G/A gene promoter polymorphisms were retrospectively evaluated in 314 subjects, including 157 controls and 157 Caucasian patients with histologically di…

MaleAntimetabolitesSettore MED/06 - Oncologia Medicamedicine.medical_treatmentchemotherapyGastroenterologysingle nucleotide polymorphismschemotherapy; gastrointestinal cancer; single nucleotide polymorphisms; tumour necrosis factor-α; venous thromboembolismsingle nucleotide polymorphismPhytogenic80 and overtumour necrosis factor-αPromoter Regions GeneticGastrointestinal NeoplasmsAged 80 and overHazard ratioSingle NucleotideHematologyMiddle AgedAntineoplasticChemotherapy regimenOncologyFemaleFluorouracilmedicine.drugAdultRiskAntimetabolites Antineoplasticmedicine.medical_specialtygastrointestinal cancervenous thromboembolismAntineoplastic AgentsSingle-nucleotide polymorphismIrinotecanPolymorphism Single NucleotidePromoter RegionsGeneticInternal medicinemedicineHumansGenetic Predisposition to DiseaseGastrointestinal cancercardiovascular diseasesPolymorphismRetrospective StudiesAgedChemotherapyTumor Necrosis Factor-alphabusiness.industryHaplotypeOdds ratiomedicine.diseaseAntineoplastic Agents PhytogenicIrinotecanHaplotypesCase-Control StudiesImmunologyCamptothecinHuman medicinePolymorphism Single Nucleotide; Antimetabolites Antineoplastic; single nucleotide polymorphisms; Humans; Retrospective Studies; Aged; Promoter Regions Genetic; Haplotypes; Aged 80 and over; Adult; gastrointestinal cancer; Genetic Predisposition to Disease; Male; tumour necrosis factor-α; Tumor Necrosis Factor-alpha; Venous Thromboembolism; Camptothecin; chemotherapy; Risk; Fluorouracil; Case-Control Studies; Gastrointestinal Neoplasms; Middle Aged; venous thromboembolism; Antineoplastic Agents Phytogenic; Femalebusiness
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Inhibition of DNA methylation sensitizes glioblastoma for tumor necrosis factor-related apoptosis-inducing ligand-mediated destruction.

2005

AbstractLife expectancy of patients affected by glioblastoma multiforme is extremely low. The therapeutic use of tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) has been proposed to treat this disease based on its ability to kill glioma cell lines in vitro and in vivo. Here, we show that, differently from glioma cell lines, glioblastoma multiforme tumors were resistant to TRAIL stimulation because they expressed low levels of caspase-8 and high levels of the death receptor inhibitor PED/PEA-15. Inhibition of methyltransferases by decitabine resulted in considerable up-regulation of TRAIL receptor-1 and caspase-8, down-regulation of PED/PEA-15, inhibition of cell growth, and …

MaleCancer ResearchMethyltransferaseNudeDrug ResistanceApoptosisReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandCASPASE-8 EXPRESSIONMiceNude mouseSIGNALING COMPLEXReceptorsAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedDNA Modification MethylasesIN-VIVOHeterologousCaspase 8CulturedMembrane GlycoproteinsbiologyIntracellular Signaling Peptides and ProteinsMiddle AgedTumor CellsGene Expression Regulation NeoplasticMALIGNANT GLIOMA-CELLSOncologyCaspasesDNA methylationAzacitidineTumor necrosis factor alphaFemalemedicine.drugSignal TransductionAdultBRAIN-TUMORSTransplantation HeterologousCHEMOTHERAPEUTIC-AGENTSDecitabineMice NudeDecitabineDRUG-INDUCED APOPTOSISDEATH RECEPTOR5-AZA-2'-DEOXYCYTIDINEIn vivoSettore MED/04 - PATOLOGIA GENERALEmedicineAnimalsHumansneoplasmsAgedTransplantationNeoplasticCell growthTumor Necrosis Factor-alphaHistocompatibility Antigens Class IDNA Methylationbiology.organism_classificationPhosphoproteinsReceptors TNF-Related Apoptosis-Inducing LigandGene Expression RegulationApoptosisDrug Resistance NeoplasmImmunologyCancer researchNeoplasmAdult; Aged; Animals; Antineoplastic Combined Chemotherapy Protocols; Apoptosis; Apoptosis Regulatory Proteins; Azacitidine; Caspase 8; Caspases; DNA Modification Methylases; Drug Resistance Neoplasm; Female; Glioblastoma; Histocompatibility Antigens Class I; Humans; Intracellular Signaling Peptides and Proteins; Male; Membrane Glycoproteins; Mice; Mice Nude; Middle Aged; Phosphoproteins; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor; Signal Transduction; TNF-Related Apoptosis-Inducing Ligand; Transplantation Heterologous; Tumor Cells Cultured; Tumor Necrosis Factor-alpha; DNA Methylation; Gene Expression Regulation Neoplastic; Cancer Research; OncologyTumor Necrosis FactorTRAIL-INDUCED APOPTOSISApoptosis Regulatory ProteinsGlioblastomaCancer research
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Oncogene-driven intrinsic inflammation induces leukocyte production of tumor necrosis factor that critically contributes to mammary carcinogenesis.

