Search results for "Apoptosis ."

showing 10 items of 177 documents

Addition of AEG35156 XIAP antisense oligonucleotide in reinduction chemotherapy does not improve remission rates in patients with primary refractory …

2011

Background XIAP (X-linked inhibitor of apoptosis protein) is an inhibitor of caspases 3 and 9 that is overexpressed in acute myeloid leukemia (AML) and may contribute to chemoresistance. We report an open-label randomized phase II trial of reinduction chemotherapy with and without the XIAP antisense oligonucleotide AEG35156 in patients with AML who did not achieve remission with initial induction chemotherapy. Methods Twenty-seven patients with AML who were refractory to initial induction chemotherapy were randomized and treated with AEG35156 (650 mg) in combination with high-dose cytarabine and idarubicin. Thirteen patients were randomized and treated with high-dose cytarabine and idarubic…

AdultMaleOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentOligonucleotidesMedizinPhases of clinical researchX-Linked Inhibitor of Apoptosis ProteinPharmacologyYoung AdultInternal medicineAntineoplastic Combined Chemotherapy ProtocolsmedicineHumansIdarubicinAgedAged 80 and overChemotherapybusiness.industryRemission InductionInduction chemotherapyMyeloid leukemiaHematologyMiddle Agedmedicine.diseaseXIAPLeukemia Myeloid AcuteLeukemiaTreatment OutcomeOncologyCytarabineFemalebusinessmedicine.drug
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Apoptosis resistance in epithelial tumors is mediated by tumor-cell-derived interleukin-4

2008

We investigated the mechanisms involved in the resistance to cell death observed in epithelial cancers. Here, we identify that primary epithelial cancer cells from colon, breast and lung carcinomas express high levels of the antiapoptotic proteins PED, cFLIP, Bcl-xL and Bcl-2. These cancer cells produced interleukin-4 (IL-4), which amplified the expression levels of these antiapoptotic proteins and prevented cell death induced upon exposure to TRAIL or other drug agents. IL-4 blockade resulted in a significant decrease in the growth rate of epithelial cancer cells and sensitized them, both in vitro and in vivo, to apoptosis induction by TRAIL and chemotherapy via downregulation of the antia…

AdultMaleProgrammed cell deathLung NeoplasmsTime Factorsapoptosis interleukin-4 cancer stem cells cancer chemiotherapy cytokinesCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinAntineoplastic AgentsApoptosisBreast NeoplasmsBiologyTNF-Related Apoptosis-Inducing LigandTumor Cells CulturedmedicineHumansAutocrine signallingMolecular BiologyInterleukin 4AgedCell ProliferationSettore MED/04 - Patologia GeneraleCell DeathDose-Response Relationship DrugCell growthCarcinomaIntracellular Signaling Peptides and ProteinsAntibodies MonoclonalInterleukin-4 Receptor alpha SubunitCorrectionCancerCell BiologyMiddle AgedPhosphoproteinsmedicine.diseaseUp-RegulationCell biologyAutocrine CommunicationProto-Oncogene Proteins c-bcl-2Drug Resistance NeoplasmApoptosisColonic NeoplasmsCancer cellFemaleInterleukin-4Interleukin-4 Cancer stem cellsSignal transductionApoptosis Regulatory ProteinsSignal Transduction
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NF-κB protects Behçet's disease T cells against CD95-induced apoptosis up-regulating antiapoptotic proteins

2005

Objective To determine whether prolongation of the inflammatory reaction in patients with Behcet's disease (BD) is related to apoptosis resistance and is associated with the up-regulation of antiapoptotic factors. Methods The percentage of cell death was evaluated by flow cytometry in peripheral blood mononuclear cells from 35 patients with BD and 30 healthy volunteers. The expression levels of antiapoptotic factors and NF-κB regulatory proteins were measured using Western blotting and immunohistochemical analyses. To down-regulate NF-κB nuclear translocation, BD T lymphocytes were exposed in vitro to thalidomide and subjected to transfection with NF-κB small interfering RNA. Results Althou…

AdultMaleSmall interfering RNAProgrammed cell deathT-LymphocytesT cellImmunologyCASP8 and FADD-Like Apoptosis Regulating Proteinbcl-X ProteinApoptosisCaspase 3TransfectionCaspase 8RheumatologyHumansImmunology and AllergyMedicinePharmacology (medical)fas ReceptorRNA Small InterferingCells CulturedDose-Response Relationship Drugbusiness.industryBehcet SyndromeIntracellular Signaling Peptides and ProteinsNF-kappa BTransfectionFlow CytometryFas receptorThalidomideUp-Regulationmedicine.anatomical_structureGene Expression RegulationProto-Oncogene Proteins c-bcl-2ApoptosisImmunologyLeukocytes MononuclearCancer researchFemalebusinessArthritis & Rheumatism
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Dysregulated Survivin Expression in Nasal Polyps of Individuals with Aspirin Exacerbated Respiratory Disease

