Search results for "Histone Deacetylase Inhibitors"

showing 10 items of 55 documents

Inhibition of histone deacetylation rescues phenotype in a mouse model of Birk-Barel intellectual disability syndrome

2020

Mutations in the actively expressed, maternal allele of the imprinted KCNK9 gene cause Birk-Barel intellectual disability syndrome (BBIDS). Using a BBIDS mouse model, we identify here a partial rescue of the BBIDS-like behavioral and neuronal phenotypes mediated via residual expression from the paternal Kcnk9 (Kcnk9pat) allele. We further demonstrate that the second-generation HDAC inhibitor CI-994 induces enhanced expression from the paternally silenced Kcnk9 allele and leads to a full rescue of the behavioral phenotype suggesting CI-994 as a promising molecule for BBIDS therapy. Thus, these findings suggest a potential approach to improve cognitive dysfunction in a mouse model of an impri…

Male0301 basic medicinePotassium Channels[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyGeneral Physics and AstronomyDiseasePhenylenediamines[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyCraniofacial AbnormalitiesHistonesMice0302 clinical medicineIntellectual disabilityImprinting (psychology)lcsh:ScienceMice KnockoutGeneticsMultidisciplinaryBehavior AnimalbiologyNeurodevelopmental disordersDevelopmental disordersQBrainPhenotypeUp-RegulationPhenotypeHistoneGene Knockdown TechniquesBenzamidesMuscle HypotoniaFemaleLocus CoeruleusEpigeneticsScienceArticleGeneral Biochemistry Genetics and Molecular BiologyGenomic Imprinting03 medical and health sciencesDevelopmental disorders ; Neurodevelopmental disorders ; EpigeneticsIntellectual DisabilitymedicineAnimalsHumansddc:610AlleleGene[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Chemistrymedicine.diseaseHistone Deacetylase InhibitorsMice Inbred C57BLDisease Models Animal030104 developmental biologyAcetylationMutationbiology.proteinlcsh:Q030217 neurology & neurosurgery
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Phase ia/ii, two-arm, open-label, dose-escalation study of oral panobinostat administered via two dosing schedules in patients with advanced hematolo…

2013

Panobinostat is a potent oral pandeacetylase inhibitor that leads to acetylation of intracellular proteins, inhibits cellular proliferation and induces apoptosis in leukemic cell lines. A phase Ia/II study was designed to determine the maximum-tolerated dose (MTD) of daily panobinostat, administered on two schedules: three times a week every week or every other week on a 28-day treatment cycle in patients with advanced hematologic malignancies. The criteria for hematologic dose-limiting toxicities differed between patients with indications associated with severe cytopenias at baseline (leukemia and myeloid disorders) and those less commonly associated with baseline cytopenias (lymphoma and …

MaleOncologyCancer ResearchIndolesMyeloidhodgkin lymphomahydroxamic acidAdministration Oralresponse criteriaPharmacologyHydroxamic Acidst-cell lymphomaHistoneschemistry.chemical_compoundhemic and lymphatic diseasesAged 80 and overHematologyMiddle AgedLeukemiaTreatment Outcomemedicine.anatomical_structuremyelomaOncologyvorinostatHematologic NeoplasmsFemaleAdultmedicine.medical_specialtypanobinostatrefractory multiple-myelomaMaximum Tolerated DoseAntineoplastic AgentsmyelofibrosisNeutropeniahistone deacetylase inhibitorsmyelodysplastic disordersDrug Administration ScheduleYoung AdultInternal medicinePanobinostatmedicineHumansIn patientAdverse effectMyelofibrosisAgedNeoplasm Staginginternational-working-groupacetylationbusiness.industrymedicine.diseaseLymphomachemistryhistone deacetylasehypoxia-inducible factor-1-alphalbh589business
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A Phase II Study of the Histone Deacetylase Inhibitor Panobinostat (LBH589) in Pretreated Patients with Small-Cell Lung Cancer

2013

Background: In vitro data suggest that panobinostat (LBH589), a pan-deacetylase inhibitor, may add therapeutic benefit in the treatment of small-cell lung cancer (SCLC) with regression of tumors. Methods: This multicenter, nonrandomized phase 2 trial was designed to evaluate antitumor activity of LBH589 in patients with previously treated SCLC. Patients received LBH589 administered intravenously at a dose of 20 mg/mq (days 1–8) every 21 days. Results: A total of 21 patients with extensive- or limited-stage SCLC were enrolled. Patients received a median of two cycles (range, 1–6). LBH589 was well tolerated, and the most common toxicities were grade 1 to 2 gastrointestinal disorders (nausea 3…

