Search results for "Decitabine"

showing 10 items of 20 documents

Hypomethylating agents in relapsed and refractory AML: outcomes and their predictors in a large international patient cohort.

2018

Although hypomethylating agents (HMAs) are frequently used in the frontline treatment of older acute myeloid leukemia (AML) patients, little is known about their effectiveness in relapsed or primary treatment–refractory (RR)-AML. Using an international multicenter retrospective database, we studied the effectiveness of HMAs in RR-AML and evaluated for predictors of response and overall survival (OS). A total of 655 patients from 12 centers received azacitidine (57%) or decitabine (43%), including 290 refractory (44%) and 365 relapsed (56%) patients. Median age at diagnosis was 65 years. Best response to HMAs was complete remission (CR; 11%) or CR with incomplete count recovery (CRi; 5.3%). …

0301 basic medicineAdultmedicine.medical_specialtyAntimetabolites AntineoplasticMyeloidAdolescentDatabases FactualAzacitidineDecitabineSalvage therapyDecitabineCohort Studies03 medical and health sciencesYoung Adult0302 clinical medicineRefractoryInternal medicinehemic and lymphatic diseasesmedicineHumansSurvival analysisAgedRetrospective StudiesAged 80 and overSalvage TherapyMyeloid Neoplasiabusiness.industryRemission InductionRetrospective cohort studyHematologyDNA MethylationMiddle Agedmedicine.diseasePrognosisSurvival AnalysisLeukemiaLeukemia Myeloid Acute030104 developmental biologymedicine.anatomical_structureTreatment Outcome030220 oncology & carcinogenesisAdolescent; Adult; Aged; Aged 80 and over; Antimetabolites Antineoplastic; Cohort Studies; DNA Methylation; Databases Factual; Decitabine; Humans; Leukemia Myeloid Acute; Middle Aged; Prognosis; Remission Induction; Retrospective Studies; Salvage Therapy; Survival Analysis; Treatment Outcome; Young Adultbusinessmedicine.drug
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DNA demethylation caused By 5-Aza-2'-Deoxycytidine induces mitotic alterations and aneuploidy

2016

Aneuploidy, the unbalanced number of chromosomes in a cell, is considered a prevalent form of genetic instability and is largely acknowledged as a condition implicated in tumorigenesis. Epigenetic alterations like DNA hypomethylation have been correlated with cancer initiation/progression. Furthermore, a growing body of evidence suggests the involvement of epigenome-wide disruption as a cause of global DNA hypomethylation in aneuploidy generation. Here, we report that the DNA hypomethylating drug 5-aza-2′-deoxycytidine (DAC), affects the correct ploidy of nearly diploid HCT-116 human cells by altering the methylation pattern of the chromosomes. Specifically, we show that a DAC-induced reduc…

0301 basic medicineAntimetabolites Antineoplastic5-aza-2'-deoxycytidine (DAC); Aneuploidy; Chromosome methylation pattern; Chromosome Section; DNA demethylation; OncologyBlotting WesternAneuploidyMitosisApoptosisBiologymedicine.disease_causeDecitabineReal-Time Polymerase Chain ReactionChromosome Section03 medical and health scienceschromosome methylation patternChromosome instabilitymedicineTumor Cells CulturedHumansEpigeneticsaneuploidyRNA Messenger5-aza-2′-deoxycytidine (DAC)Cell ProliferationGeneticsChromosome AberrationsPloidiesReverse Transcriptase Polymerase Chain ReactionDNA Methylationmedicine.disease5-aza-2'-deoxycytidine (DAC)Gene Expression Regulation NeoplasticResearch Paper: ChromosomeSettore BIO/18 - Genetica030104 developmental biologyDNA demethylationOncologyMicroscopy FluorescenceDNA methylationColonic NeoplasmsCytogenetic AnalysisCancer researchDNA demethylationAzacitidinePloidyCarcinogenesisDNA hypomethylation
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Efficacy and epigenetic interactions of novel DNA hypomethylating agent guadecitabine (SGI-110) in preclinical models of hepatocellular carcinoma.

