Search results for "2A"

showing 10 items of 282 documents

Preliminary in vivo and ex vivo evaluation of the 5-HT2A imaging probe [18F]MH.MZ

2009

Abstract Introduction The 5-HT 2A receptor is one of the most interesting targets within the serotonergic system because it is involved in a number of important physiological processes and diseases. Methods [ 18 F]MH.MZ, a 5-HT 2A antagonistic receptor ligand, is labeled by 18 F-fluoroalkylation of the corresponding desmethyl analogue MDL 105725 with 2-[ 18 F]fluoroethyltosylate ([ 18 F]FETos). In vitro binding experiments were performed to test selectivity toward a broad spectrum of neuroreceptors by radioligand binding assays. Moreover, first micro-positron emission tomography (μPET) experiments, ex vivo organ biodistribution, blood cell and protein binding and brain metabolism studies of…

MaleCancer ResearchBiodistributionPharmacologychemistry.chemical_compoundPiperidinesIn vivoAnimalsHumansReceptor Serotonin 5-HT2ATissue DistributionRadiology Nuclear Medicine and imagingReceptor5-HT receptorBrainBinding potentialLigand (biochemistry)RatsFluorobenzenesRadioactivitychemistryPositron-Emission TomographyAltanserinBiophysicsAutoradiographyMolecular MedicineEx vivoNuclear Medicine and Biology
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation.

2014

The Ewing sarcoma family of tumors (EFT) is a group of highly malignant small round blue cell tumors occurring in children and young adults. We report here the largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines). Using a combination of whole genome sequencing and targeted sequencing approaches, we discover that EFT has a very low mutational burden (0.15 mutations/Mb) but frequent deleterious mutations in the cohesin complex subunit STAG2 (21.5% tumors, 44.4% cell lines), homozygous deletion of CDKN2A (13.8% and 50%) and mutations of TP53 (6.2% and 71.9%). We additionally note an increased prevalence of the BRCA2 K3326X polymorphism in EFT patient samples (7.3%) compared …

MaleCancer ResearchCell Cycle Proteinsmedicine.disease_causeFusion geneCDKN2AMedicine and Health Sciences2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)CancerPediatricMutationTissue microarrayTumorGenomeSarcomasHigh-Throughput Nucleotide SequencingAntigens NuclearSarcomaNeoplasm ProteinsOncologyChild PreschoolFemaleSarcomaResearch ArticleBiotechnologyHumanAdultPediatric Research Initiativelcsh:QH426-470Cohesin complexAdolescentPediatric CancerEwing SarcomaSarcoma EwingBiologyDisease-Free SurvivalFrameshift mutationCell LineGermline mutationRare DiseasesCell Line TumorEwingCancer GeneticsmedicineGeneticsHumansNuclearGenetic TestingAntigensPreschoolMolecular BiologyEcology Evolution Behavior and SystematicsGenome HumanHuman GenomeBiology and Life SciencesCancers and NeoplasmsInfantmedicine.diseaselcsh:GeneticsOrphan DrugMutationCancer researchGene DeletionDevelopmental Biology
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18F-labeling and evaluation of novel MDL 100907 derivatives as potential 5-HT2A antagonists for molecular imaging.

2009

Abstract Introduction The serotonergic system, especially the 5-HT2A receptor, is involved in various diseases and conditions. It is a very interesting target for medicinal applications. Methods Two novel 5-HT2A tracers, namely, [ 18 F]DD-1 and the enantiomeric pure ( R )-[ 18 F]MH.MZ, were radiolabeled by 18 F-fluoroalkylation of the corresponding desmethyl analogue. In vitro binding autoradiography on rat brain slices was performed to test the affinity and selectivity of these tracers. Moreover, first μPET experiments of ( R )-[ 18 F]MH.MZ were carried out in Sprague-Dawley rats. Results [ 18 F]DD-1 ( K i =3.23 nM) and ( R )-[ 18 F]MH.MZ ( K i =0.72 nM) were 18 F-fluoroalkylated by the se…

MaleCancer ResearchFluorine RadioisotopesStereochemistryRats Sprague-DawleyPiperidinesAnimalsRadiology Nuclear Medicine and imagingReceptor Serotonin 5-HT2ARadioactive TracersRadiochemistryChemistrySynthonBinding potentialDesmethylCortex (botany)Molecular ImagingRatsFluorobenzenesPositron-Emission TomographySerotonin 5-HT2 Receptor AntagonistsMolecular MedicineAutoradiographySpecific activitySteady state (chemistry)EnantiomerSelectivityNuclear medicine and biology
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Detection and clinical implications of a novel BCR-ABL1 E12A2 insertion/deletion in a CML patient expressing the E13A2 isoform