MalePulmonary and Respiratory Medicinemedicine.medical_specialtyIndolesLung Neoplasmsmedicine.drug_classNauseaPhases of clinical researchAntineoplastic AgentsHydroxamic AcidsGastroenterologySmall-cell lung cancerDeacetylase inhibitor.chemistry.chemical_compoundInternal medicinePanobinostatPanobinostatmedicineHumansLung cancerAgedbusiness.industryHistone deacetylase inhibitorMiddle Agedmedicine.diseaseSmall Cell Lung CarcinomaSurgeryHistone Deacetylase InhibitorsLBH58Clinical trialDiarrheaOncologychemistryVomitingFemalePhase II trialmedicine.symptombusinessJournal of Thoracic Oncology
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Changes in histone acetylation in the prefrontal cortex of ethanol-exposed adolescent rats are associated with ethanol-induced place conditioning

2012

Alcohol drinking during adolescence can induce long-lasting effects on the motivation to consume alcohol. Abnormal plasticity in reward-related processes might contribute to the vulnerability of adolescents to drug addiction. We have shown that binge-like ethanol treatment in adolescent rats induces alterations in the dopaminergic system and causes histone modifications in brain reward regions. Considering that histone acetylation regulates transcriptional activity and contributes to drug-induced alterations in gene expression and behavior, we addressed the hypothesis that ethanol is capable of inducing transcriptional changes by histone modifications in specific gene promoters in adolescen…

Malemedicine.medical_specialtyPrefrontal CortexHDAC inhibitionChromatin remodelingHistonesCellular and Molecular Neurosciencechemistry.chemical_compoundInternal medicineConditioning PsychologicalmedicineAnimalsEpigeneticsRats WistarConditioned place aversionPharmacologyEthanolbiologyHistone modificationsAge FactorsAcetylationSodium butyrateRatsAdolescenceHistone Deacetylase InhibitorsHistoneEndocrinologychemistryBiochemistryAcetylationbiology.proteinBrain stimulation rewardBinge-like ethanol treatmentHistone deacetylaseFOSBNeuropharmacology
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Role of Redox Signaling, Protein Phosphatases and Histone Acetylation in the Inflammatory Cascade in Acute Pancreatitis: Therapeutic Implications

2010

Acute pancreatitis starts as a local inflammation of the pancreatic tissue but often leads to the systemic inflammatory response syndrome and death by multiple organ failure. Pro-inflammatory cytokines, particularly TNF-alpha and Il-1beta, play a pivotal role together with oxidative stress and glutathione depletion in the inflammatory response in this disease. Most inflammatory mediators act through mitogen activated protein kinases and nuclear factor kB. Nevertheless, elucidation of the precise mechanisms involved in activation and attenuation phases of the inflammatory cascade is still underway. Redox signaling mediated by inactivation of protein phosphatases and histone acetylation trigg…

Phosphodiesterase InhibitorsImmunologyPhosphataseBiologyHistonesDual-specificity phosphatasePhosphoprotein PhosphatasesHumansImmunology and AllergyPancreasHistone AcetyltransferasesInflammationPharmacologyHistone AcetyltransferasesKinaseAcetylationGeneral MedicineProtein phosphatase 2ChromatinCell biologyHistone Deacetylase InhibitorsHistonePancreatitisBiochemistryAcetylationAcute Diseasebiology.proteinSignal transductionOxidation-ReductionSignal TransductionInflammation & Allergy - Drug Targets
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Image-Guided Synthesis Reveals Potent Blood-Brain Barrier Permeable Histone Deacetylase Inhibitors

2014

Recent studies have revealed that several histone deacetylase (HDAC) inhibitors, which are used to study/treat brain diseases, show low blood-brain barrier (BBB) penetration. In addition to low HDAC potency and selectivity observed, poor brain penetrance may account for the high doses needed to achieve therapeutic efficacy. Here we report the development and evaluation of highly potent and blood-brain barrier permeable HDAC inhibitors for CNS applications based on an image-guided approach involving the parallel synthesis and radiolabeling of a series of compounds based on the benzamide HDAC inhibitor, MS-275 as a template. BBB penetration was optimized by rapid carbon-11 labeling and PET im…

PhysiologyCognitive NeuroscienceHistone Deacetylase 2Vascular permeabilityHistone Deacetylase 1Blood–brain barrierBiochemistrylaw.inventionCapillary Permeabilitychemistry.chemical_compoundlawmedicineAnimalsHumansCarbon RadioisotopesBenzamideHistone deacetylase 2BrainCell BiologyGeneral MedicinePenetration (firestop)Papio anubisHDAC1Recombinant ProteinsHistone Deacetylase Inhibitorsmedicine.anatomical_structurechemistryBiochemistryBlood-Brain BarrierPositron-Emission TomographyBenzamidesRecombinant DNABiophysicsDrug EvaluationFemaleHistone deacetylaseRadiopharmaceuticals
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Combined inhibition of Bcl-2 and NFκB synergistically induces cell death in cutaneous T-cell lymphoma.