2016

ABSTRACT Hepatocellular carcinoma (HCC) is a deadly malignancy characterized at the epigenetic level by global DNA hypomethylation and focal hypermethylation on the promoter of tumor suppressor genes. In most cases it develops on a background of liver steatohepatitis, fibrosis, and cirrhosis. Guadecitabine (SGI-110) is a second-generation hypomethylating agent, which inhibits DNA methyltransferases. Guadecitabine is formulated as a dinucleotide of decitabine and deoxyguanosine that is resistant to cytidine deaminase (CDA) degradation and results in prolonged in vivo exposure to decitabine following small volume subcutaneous administration of guadecitabine. Here we found that guadecitabine i…

0301 basic medicineCancer ResearchMethyltransferasesteatohepatitisDecitabineBiologyDecitabineDNA methylation Decitabine guadecitabine hepatocellular carcinoma (HCC) histone macroH2A1 steatohepatitishepatocellular carcinoma (HCC)03 medical and health scienceschemistry.chemical_compoundCDKN2AmedicineEpigeneticsMolecular BiologyneoplasmsDNA methylationGuadecitabineguadecitabinehistone macroH2A1steatohepatitidigestive system diseases3. Good healthDemethylating agent030104 developmental biologychemistryHypomethylating agentDNA methylationCancer researchResearch Papermedicine.drug
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The SCO1731 methyltransferase modulates actinorhodin production and morphological differentiation of Streptomyces coelicolor A3(2)

2018

AbstractStreptomyces coelicolor is a Gram-positive microorganism often used as a model of physiological and morphological differentiation in streptomycetes, prolific producers of secondary metabolites with important biological activities. In the present study, we analysed Streptomyces coelicolor growth and differentiation in the presence of the hypo-methylating agent 5′-aza-2′-deoxycytidine (5-aza-dC) in order to investigate whether cytosine methylation has a role in differentiation. We found that cytosine demethylation caused a delay in spore germination, aerial mycelium development, sporulation, as well as a massive impairment of actinorhodin production. Thus, we searched for putative DNA…

0301 basic medicineScienceMutantAnthraquinonesStreptomyces coelicolorDecitabineSettore BIO/19 - Microbiologia GeneraleDNA methyltransferaseArticleActinorhodin03 medical and health scienceschemistry.chemical_compoundBacterial ProteinsSpore germinationSpores BacterialRegulation of gene expressionMultidisciplinaryMyceliumbiologyStreptomyces coelicolorfungiQRActinorhodin ProductionCell DifferentiationGene Expression Regulation BacterialMethyltransferasesbiology.organism_classificationTn5 Mutant Strains030104 developmental biologychemistryBiochemistryHypomethylating AgentsStreptomyces coelicolor bacterial differentiation epigenetic cytosine methylationDNA methylationMedicineCytosineCytosine Methylation
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The Use of Hypomethylating Agents (HMAs) in Patients with Relapsed and Refractory Acute Myeloid Leukemia (RR-AML): Clinical Outcomes and Their Predic…

2016

Abstract Introduction: Patients with RR-AML, particularly older adults, have dismal outcomes and limited therapy options. Given low response rates and high toxicity with salvage intensive chemotherapy, and frequent ineligibility for allogeneic stem cell transplantation (alloSCT), many patients are treated with HMAs. Robust data regarding use of HMAs in AML predominates in the frontline setting, while their use in RR-AML has limited supportive data. Here wesought to analyze theoutcomes and their predictors in patients with RR-AML treated with HMAs. Methods:We collected data, spanning a period from 2006 to 2016, from 7 centers in the United States and 4 centers in Europe regarding patients tr…

0301 basic medicinemedicine.medical_specialtybusiness.industryImmunologyComplete remissionDecitabineCell BiologyHematologyBiochemistryTransplantationClinical trial03 medical and health sciences030104 developmental biology0302 clinical medicineRefractoryInterquartile range030220 oncology & carcinogenesisInternal medicineCohortmedicineIn patientbusinessmedicine.drugBlood
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Blastic plasmacytoid dendritic cell neoplasm: genomics mark epigenetic dysregulation as a primary therapeutic target

2018

Blastic Plasmacytoid Dendritic Cell Neoplasm is a rare and aggressive hematological malignancy currently lacking an effective therapy. To possibly identify genetic alterations useful for a new treatment design, we analyzed by whole-exome sequencing fourteen Blastic Plasmacytoid Dendritic Cell Neoplasm patients and the patient-derived CAL-1 cell line. The functional enrichment analysis of mutational data reported the epigenetic regulatory program as the most significantly undermined (P<.0001). In particular, twenty-five epigenetic-modifiers were found mutated (e.g., ASXL1, TET2, SUZ12, ARID1A, PHF2, CHD8); ASXL1 was the most frequently affected (28.6% of cases). To evaluate the impact of …