2010

Abstract Oncogene activation promotes an intrinsic inflammatory pathway that is crucial for cancer development. Here, we have investigated the actual effect of the inflammatory cytokine tumor necrosis factor (TNF) on the natural history of spontaneous mammary cancer in the HER2/neuT (NeuT) transgenic mouse model. Bone marrow transplantation from TNF knockout mice into NeuT recipients significantly impaired tumor growth, indicating that the source of TNF fostering tumor development was of bone marrow origin. We show that the absence of leukocyte-derived TNF disarranged the tumor vasculature, which lacked pericyte coverage and structural integrity, leading to diffuse vascular hemorrhage and s…

MaleCancer ResearchStromal cellmedicine.medical_treatmentInflammationmedicine.disease_causeAntibodiesArticleMicemedicineLeukocytesAnimalsHumansReceptors Tumor Necrosis Factor Type IItumor necrosis factor mammary carcinogenesis.Crosses GeneticBone Marrow TransplantationInflammationMice KnockoutOncogenebusiness.industryTumor Necrosis Factor-alphaCancerMammary Neoplasms ExperimentalOncogenesmedicine.diseaseImmunohistochemistryMice Inbred C57BLPlatelet Endothelial Cell Adhesion Molecule-1medicine.anatomical_structureCytokineOncologyReceptors Tumor Necrosis Factor Type IImmunologyTumor necrosis factor alphaFemaleBone marrowmedicine.symptomCarcinogenesisbusinessCancer research
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Neuroprotective effect of Fn14 deficiency is associated with induction of the granulocyte-colony stimulating factor (G-CSF) pathway in experimental s…

2010

Using a transgenic mouse model of ischemic stroke we checked for a possible interaction of antiphospholipid antibodies (aPL) which often cause thromboses as well as central nervous system (CNS) involvement under non-thrombotic conditions and the TWEAK/Fn14 pathway known to be adversely involved in inflammatory and ischemic brain disease. After 7 days, infarct volumes were reduced in Fn14 deficient mice and were further decreased by aPL treatment. This was associated with strongest increase of the endogenous neuroprotective G-CSF/G-CSF receptor system. This unexpected beneficial action of aPL is an example for a non-thrombogenic action and the double-edged nature of aPL.

MaleGenetically modified mouseImmunologyMice TransgenicBiologyNeuroprotectionReceptors Tumor Necrosis FactorBrain IschemiaMiceRandom AllocationTissue factorimmune system diseasesAntiphospholipid syndromeGranulocyte Colony-Stimulating FactormedicineAnimalsHumansImmunology and AllergyneoplasmsStrokeLupus anticoagulantmedicine.diseaseMice Inbred C57BLDisease Models AnimalNeurologyTWEAK ReceptorReceptors Granulocyte Colony-Stimulating FactorImmunologyAntibodies AntiphospholipidTumor necrosis factor alphaNeurology (clinical)Inflammation MediatorsGranulocyte colony-stimulating factor receptorSignal TransductionJournal of Neuroimmunology
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Extended analysis of a genome-wide association study in primary sclerosing cholangitis detects multiple novel risk loci

2012

Background & Aims: A limited number of genetic risk factors have been reported in primary sclerosing cholangitis (PSC). To discover further genetic susceptibility factors for PSC, we followed up on,a second tier of single nucleotide polymorphisms (SNPs) from a genome-wide association study (GWAS). Methods: We analyzed 45 SNPs in 1221 PSC cases and 3508 controls. The association results from the replication analysis and the original GWAS (715 PSC cases and 2962 controls) were combined in a meta-analysis comprising 1936 PSC cases and 6470 controls. We performed an analysis of bile microbial community composition in 39 PSC patients by 16S rRNA sequencing. Results: Seventeen SNPs representing 1…

