Search results for "azacitidine"

showing 10 items of 38 documents

Both mature KIR+ and immature KIR- NK cells control pediatric acute B-cell precursor leukemia in NOD.Cg-Prkdcscid IL2rgtmWjl/Sz mice.

2014

Therapeutic natural killer (NK)-cell-mediated alloreactivity toward acute myeloid leukemia has largely been attributed to mismatches between killer immunoglobulin-like receptors (KIRs) on NK cells and their ligands, HLA class I molecules, on target cells. While adult acute B-cell precursor leukemia (BCP-ALL) appears to be resistant to NK-cell-mediated lysis, recent data indicate that pediatric BCP-ALL might yet be a target of NK cells. In this study, we demonstrate in a donor-patient-specific NOD.Cg-Prkdc(scid) IL2rg(tmWjl)/Sz (NSG) xenotransplantation model that NK cells mediate considerable alloreactivity toward pediatric BCP-ALL in vivo. Notably, both adoptively transferred mature KIR(+)…

Cytotoxicity ImmunologicGenotypeXenotransplantationmedicine.medical_treatmentImmunologyTransplantation HeterologousAntineoplastic AgentsGraft vs Leukemia EffectHuman leukocyte antigenBiochemistryMiceImmune systemReceptors KIRMice Inbred NODPrecursor B-Cell Lymphoblastic Leukemia-LymphomamedicineAnimalsHumansChildB cellSevere combined immunodeficiencybusiness.industryHematopoietic Stem Cell TransplantationMyeloid leukemiaCell BiologyHematologyDNA Methylationmedicine.diseasePrognosisTransplantationKiller Cells NaturalLeukemiaDisease Models Animalmedicine.anatomical_structureImmunologyAzacitidineCytokinesInterleukin-2businessBlood
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Establishment and functional validation of a structural homology model for human DNA methyltransferase 1

2003

Changes in DNA methylation patterns play an important role in tumorigenesis. The DNA methyltransferase 1 (DNMT1) protein represents a major DNA methyltransferase activity in human cells and is therefore a prominent target for experimental cancer therapies. However, there are only few available inhibitors and their high toxicity and low specificity have so far precluded their broad use in chemotherapy. Based on the strong conservation of catalytic DNA methyltransferase domains we have used a homology modeling approach to determine the three-dimensional structure of the DNMT1 catalytic domain. Our results suggest an overall structural conservation with other DNA methyltransferases but also in…

DNA (Cytosine-5-)-Methyltransferase 1Models MolecularMethyltransferaseMolecular Sequence DataBiophysicsDNA Methyltransferase InhibitorComputational biologyBiologymedicine.disease_causeModels BiologicalBiochemistryDNA methyltransferasechemistry.chemical_compoundCatalytic DomainTumor Cells CulturedmedicineHumansAmino Acid SequenceDNA (Cytosine-5-)-MethyltransferasesHomology modelingEnzyme InhibitorsMolecular BiologyGeneticsSequence Homology Amino AcidCell BiologyDNA MethylationModels ChemicalchemistryDNA methylationAzacitidineDNMT1Nucleic Acid ConformationCarcinogenesisDNABiochemical and Biophysical Research Communications
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Antitumor Effects of a Combined 5-Aza-2′Deoxycytidine and Valproic Acid Treatment on Rhabdomyosarcoma and Medulloblastoma in Ptch Mutant Mice

2009

Abstract Patched (Ptch) heterozygous mice develop medulloblastoma (MB) and rhabdomyosarcoma (RMS) resembling the corresponding human tumors. We have previously shown that epigenetic silencing of the intact Ptch allele contributes to tumor formation in this model. Here, we investigated whether targeting of epigenetic silencing mechanisms could be useful in the treatment of Ptch-associated cancers. A reduction of endogenous DNA methyltransferase1 (Dnmt1) activity significantly reduced tumor incidence in heterozygous Ptch knockout mice. A combined treatment with the Dnmt inhibitor 5-aza-2′deoxycytidine (5-aza-dC) and the histone deacetlyase (HDAC) inhibitor valproic acid (VPA) efficiently prev…

DNA (Cytosine-5-)-Methyltransferase 1Patched ReceptorsPatchedCancer Researchmedicine.drug_classGene ExpressionDecitabineReceptors Cell SurfaceBiologyDecitabineHistone DeacetylasesHistonesMice03 medical and health sciences0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsRhabdomyosarcomamedicineAnimalsDNA (Cytosine-5-)-MethyltransferasesGene SilencingMuscle SkeletalRhabdomyosarcoma030304 developmental biologyMedulloblastomaMice Inbred BALB C0303 health sciencesValproic AcidHistone deacetylase inhibitorCancerAcetylationDNA Methylationmedicine.disease3. Good healthHistone Deacetylase InhibitorsMice Inbred C57BLPatched-1 Receptorstomatognathic diseasesOncology030220 oncology & carcinogenesisAzacitidineCancer researchDNMT1Epigenetic therapyMedulloblastomamedicine.drugCancer Research
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The high rate of endoreduplication in the repair deficient CHO mutant EM9 parallels a reduced level of methylated deoxycytidine in DNA

