Search results for "Decitabine"

showing 10 items of 20 documents

Genome-wide promoter methylation analysis in neuroblastoma identifies prognostic methylation biomarkers.

2012

Background: Accurate outcome prediction in neuroblastoma, which is necessary to enable the optimal choice of risk-related therapy, remains a challenge. To improve neuroblastoma patient stratification, this study aimed to identify prognostic tumor DNA methylation biomarkers.Results: To identify genes silenced by promoter methylation, we first applied two independent genome-wide methylation screening methodologies to eight neuroblastoma cell lines. Specifically, we used re-expression profiling upon 5-aza-2'-deoxycytidine (DAC) treatment and massively parallel sequencing after capturing with a methyl-CpG-binding domain (MBD-seq). Putative methylation markers were selected from DAC-upregulated …

EpigenomicsMYCN Single CopyMedizinPrimary Neuroblastoma TumorBioinformaticsNeuroblastoma0302 clinical medicineRisk FactorsMYCN StatusDatabases GeneticPromoter MethylationGTP-Binding Protein alpha Subunits GsHazard Ratio PatientPromoter Regions GeneticEpigenomicsRegulation of gene expression0303 health sciencesMassive parallel sequencingHigh-Throughput Nucleotide SequencingMethylation3. Good healthGene Expression Regulation NeoplasticMedizinische Fakultät » Universitätsklinikum Essen » Zentrum für Kinder- und Jugendmedizin030220 oncology & carcinogenesisDNA methylationAzacitidineBiologieBiologyDecitabine03 medical and health sciencesneuroblastomaCell Line TumorNeuroblastomaBiomarkers TumorChromograninsmedicineHumansddc:61ddc:610Epigenetics030304 developmental biologyepigeneticsGenome HumanResearchBiology and Life SciencesbiomarkersSequence Analysis DNADNA MethylationHCT116 Cellsmedicine.diseaseSurvival AnalysisCancer researchHuman genomeDNA-methylation
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Luspatercept Treatment Leads to Long Term Increases in Hemoglobin and Reductions in Transfusion Burden in Patients with Low or Intermediate-1 Risk My…

2015

Background: Luspatercept is a fusion protein (modified activin receptor IIB-IgG Fc) being investigated for the treatment of anemias with ineffective erythropoiesis. MDS patients have increased Smad2/3 signaling in the bone marrow, leading to ineffective erythropoiesis. Luspatercept inhibits Smad2/3 signaling and promotes late-stage erythroid differentiation, thereby correcting the ineffective erythropoiesis. Aims: This is an ongoing, phase 2, multicenter, open-label, 24-month extension study (following a 3-month base study) to evaluate the longer-term effects of luspatercept on anemia in patients (pts) with low/int-1 risk MDS (IPSS classification). Study outcomes include erythroid response…

Ineffective erythropoiesismedicine.medical_specialtyAnemiaImmunologyDecitabinemedicine.disease_causeLower riskBiochemistry03 medical and health sciences0302 clinical medicineInternal medicineMedicineAdverse effectLenalidomidebusiness.industryMyelodysplastic syndromesCell BiologyHematologymedicine.disease3. Good healthSurgery030220 oncology & carcinogenesisCohortbusiness030215 immunologymedicine.drugBlood
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Transcription intermediary factor 1γ is a tumor suppressor in mouse and human chronic myelomonocytic leukemia.

2011

Transcription intermediary factor 1γ (TIF1γ) was suggested to play a role in erythropoiesis. However, how TIF1γ regulates the development of different blood cell lineages and whether TIF1γ is involved in human hematological malignancies remain to be determined. Here we have shown that TIF1γ was a tumor suppressor in mouse and human chronic myelomonocytic leukemia (CMML). Loss of Tif1g in mouse HSCs favored the expansion of the granulo-monocytic progenitor compartment. Furthermore, Tif1g deletion induced the age-dependent appearance of a cell-autonomous myeloproliferative disorder in mice that recapitulated essential characteristics of human CMML. TIF1γ was almost undetectable in leukemic ce…