MaleLinkage disequilibriumendocrine system diseasesGenome-wide association studyPrimary biliary cirrhosisGenotypeBLOOD-GROUPBileChildPOPULATIONAged 80 and overGeneticseducation.field_of_studyPrimary sclerosing cholangitisdigestive oral and skin physiologyMiddle AgedFucosyltransferasesChild PreschoolDISEASESFemaleNeprilysinReceptors Tumor Necrosis Factor Member 14B-LYMPHOCYTEAdultRiskGenome-wide association studyAdolescentGenotypeSUSCEPTIBILITY LOCIFUT2Cholangitis SclerosingPopulationT-LYMPHOCYTE ATTENUATORSingle-nucleotide polymorphismBiologyPolymorphism Single Nucleotidedigestive systemArticlePrimary sclerosing cholangitisGenetic predispositionmedicineImmunogeneticsHumansGenetic Predisposition to DiseaseeducationMETAANALYSISAgedNON-SECRETOR STATUSHepatologymedicine.diseaseGENEdigestive system diseasesSingle nucleotide polymorphismGenetic LociImmunology
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Inflammation and Aortic Pulse Wave Velocity: A Multicenter Longitudinal Study in Patients With Inflammatory Bowel Disease

2019

Background Inflammatory bowel disease ( IBD ) is characterized by a low prevalence of traditional risk factors, an increased aortic pulse‐wave velocity ( aPWV ), and an excess of cardiovascular events. We have previously hypothesized that the cardiovascular risk excess reported in these patients could be explained by chronic inflammation. Here, we tested the hypothesis that chronic inflammation is responsible for the increased aPWV previously reported in IBD patients and that anti‐TNFa (anti‐tumor necrosis factor‐alpha) therapy reduce aPWV in these patients. Methods and Results This was a multicenter longitudinal study. We enrolled 334 patients: 82 patients with ulcerative colitis, 85 pati…

MaleLongitudinal studyTime FactorsSettore MED/09 - Medicina InternaAorta ThoracicBlood Pressure030204 cardiovascular system & hematologyGastroenterologyInflammatory bowel diseaseulcerative coliti0302 clinical medicineRisk Factorsarterial stiffneVascular DiseaseTumor necrosis factor-alphaEndoscopy Digestive SystemProspective Studies030212 general & internal medicinePulse wave velocityOriginal ResearchCrohn diseasetumor necrosis factor‐alphaUlcerative colitisC-Reactive Proteinarterial stiffnessCardiovascular DiseasesHypertensionFemaleTumor necrosis factor alphamedicine.symptomCardiology and Cardiovascular MedicineAdultmedicine.medical_specialtypulse wave velocityInflammationPulse Wave Analysis03 medical and health sciencesVascular StiffnessInternal medicinemedicineHumansIn patientulcerative colitisbusiness.industryInflammatory Bowel Diseasesmedicine.diseasearterial stiffness; Crohn disease; inflammation; pulse wave velocity; tumor necrosis factor‐alpha; ulcerative colitis; Cardiology and Cardiovascular MedicineinflammationArterial stiffnessbusinessBiomarkersFollow-Up Studies
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Dietary polyunsaturated fatty acids reduce retinal stress induced by an elevation of intraocular pressure in rats.

2011

International audience; N-6 and n-3 polyunsaturated fatty acids (PUFAs) have been shown to prevent tissue release of inflammatory molecules. We have shown that a combination of n-6 and n-3 PUFAs is more efficient than single supplementations on the long-term consequences of intraocular pressure elevation. We hypothesized that such an association is also more effective during early retinal stress by modifying retinal proinflammatory prostaglandin and cytokine productions. Rats were supplemented for 3 months with n-6 PUFAs, n-3 PUFAs, or both n-6 and n-3 PUFAs. After 3 months, a surgical elevation of intraocular pressure was induced. Retinal morphometry and glial cell activation were evaluate…

MaleMESH : RNA MessengerMESH: Eicosapentaenoic AcidEndocrinology Diabetes and Metabolismmedicine.medical_treatment[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionInterleukin-1betaMESH: Dietary SupplementsMESH: Rats Sprague-DawleyRats Sprague-Dawleychemistry.chemical_compound0302 clinical medicineEndocrinologyMESH: Interleukin-1betaratMESH: AnimalsProstaglandin E2Prostaglandin E1MESH : Tumor Necrosis Factor-alphaMESH : Intraocular Pressure0303 health sciencesNutrition and DieteticsMESH : RatsMESH : NeurogliaMESH: RetinaMESH: Dinoprostonepression intraoculaireMESH: AlprostadilMESH: Docosahexaenoic AcidsBiochemistryEicosapentaenoic AcidDocosahexaenoic acidlipids (amino acids peptides and proteins)MESH: NeurogliaProstaglandin D2Cell activationNeurogliaMESH : Alprostadilmedicine.drugProstaglandin Emedicine.medical_specialtyMESH : DinoprostoneMESH : Interleukin-6Docosahexaenoic AcidsMESH: RatsMESH : MaleProstaglandinBiologyMESH : Interleukin-1betaDinoprostoneRetinaMESH : Diet03 medical and health sciencesMESH: DietMESH: Intraocular PressureInternal medicinemedicineMESH : Eicosapentaenoic AcidAnimalsMESH : Dietary SupplementsRNA MessengerAlprostadilprostanoids030304 developmental biologyMESH: RNA MessengerInterleukin-6Tumor Necrosis Factor-alphadietary polyunsatured fatty acidretinal stressMESH : RetinaRetinalN-6MESH: Interleukin-6MESH : Rats Sprague-Dawleyeye diseasesMESH: MaleMESH : Docosahexaenoic AcidsDietRatsN-3EndocrinologychemistryMESH: Tumor Necrosis Factor-alphaDietary Supplements030221 ophthalmology & optometryMESH : Animalssense organs[SDV.AEN]Life Sciences [q-bio]/Food and Nutritionintraocular pressure
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Mast cell targeting hampers prostate adenocarcinoma development but promotes the occurrence of highly malignant neuroendocrine cancers