Acute Myeloid LeukemiaBlastic plasmacytoid dendritic cell neoplasm epigenetic mutationsSkin NeoplasmsAzacitidineDecitabinePlasmacytoid dendritic cellGene mutationBiologyDecitabineBPDCNArticleEpigenesis Genetic03 medical and health sciences0302 clinical medicineHistone methylation5’-Azacytidine; Acute Myeloid Leukemia; BPDCN; Decitabine; WESmedicineHumansEpigeneticsExome sequencingRegulation of gene expressionMyeloproliferative DisordersDendritic CellsGenomicsHematology5 -AzacytidineMyeloid Neoplasms5’-AzacytidineCancer researchWES030215 immunologymedicine.drugHaematologica
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53 LUSPATERCEPT INCREASES HEMOGLOBIN AND REDUCES TRANSFUSION BURDEN IN PATIENTS WITH LOW OR INTERMEDIATE-1 RISK MYELODYSPLASTIC SYNDROMES (MDS): PREL…

2015

Introduction. ACE-536, a recombinant fusion protein containing modified activin receptor type IIB and IgG Fc, is being developed for the treatment of anemias due to ineffective erythropoiesis, such as myelodysplastic syndromes (MDS). Patients with MDS often have elevated levels of erythropoietin (EPO) and may be non-responsive or refractory to erythropoiesis-stimulating agents (ESAs). MDS patients have also been shown to have increased serum GDF11 levels (Suragani R et al., Nature Medicine 2014) and increased Smad 2/3 signaling in the bone marrow (Zhou L et al., Blood 2008). ACE-536 binds to ligands in the TGF-s superfamily, including GDF11, inhibits Smad 2/3 signaling, and promotes late-st…

Cancer Researchmedicine.medical_specialtybusiness.industryAnemiaMyelodysplastic syndromesPhases of clinical researchDecitabineHematologymedicine.diseaseGastroenterologyGranulocyte colony-stimulating factorOncologyErythropoietinInternal medicinemedicineAbsolute neutrophil countbusinessIntensive care medicineLenalidomidemedicine.drugLeukemia Research
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Differential Promotion of Glutamate Transporter Expression and Function by Glucocorticoids in Astrocytes from Various Brain Regions

2005

Steroids that activate glucocorticoid receptors (GRs) and mineralocorticoid receptors have important regulatory effects on neural development, plasticity, and the body's stress response. Here, we investigated the role of corticosteroids in regulating the expression of the glial glutamate transporters glial glutamate transporter-1 (GLT-1) and glutamate-aspartate transporter (GLAST) in rat primary astrocytes. The synthetic glucocorticoid dexamethasone provoked a marked increase of GLT-1 transcription and protein levels in cortical astrocytes, whereas GLAST expression remained unaffected. Up-regulation of GLT-1 expression was accompanied by an enhanced glutamate uptake, which could be blocked …

Central Nervous SystemTime FactorsAmino Acid Transport System X-AGLigandsBiochemistryDexamethasoneRats Sprague-Dawleychemistry.chemical_compoundGlucocorticoid receptorMineralocorticoid receptorAdrenal Cortex HormonesCorticosteroneCerebellumGene expressionLuciferasesReceptorDNA Modification MethylasesKainic AcidReverse Transcriptase Polymerase Chain ReactionGlutamate receptorBrainImmunohistochemistryUp-RegulationMifepristoneAzacitidineNeurogliaGlucocorticoidmedicine.drugmedicine.medical_specialtymedicine.drug_classBlotting WesternDetergentsBiologyDecitabineTransfectionMembrane MicrodomainsInternal medicinemedicineAnimalsGlucocorticoidsMolecular BiologyDNA PrimersFluorescent DyesDose-Response Relationship DrugCell BiologyDNA MethylationRatsReceptors MineralocorticoidEndocrinologychemistryMineralocorticoidAstrocytesCorticosteroneJournal of Biological Chemistry
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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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Reactivation of SNURF-SNRPN gene by DNA Methyltransferase inhibitors in a Prader-Willi lymphoblastoid cell line.

2014

ECGCDNMT1DNMTDNA Methyltransferase inhibitorRG108ZebularineDecitabinePrader-Willi SyndromeSNURF-SNRPN geneSettore MED/13 - Endocrinologia
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