2012

Background A derailed balance of cell proliferation and apoptosis is presumed to result in cell hyperplasia as a typical feature of nasal polyps. Survivin, a protein of the inhibitors of the apoptosis family is proposed to promote polyp formation. However, studies concerning survivin expression in chronic rhinosinusitis (CRS) with nasal polyps are rare and the specificity of the survivin expression in nasal polyps from individuals with aspirin-exacerbated respiratory disease (AERD) has not been investigated. Methods Immunohistochemical survivin expression analysis was performed. Samples were taken from the ethmoid sinus of individuals with CRS with nasal polyps with and without AERD during …

AdultMaleVascular Endothelial Growth Factor APathologymedicine.medical_specialtySurvivinApoptosisInhibitor of Apoptosis ProteinsDrug HypersensitivityYoung AdultNasal PolypsEthmoid SinusWestern blotSurvivinotorhinolaryngologic diseasesmedicineHumansImmunology and AllergyNasal polypsSinusitisneoplasmsCells CulturedRhinitisAspirinmedicine.diagnostic_testbusiness.industryRespiratory diseaseGeneral MedicineMiddle AgedHyperplasiamedicine.diseasePathophysiologyOtorhinolaryngologyApoptosisChronic DiseaseDisease ProgressionImmunohistochemistryFemalebusinessAmerican Journal of Rhinology & Allergy
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Control of target cell survival in thyroid autoimmunity by T helper cytokines via regulation of apoptotic proteins

2000

After autoimmune inflammation, interactions between CD95 and its ligand (CD95L) mediate thyrocyte destruction in Hashimoto's thyroiditis (HT). Conversely, thyroid autoimmune processes that lead to Graves' disease (GD) result in autoantibody-mediated thyrotropin receptor stimulation without thyrocyte depletion. We found that GD thyrocytes expressed CD95 and CD95L in a similar manner to HT thyrocytes, but did not undergo CD95-induced apoptosis either in vivo or in vitro. This pattern was due to the differential production of TH1 and TH2 cytokines. Interferon gamma promoted caspase up-regulation and CD95-induced apoptosis in HT thyrocytes, whereas interleukin 4 and interleukin 10 protected GD …

Adultendocrine systemmedicine.medical_specialtyFas Ligand Proteinendocrine system diseasesCell SurvivalImmunologyCASP8 and FADD-Like Apoptosis Regulating ProteinThyroid Glandbcl-X ProteinApoptosisMice TransgenicIn Vitro TechniquesThyroiditisThyrotropin receptorMiceTh2 CellsSettore MED/04 - PATOLOGIA GENERALEInternal medicinemedicineImmunology and AllergyAnimalsHumansInterferon gammafas ReceptorInterleukin 4CaspaseMembrane GlycoproteinsbiologyThyroidIntracellular Signaling Peptides and ProteinsThyroiditis AutoimmuneT-Lymphocytes Helper-InducerMiddle AgedTh1 CellsFas receptormedicine.diseaseGraves DiseaseInterleukin 10medicine.anatomical_structureEndocrinologyProto-Oncogene Proteins c-bcl-2biology.proteinCytokinesCarrier Proteinsmedicine.drug
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Induction of apoptosis by the adenosine derivative IB-MECA in parental or multidrug-resistant HL-60 leukemia cells: possible relationship to the effe…

2004

<i>Background:</i> The effects of the A<sub>3</sub> adenosine receptor (A<sub>3</sub>AR) agonist IB-MECA were examined in HL-60 leukemia and in its multidrug-resistant variant HL-60R cells. <i>Methods:</i> Cytotoxicity was evaluated by MTS assays and apoptosis by flow cytometry analyses of DNA fragmentation and phosphatidylserine exposure. The mRNAs of A<sub>3</sub>AR and inhibitor of apoptosis proteins (IAPs) were determined by RT-PCR. <i>Results:</i> A<sub>3</sub>AR expression was similar in HL-60 and HL-60R cells. At ≧100 µ<i>M</i>, IB-MECA exhibited strong cytotoxic and apoptotic effects in H…

AgonistProgrammed cell deathAdenosinemedicine.drug_classApoptosisHL-60 CellsBiologyInhibitor of apoptosisInhibitor of Apoptosis ProteinsDrug DiscoverymedicineNeoplasmHumansPharmacology (medical)PharmacologyGeneral Medicinemedicine.diseaseAdenosine A3 receptorFlow CytometryAdenosineDrug Resistance MultipleLeukemiaInfectious DiseasesOncologyBiochemistryApoptosisDrug Resistance NeoplasmA 3 adenosine receptor IB-MECA Apoptosis Multidrug resistance Inhibitor of apoptosis proteinsCancer researchmedicine.drugChemotherapy
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DNA replication arrest in response to genotoxic stress provokes early activation of stress-activated protein kinases (SAPK/JNK).