2011

Abstract Mast cells (MC) are c-Kit–expressing cells, best known for their primary involvement in allergic reactions, but recently reappraised as important players in either cancer promotion or inhibition. Here, we assessed the role of MCs in prostate tumor development. In prostate tumors from both tumor-prone transgenic adenocarcinoma of the mouse prostate (TRAMP) mice and human patients, MCs are specifically enriched and degranulated in areas of well-differentiated (WD) adenocarcinoma but not around poorly differentiated (PD) foci that coexist in the same tumors. We derived novel TRAMP tumor cell lines, representative of WD and PD variants, and through pharmacologic stabilization or geneti…

MaleOncologyCancer Researchmedicine.medical_specialtyEpithelial-Mesenchymal TransitionMice TransgenicAdenocarcinomaBiologymedicine.disease_causeCell DegranulationMiceProstate cancerProstateCell Line TumorInternal medicineTumor MicroenvironmentmedicineMast CellAnimalsHumansMast CellsReceptors Tumor Necrosis Factor Member 25Tumor microenvironmentAdenocarcinoma; Animals; Carcinoma Neuroendocrine; Cell Degranulation; Cell Line Tumor; Disease Progression; Epithelial-Mesenchymal Transition; Humans; Male; Mast Cells; Matrix Metalloproteinase 9; Mice; Mice Inbred C57BL; Mice Transgenic; Prostatic Neoplasms; Proto-Oncogene Proteins c-kit; Receptors Tumor Necrosis Factor Member 25; Tumor Microenvironment; Cancer Research; OncologyAnimalProstatic NeoplasmsCancermedicine.diseasehumanitiesCarcinoma NeuroendocrineMice Inbred C57BLProto-Oncogene Proteins c-kitmedicine.anatomical_structureMatrix Metalloproteinase 9OncologyTumor progressionProstatic NeoplasmDisease ProgressionAdenocarcinomaCarcinogenesisHumanTramp
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Expression of Interleukin-32 in the Inflamed Arteries of Patients With Giant Cell Arteritis

2011

Objective Giant cell (temporal) arteritis (GCA) is a vasculitis that mainly affects the large and medium arteries, especially the branches of the proximal aorta. Interleukin-32 (IL-32) is a recently described Th1 proinflammatory cytokine, and is mainly induced by interferon-γ (IFNγ), IL-1β, and tumor necrosis factor α (TNFα). This study was undertaken to investigate the expression and tissue distribution of IL-32 in artery biopsy specimens from patients with GCA. Methods Quantitative gene expression analysis of IL-32, IL-1β, TNFα, IFNγ, IL-6, and IL-27 was performed in artery biopsy specimens obtained from 18 patients with GCA and 15 controls. Immunohistochemistry analysis was performed to …

MalePathologyInterleukin-1betaMessenger80 and overImmunology and AllergyPharmacology (medical)Giant Cell ArteritiAged 80 and overeducation.field_of_studyReverse Transcriptase Polymerase Chain ReactionInterleukin-17StatisticsArteriesMiddle AgedFlow CytometryImmunohistochemistryTh1 responseFemaleInterleukin 17VasculitisInterleukin-32; Giant Cell Arteritis; Th1 responsemedicine.medical_specialtyGiant Cell ArteritisImmunologyPopulationBiologyStatistics NonparametricProinflammatory cytokineInterferon-gammaRheumatologymedicine.arterymedicineHumansNonparametricRNA MessengerArteritiseducationAgedAortaAged; Aged 80 and over; Arteries; Female; Flow Cytometry; Giant Cell Arteritis; Humans; Immunohistochemistry; Interferon-gamma; Interleukin-17; Interleukin-1beta; Interleukin-6; Interleukins; Male; Middle Aged; RNA Messenger; Reverse Transcriptase Polymerase Chain Reaction; Statistics Nonparametric; Th1 Cells; Tumor Necrosis Factor-alphaInterleukin-6Tumor Necrosis Factor-alphaInterleukinsTh1 Cellsmedicine.diseaseInterleukin-32Giant cell arteritisGiant cellImmunologyRNA
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