2019

Abstract Therapeutic options for cutaneous T-cell lymphoma (CTCL) are limited and curative treatment regimens are not available. Thus, new targeted and well-tolerated therapeutic approaches are urgently needed. In this respect, we have recently shown that dimethyl fumerate (DMF) inhibits NF-κB acting as a survival factor in CTCL. Similarly, inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) has been shown to induce cell death in CTCL especially when combined with histone deacetylase inhibitors. Therefore, we hypothesized that inhibition of Bcl-2 should potentiate NF-κB inhibition in a novel combination treatment of CTCL. We show that, in vitro, the Bcl-2 inhibitors ABT-199 an…

Programmed cell deathT cellImmunologyAntineoplastic AgentsApoptosisBiochemistryMicehemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansRNA Small InterferingCell ProliferationNeoplasm StagingCell DeathDose-Response Relationship Drugbusiness.industryCutaneous T-cell lymphomaNF-kappa BDrug SynergismCell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysLymphomaLymphoma T-Cell CutaneousHistone Deacetylase InhibitorsDisease Models Animalmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCancer researchRNA InterferenceHistone deacetylaseSignal transductionbusinessProtein BindingBlood
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The synergistic effect of SAHA and parthenolide in MDA-MB231 breast cancer cells

2014

Abstract: The sesquiterpene lactone Parthenolide (PN) exerted a cytotoxic effect on MDA-MB231 cells, a triple-negative breast cancer (TNBC) cell line, but its effectiveness was scarce when employed at low doses. This represents an obstacle for a therapeutic utilization of PN. In order to overcome this difficulty we associated to PN the suberoylanilide hydroxamic acid (SAHA), an histone deacetylase inhibitor. Our results show that SAHA synergistically sensitized MDA-MB231 cells to the cytotoxic effect of PN. It is noteworthy that treatment with PN alone stimulated the survival pathway Akt/mTOR and the consequent nuclear translocation of Nrf2, while treatment with SAHA alone induced autophagi…

SesquiterpenePhysiologyClinical BiochemistryDown-RegulationApoptosisBreast NeoplasmsApoptosis; Autophagy; Breast Neoplasms; Cell Line Tumor; Down-Regulation; Drug Synergism; Female; Histone Deacetylase Inhibitors; Humans; Hydroxamic Acids; NF-kappa B; Sesquiterpenes; Clinical Biochemistry; Cell Biology; Physiology; Medicine (all)Hydroxamic AcidsHydroxamic AcidSettore BIO/10 - BiochimicaCell Line TumorHistone Deacetylase InhibitorAutophagyHumansBiologyVorinostatMedicine (all)NF-kappa BApoptosiDrug SynergismCell BiologyHistone Deacetylase InhibitorsFemaleHuman medicineSesquiterpenesBreast NeoplasmHumanJournal of cellular physiology
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Epigenetic agents as an adjunct to active chemotherapy in hematological tumor cell lines

2012

Epigenetic therapy is a new promising area in cancer research that is based on the use of a series of molecules capable of affecting tumor cell growth, differentiation and death by modifying the cellular mechanisms underlying the control of gene expression. Significant enhancement of traditional anticancer drug effects has been also reported by several authors. Our recent research focused on the identification of new epigenetic agent-containing drug combinations to be employed in the therapy of leukemia. The results showed that the new combination of an histone deacetylase (HDAC) inhibitor and the ribonucleotide reductase (RR) inhibitor 3’-methyl-adenosine (3’-Me-Ado) is endowed with a sign…

Settore BIO/14 - Farmacologiaepigenetics leukemia histone deacetylase inhibitors ribonucleotide reductase inhibitors bifunctional agents
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Hepatocellular carcinoma treatment over sorafenib: epigenetics, microRNAs and microenvironment. Is there a light at the end of the tunnel?

2015

Introduction: Sorafenib is currently the only approved therapy in hepatocellular carcinoma (HCC). Alternative first- and second-line treatments are a significant unmet medical need, and several biologic agents have been tested in recent years, with poor results. Therefore, angiogenic pathways and the cytokine cascade remain possible targets in HCC. Recent studies suggest a role of epigenetic processes, associated with the initiation and development of HCC. In this field, DNA methylation, micro-RNAs (miRNAs) and tumor microenvironment cells became a possible new target for HCC treatment. Areas covered: This review explains the possible role of DNA methylation and histone deacetylase inhibito…

Settore MED/06 - Oncologia MedicaClinical BiochemistrytivantinibEpigenesis GeneticAntineoplastic Agentchemistry.chemical_compoundHistone Deacetylase InhibitorDrug DiscoveryTumor MicroenvironmentMolecular Targeted TherapyplateletmicroRNALiver Neoplasmshepatocellular carcinomaSorafenibVEGFLiver NeoplasmHepatocellular carcinomaDNA methylationMolecular MedicineepigeneticHumanmedicine.drugPhenylurea CompoundSorafenibNiacinamideCarcinoma HepatocellularAntineoplastic AgentsBiologymicroRNAmedicineAnimalsHumansEpigeneticsTivantinibPharmacologyTumor microenvironmentAnimalDrug Discovery3003 Pharmaceutical SciencePhenylurea CompoundsDNA Methylationmedicine.diseasedigestive system diseasesHistone Deacetylase InhibitorsMicroRNAschemistryDrug DesignImmunologyCancer researchHistone deacetylaseExpert opinion on therapeutic targets
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