MaleAgingAntimetabolites AntineoplasticTumor suppressor geneCellular differentiationMolecular Sequence DataChronic myelomonocytic leukemiaReceptor Macrophage Colony-Stimulating FactorBiologyDecitabinechemistry.chemical_compoundMicemedicineAnimalsHumansGenes Tumor SuppressorPromoter Regions GeneticTranscription factorAgedAged 80 and overMice KnockoutBase SequenceGene Expression Regulation LeukemicCell DifferentiationLeukemia Myelomonocytic ChronicGeneral MedicineDNA MethylationMiddle Agedmedicine.diseaseTRIM33Hematopoietic Stem CellsMolecular biologyDemethylating agentHematopoiesisNeoplasm ProteinsSpecific Pathogen-Free OrganismsHaematopoiesischemistryDNA methylationCancer researchAzacitidineFemaleTranscription FactorsResearch ArticleThe Journal of clinical investigation
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Outcome of lower-risk patients with myelodysplastic syndromes without 5q deletion after failure of erythropoiesis-stimulating agents

2017

Purpose Most anemic patients with non-deleted 5q lower-risk myelodysplastic syndromes (MDS) are treated with erythropoiesis-stimulating agents (ESAs), with a response rate of approximately 50%. Second-line treatments, including hypomethylating agents (HMAs), lenalidomide (LEN), and investigational drugs, may be used after ESA failure in some countries, but their effect on disease progression and overall survival (OS) is unknown. Here, we analyzed outcome after ESA failure and the effect of second-line treatments. Patients and Methods We examined an international retrospective cohort of 1,698 patients with non-del(5q) lower-risk MDS treated with ESAs. Results Erythroid response to ESAs was 6…

MaleCancer Research0302 clinical medicineRecurrenceRisk Factorshemic and lymphatic diseasesHydroxyureaCumulative incidenceTreatment FailureEnzyme InhibitorsLenalidomideAged 80 and overCytarabineAnemiaMiddle AgedThalidomideMelodysplastic syndromeSurvival RateLeukemia Myeloid AcuteOncologyInternational Prognostic Scoring System030220 oncology & carcinogenesisRetreatmentAzacitidineCyclosporineDisease ProgressionChromosomes Human Pair 5FemaleChromosome DeletionErythrocyte Transfusionmedicine.drugmedicine.medical_specialtyMelodysplastic syndrome erytropoiesis stimulating agents 5q-erytropoiesis stimulating agentsDecitabineAntineoplastic AgentsTretinoinDecitabineLower risk5q-Arsenic03 medical and health sciencesInternal medicinemedicineHumansImmunologic FactorsSurvival rateAgedAntilymphocyte SerumRetrospective StudiesLenalidomidebusiness.industryValproic AcidMyelodysplastic syndromesRetrospective cohort studymedicine.diseaseMyelodysplastic SyndromesHematinicsPhysical therapybusiness030215 immunology
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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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Validation of response assessment according to international consortium for MDS/MPN criteria in chronic myelomonocytic leukemia treated with hypometh…

2017

Validation of response assessment according to international consortium for MDS/MPN criteria in chronic myelomonocytic leukemia treated with hypomethylating agents

OncologyAdultMalemedicine.medical_specialtyAntimetabolites AntineoplasticeducationAzacitidineChronic myelomonocytic leukemiaDecitabine03 medical and health sciences0302 clinical medicineMyelodysplastic–myeloproliferative diseaseshemic and lymphatic diseasesInternal medicinemedicineHumansLetter to the Editorhealth care economics and organizationsAgedHematologybusiness.industryMyelodysplastic syndromesTranslational biologyfood and beveragesLeukemia Myelomonocytic Chronic[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematologyDNA MethylationMiddle Agedmedicine.diseaseMyelodysplastic-Myeloproliferative DiseasesSurvival Analysis3. Good healthResponse assessmentLeukemiaTreatment OutcomeOncology030220 oncology & carcinogenesisMyelodysplastic SyndromesImmunologyAzacitidineFemalebusiness030215 immunologymedicine.drug
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Molecular predictors of response to decitabine in advanced chronic myelomonocytic leukemia: a phase 2 trial.