2009

Abstract The impact of DNA damage-induced replication blockage for early activation of stress kinases [stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK)] is largely unknown. Here, we show that induction of dual phosphorylation of SAPK/JNK by the DNA polymerase inhibitor aphidicolin was not ameliorated by additional exposure to ultraviolet (UV) light, indicating that overlapping mechanisms participate in signaling to SAPK/JNK triggered by both agents. UV-induced DNA replication blockage, cyclobutane pyrimidine dimer formation and DNA strand break induction coincided with SAPK/JNK phosphorylation at early (≤ 30 min) but not late (≥ 2 h) time points after exposure. Genotoxin…

AphidicolinDNA ReplicationDNA damageUltraviolet RaysPoly ADP ribose polymeraseCell Linechemistry.chemical_compoundMiceAphidicolinStructural BiologyCricetinaeAnimalsHumansLymphocytesPhosphorylationProtein kinase AMolecular BiologyNucleic Acid Synthesis InhibitorsBRCA2 ProteinMice KnockoutbiologyKinaseCell CycleDNA replicationJNK Mitogen-Activated Protein KinasesFibroblastsMolecular biologyProliferating cell nuclear antigenDNA-Binding ProteinsEnzyme ActivationchemistryPyrimidine Dimersbiology.proteinPhosphorylationApoptosis Regulatory ProteinsDNA DamageJournal of molecular biology
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Apoptosis linfocitaria según receptor TCR- αβ y TCR- γδ en sujetos sanos

2015

Durante décadas, los LTγδ han generado cierto desconcierto debido a su preponderancia en los tejidos periféricos sobre la sangre periférica y a la presencia de fenotipos activados y de memoria mayoritariamente, así como por su capacidad para reconocer un amplio repertorio de antígenos, alguno de los cuales no requieren ser procesados por el MHC. Los LTγδ forman parte de un sistema inmunológico superpuesto entre la inmunidad innata y la adquirida. Estas células están en constante contacto con sustancias medioambientales, identificando posibles patógenos para presentarlos a otras células o eliminarlos (células T γδ activadas), memorizando su estructura antigénica para posteriores contactos (c…

Apoptosis Linfocito TCR- αβ Linfocito TCR- γδ
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Induction of annexin-1 during TRAIL-induced apoptosis in thyroid carcinoma cells

2005

We investigated the expression of annexin-1 (ANXA1) in thyroid carcinoma cell lines and in thyroid cancers with a different degree of differentiation. The highest level of ANXA1 expression examined by Western blotting was detected in the papillary carcinoma cells (NPA) and in the follicular cells (WRO). On the other hand, the most undifferentiated thyroid carcinoma cells (ARO and FRO) presented the lowest level of ANXA1 expression. In surgical tissue specimens from 32 patients with thyroid cancers, we found high immunoreactivity for ANXA1 in papillary (PTC) and follicular (FTC) thyroid cancers while in undifferentiated thyroid cancers (UTC) the expression of the protein was barely detectabl…

ApoptosisTNF-Related Apoptosis-Inducing LigandApoptosis Regulatory ProteinsthyroidThyroid carcinomaTNF-Related Apoptosis-Inducing LigandText miningAnnexinMedicineHumansThyroid NeoplasmsMolecular BiologyThyroid NeoplasmAnnexin A1Apoptosis Regulatory ProteinMembrane Glycoproteinsbusiness.industryTumor Necrosis Factor-alphaApoptosiCell BiologyApoptosisCancer researchMembrane GlycoproteinbusinessApoptosis Regulatory ProteinsHuman
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Pharmacological blockade of the fatty acid amide hydrolase (FAAH) alters neural proliferation, apoptosis and gliosis in the rat hippocampus, hypothal…

2015

Endocannabinoids participate in the control of neurogenesis, neural cell death and gliosis. The pharmacological effect of the fatty acid amide hydrolase (FAAH) inhibitor URB597, which limits the endocannabinoid degradation, was investigated in the present study. Cell proliferation (phospho-H3(+) or BrdU(+) cells) of the main adult neurogenic zones as well as apoptosis (cleaved caspase-3(+)), astroglia (GFAP(+)), and microglia (Iba1(+) cells) were analyzed in the hippocampus, hypothalamus and striatum of rats intraperitoneally treated with URB597 (0.3 mg/kg/day) at one dose/4-days resting or 5 doses (1 dose/day). Repeated URB597 treatment increased the plasma levels of the N-acylethanolamine…