2008

It has been recently proposed that hypomethylation of DNA induced by 5-azacytidine (5-azaC) leads to reduced chromatid decatenation that ends up in endoreduplication, most likely due to a failure in topo II function [S. Mateos, I. Domínguez, N. Pastor, G. Cantero, F. Cortés, The DNA demethylating 5-azaC induces endoreduplication in cultured Chinese hamster cells, Mutat. Res. 578 (2005) 33-42]. The Chinese hamster mutant cell line EM9 has a high spontaneous frequency of endoreduplication as compared to its parental line AA8. In order to see if this is related to the degree of DNA methylation, we have investigated the basal levels of both endpoints in AA8 and EM9, as well as the effect of ext…

DNA ReplicationDNA RepairHealth Toxicology and MutagenesisMutantCHO CellsChromosome segregationamedicine.disease_causeDeoxycytidineChromosomesChinese hamsterHypomethylation of DNAchemistry.chemical_compoundCricetulusCricetinaeGeneticsmedicineAnimalsEndoreduplicationMolecular BiologyMutationbiologyChinese hamster ovary cellEndoreduplicationDNA Methylationbiology.organism_classificationTopoisomerase IIMolecular biologychemistryMutationDNA methylationAzacitidineChromatidDNAMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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DNA-methylation dependent regulation of embryo-specific 5S ribosomal DNA cluster transcription in adult tissues of sea urchin Paracentrotus lividus

2013

Abstract We have previously reported a molecular and cytogenetic characterization of three different 5S rDNA clusters in the sea urchin Paracentrotus lividus and recently, demonstrated the presence of high heterogeneity in functional 5S rRNA. In this paper, we show some important distinctive data on 5S rRNA transcription for this organism. Using single strand conformation polymorphism (SSCP) analysis, we demonstrate the existence of two classes of 5S rRNA, one which is embryo-specific and encoded by the smallest (700 bp) cluster and the other which is expressed at every stage and encoded by longer clusters (900 and 950 bp). We also demonstrate that the embryo-specific class of 5S rRNA is ex…

Embryo NonmammalianTranscription GeneticBase pairDNA RibosomalParacentrotus lividusEpigenesis Geneticsea urchin5S ribosomal RNASingle-Strand conformation polymorphism (SSCP)Transcription (biology)biology.animalGeneticsAnimalsGene SilencingSea urchinRibosomal DNAPolymorphism Single-Stranded ConformationalGeneticsbiologyRNA Ribosomal 5SDNA Methylation5S ribosomal RNARibosomal RNAbiology.organism_classificationSettore BIO/18 - GeneticaOrgan Specificity5S ribosomal genesilencingDNA methylationAzacitidineOocytesParacentrotusFemaleepigeneticGenomics
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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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Role and importance of polymorphisms with respect to DNA methylation for the expression of CYP2E1 enzyme

2014

Different individuals possess slightly different genetic information and show genetically-determined differences in several enzyme activities due to genetic variability. Following an integrated approach, we studied the polymorphisms and methylation of sites contained in the 5' flanking region of the metabolizing enzyme CYP2E1 in correlation to its expression in both tumor and non-neoplastic liver cell lines, since to date little is known about the influence of these (epi)genetic elements in basal conditions and under induction by the specific inductor and a demethylating agent. In treated cells, reduced DNA methylation, assessed both at genomic and gene level, was not consistently associate…

Genotype5' Flanking RegionCell Survival5' flanking regionMinisatellite RepeatsBiologyGene Expression Regulation EnzymologicGenotypeGeneticsCYP2E1 gene polymorphismTumor Cells CulturedHumansGeneHepatocellular carcinoma cell lines; CYP2E1 gene polymorphisms; DNA methylation; 5-Azacytidine; Ethanol;GeneticsPolymorphism GeneticEthanolLiver cellHaplotype5-AzacytidineCytochrome P-450 CYP2E1General MedicineMethylationHep G2 CellsHepatocellular carcinoma cell lineDNA MethylationMolecular biologySettore BIO/18 - GeneticaDNA methylationAzacitidineRestriction fragment length polymorphismPolymorphism Restriction Fragment Length
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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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