2011

Abstract Hydroxyurea is the standard therapy of chronic myelomonocytic leukemia (CMML) presenting with advanced myeloproliferative and/or myelodysplastic features. Response to hypomethylating agents has been reported in heterogeneous series of CMML. We conducted a phase 2 trial of decitabine (DAC) in 39 patients with advanced CMML defined according to a previous trial. Median number of DAC cycles was 10 (range, 1-24). Overall response rate was 38% with 4 complete responses (10%), 8 marrow responses (21%), and 3 stable diseases with hematologic improvement (8%). Eighteen patients (46%) demonstrated stable disease without hematologic improvement, and 6 (15%) progressed to acute leukemia. With…

OncologyNeuroblastoma RAS viral oncogene homologMalemedicine.medical_specialtyAntimetabolites AntineoplasticImmunologyDecitabineChronic myelomonocytic leukemiamedicine.disease_causeDecitabineBiochemistryhemic and lymphatic diseasesInternal medicinemedicineHumansSurvival analysisAgedAged 80 and overAcute leukemiaHematologybusiness.industryGene Expression Regulation LeukemicLeukemia Myelomonocytic ChronicCell BiologyHematologyMiddle Agedmedicine.diseasePrognosisSurvival AnalysisLeukemiaImmunologyMutationAzacitidineFemaleKRASbusinessmedicine.drugBlood
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Validation of the High-Risk Prognostic Score Defined By the Presence of Mutations in NRAS or TP53 in a Cohort of 497 Patients with Acute Myeloid Leuk…

2020

INTRODUCTION Older AML patients have a different mutational landscape compared to younger patients. The prognostic classification of AML proposed by the European Leukemia Net (2017) is based on the presence of mutations in FLT3 (ITD), NPM1, CEBPA, RUNX1, ASXL1 and TP53. However, our group has identified a high-risk prognostic score in older patients with AML, who are undergoing treatment with azacitidine or low-dose cytarabine plus fludarabine, which predict a shorter survival. OBJECTIVE Validation of the previously identified high-risk prognostic score, defined by the presence of mutations in NRAS or TP53, in 3 cohorts of patients with AML who have been studied by NGS with a custom panel i…

OncologyNeuroblastoma RAS viral oncogene homologmedicine.medical_specialtyHematologybusiness.industryImmunologyAzacitidineDecitabineCell BiologyHematologyBiochemistryFludarabineInternal medicineCEBPACohortCytarabineMedicinebusinessmedicine.drugBlood
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Treatment of Relapse after Allogeneic Hematopoietic Stem Cell Transplantation with Venetoclax, Hypomethylating Agents and DLI - a Retrospective Multi…

2019

Introduction: The most common cause of treatment failure after allogeneic hematopoetic stem cell transplantation (aHSCT) is relapse. The combination of venetoclax and the hypomethylating agents (HMA) azacitidine (AZA) or decitabine (DAC) have shown promising efficacy in elderly patients with AML. We here present clinical data on 32 patients, who were treated with an HMA/venetoclax combination therapy (HMAClax) for relapse of a myeloid malignancy after aHSCT, collected retrospectively from 11 German centers. Results: Sixteen patients (50%) were male, median age was 54 years (30.8-71.5). Diagnoses at aHSCT were 25 AML (17 primary, 8 emerging from MDS, CMML or OMF), 5 MDS, 1 CMML and one atypi…

Oncologymedicine.medical_specialtyVenetoclaxbusiness.industrymedicine.medical_treatmentImmunologyAzacitidineMedizinDecitabineSalvage therapyCell BiologyHematologyHematopoietic stem cell transplantationmedicine.diseaseBiochemistryTransplantationTumor lysis syndromechemistry.chemical_compoundchemistryInternal medicinemedicinebusinessLenalidomidemedicine.drug
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Use of Venetoclax in Patients with Relapsed or Refractory Acute Myeloid Leukemia: The Pethema Registry Experience

2020

Introduction The prognosis of patients with recurrent or refractory acute myeloid leukemia (AML-RR) is very poor, especially if they are not candidates for allogeneic transplantation (allo-SCT) after a second complete response (CR). Venetoclax, a potent and selective inhibitor of the antiapoptotic protein BCL-2, was approved by the FDA in combination with hypomethylating agents (HMAs) or low-dose cytarabine (LDAC) in patients with newly diagnosed AML of age ≥ 75 years, or who have comorbidities that preclude the use of intensive chemotherapy. However, the evidence in AML-RR patients is still scarce. For this reason, the objective of our study is to retrospectively analyze the efficacy of th…

medicine.medical_specialtyVenetoclaxbusiness.industryImmunologyDecitabineCell BiologyHematologymedicine.diseaseBiochemistryDiscontinuationRegimenchemistry.chemical_compoundLeukemiachemistryRefractoryInternal medicineCohortmedicineCytarabinebusinessmedicine.drugBlood
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