AstrocitosNeurobiologia del desenvolupamentAmidohidrolasasCannabinoid receptorCarbamatos:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Intracellular Signaling Peptides and Proteins::Apoptosis Regulatory Proteins::Caspases [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Differentiation::Neurogenesis [Medical Subject Headings]medicine.medical_treatment:Chemicals and Drugs::Carbohydrates::Monosaccharides::Hexoses::Glucose [Medical Subject Headings]Apoptosis:Phenomena and Processes::Physiological Phenomena::Body Constitution::Body Weights and Measures::Body Size::Body Weight [Medical Subject Headings]chemistry.chemical_compound:Chemicals and Drugs::Amino Acids Peptides and Proteins::Proteins::Membrane Proteins::Receptors Cell Surface::Receptors G-Protein-Coupled::Receptors Cannabinoid::Receptor Cannabinoid CB1 [Medical Subject Headings]0302 clinical medicine:Chemicals and Drugs::Organic Chemicals::Carboxylic Acids::Acids Acyclic::Carbamates [Medical Subject Headings]Fatty acid amide hydrolaseReceptor cannabinoide CB1:Organisms::Eukaryota::Animals [Medical Subject Headings]FAAHGliosishealth care economics and organizations:Chemicals and Drugs::Nucleic Acids Nucleotides and Nucleosides::Nucleosides::Deoxyribonucleosides::Deoxyuridine::Bromodeoxyuridine [Medical Subject Headings]:Chemicals and Drugs::Lipids::Glycerides::Triglycerides [Medical Subject Headings]Original Research0303 health sciencesNeurogenesisBenzamidas:Chemicals and Drugs::Polycyclic Compounds::Steroids::Cholestanes::Cholestenes::Cholesterol [Medical Subject Headings]Endocannabinoid systemEtanolaminas3. Good healthEndocannabinoides:Chemicals and Drugs::Lipids::Fatty Acids::Fatty Acids Unsaturated::Fatty Acids Monounsaturated::Oleic Acids [Medical Subject Headings]CannabinoidesMicroglíalipids (amino acids peptides and proteins)medicine.symptomColesterol:Chemicals and Drugs::Organic Chemicals::Hydrocarbons::Terpenes::Cannabinoids [Medical Subject Headings]:Chemicals and Drugs::Lipids::Fatty Acids::Palmitic Acids [Medical Subject Headings]psychological phenomena and processesProliferación celularmedicine.medical_specialtyCerebroNeurogenesiseducationBiologyBromodesoxiuridina:Anatomy::Nervous System::Neuroglia::Microglia [Medical Subject Headings]Triglicéridoslcsh:RC321-571Ácidos oléicosRatas03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineHipocampomedicineCaspasa 3:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hippocampus [Medical Subject Headings]:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Growth Processes::Cell Proliferation [Medical Subject Headings]lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry030304 developmental biologyPalmitoylethanolamide:Chemicals and Drugs::Chemical Actions and Uses::Pharmacologic Actions::Molecular Mechanisms of Pharmacological Action::Neurotransmitter Agents::Endocannabinoids [Medical Subject Headings]:Chemicals and Drugs::Enzymes and Coenzymes::Enzymes::Hydrolases::Amidohydrolases [Medical Subject Headings]Cannabinoids:Anatomy::Cells::Neuroglia::Astrocytes [Medical Subject Headings]Peso corporalEnergy metabolism:Anatomy::Nervous System::Central Nervous System::Brain [Medical Subject Headings]:Anatomy::Nervous System::Central Nervous System::Brain::Limbic System::Hypothalamus [Medical Subject Headings]URB597:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death [Medical Subject Headings]:Diseases::Pathological Conditions Signs and Symptoms::Pathologic Processes::Gliosis [Medical Subject Headings]:Chemicals and Drugs::Organic Chemicals::Amines::Amino Alcohols::Ethanolamines [Medical Subject Headings]Muerte celular:Phenomena and Processes::Cell Physiological Phenomena::Cell Physiological Processes::Cell Death::Apoptosis [Medical Subject Headings]:Organisms::Eukaryota::Animals::Chordata::Vertebrates::Mammals::Rodentia::Muridae::Murinae::Rats [Medical Subject Headings]EndocrinologyURB597chemistryGliosisnervous systemGlucosaCannabinoidEnergy Metabolism:Chemicals and Drugs::Organic Chemicals::Amides::Benzamides [Medical Subject Headings]HipotálamoÁcidos palmíticos030217 neurology & neurosurgeryNeuroscienceFrontiers in Cellular Neuroscience
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