2019

Background/Aim: The Philadelphia chromosome is the most frequent cytogenetic abnormality in chronic myelogenous (CML). More than 95% of CML patients are diagnosed with the e13a2 or e14a2 BCR-ABL1 fusion transcripts while, in about 1% of these individuals, the break generates the e1a2 rearrangement. Furthermore, about 5% of CML patients are diagnosed with rare BCR-ABL1 fusion transcripts, such as e19a2, e8a2, e13a3, e14a3, e1a3 and e6a2. However, there is limited evidence concerning the clinical and prognostic implications of these infrequent oncogenic variants for CML patients receiving tyrosine kinase inhibitors (TKIs). Case Report: We describe a novel atypical e12a2 insertion/deletion (In…

MaleCancer Researchbcr-ablFusion Proteins bcr-ablBCR-ABL1; CML; E12a2; E13a2; Nilotinib; Ponatinib; TKIs; Antineoplastic Combined Chemotherapy Protocols; Fusion Proteins bcr-abl; Humans; INDEL Mutation; Imidazoles; Leukemia Myelogenous Chronic BCR-ABL Positive; Male; Middle Aged; Protein Isoforms; Pyridazines; Pyrimidines; Treatment Outcomechemistry.chemical_compoundExon0302 clinical medicineINDEL Mutationhemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsProtein IsoformsChronicCMLLeukemiaPonatinibImidazolesGeneral MedicineMiddle AgedTKIPyridazinesTreatment OutcomeOncology030220 oncology & carcinogenesisPonatinibPyridazineTyrosine kinaseINDEL MutationE13a2Humanmedicine.drugPhiladelphia chromosome03 medical and health sciencesMyelogenousLeukemia Myelogenous Chronic BCR-ABL PositivemedicineHumansImidazoleAntineoplastic Combined Chemotherapy Protocolbusiness.industryBreakpointProtein IsoformFusion Proteinsmedicine.diseaseNilotinibBCR-ABL1PyrimidinesPyrimidinechemistryNilotinibTKIsCancer researchBCR-ABL PositivebusinessE12a2Myelogenous
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Loss of histone macroH2A1 in hepatocellular carcinoma cells promotes paracrine-mediated chemoresistance and CD4

2019

Rationale: Loss of histone macroH2A1 induces appearance of cancer stem cells (CSCs)-like cells in hepatocellular carcinoma (HCC). How CSCs interact with the tumor microenvironment and the adaptive immune system is unclear. Methods: We screened aggressive human HCC for macroH2A1 and CD44 CSC marker expression. We also knocked down (KD) macroH2A1 in HCC cells, and performed integrated transcriptomic and secretomic analyses. Results: Human HCC showed low macroH2A1 and high CD44 expression compared to control tissues. MacroH2A1 KD CSC-like cells transferred paracrinally their chemoresistant properties to parental HCC cells. MacroH2A1 KD conditioned media transcriptionally reprogrammed parental …

MaleCarcinoma HepatocellularT-Lymphocytes RegulatoryHistonesadaptive immune systemCell Line TumorParacrine CommunicationTumor MicroenvironmentHumansMetabolomicschemoresistance.neoplasmsLiver Neoplasmshistone macroH2A1Interleukin-2 Receptor alpha SubunitForkhead Transcription Factorshepatocellular carcinomaMiddle Ageddigestive system diseasesGene Expression Regulation NeoplasticHyaluronan ReceptorsDrug Resistance NeoplasmGene Knockdown TechniquesNeoplastic Stem CellsGlycolysisResearch PaperTheranostics
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Negative regulation of diacylglycerol kinase θ mediates adenosine-dependent hepatocyte preconditioning

2010

In liver ischemic preconditioning (IP), stimulation of adenosine A2a receptors (A2aR) prevents ischemia/reperfusion injury by promoting diacylglycerol-mediated activation of protein kinase C (PKC). By concerting diacylglycerol to phosphatidic acid, diacylglycerol kinases (DGKs) act as terminator of diacylglycerol signalling. This study investigates the role of DGK in the development of hepatocyte IP. DGK activity and cell viability were evaluated in isolated rat hepatocytes preconditioned by 10 min hypoxia followed by 10 min re-oxygenation or by the treatment with the A2aR agonist, CGS21680, and subsequently exposed to prolonged hypoxia. We observed that after IP or A2aR activation, a decre…

MaleDiacylglycerol Kinasemedicine.medical_specialtyAdenosineReceptor Adenosine A2Ap38 mitogen-activated protein kinasesBiologyQuinazolinonechemistry.chemical_compoundPiperidinecytoprotectionPiperidinesDownregulation and upregulationDiacylglycerol kinase thetaInternal medicinemedicineEnzyme Inhibitorhepatocytes adenosine RhoA hypoxia cytoprotectionAnimalsHepatocyteEnzyme InhibitorsRats WistarMolecular BiologyCells CulturedProtein kinase CQuinazolinonesDiacylglycerol kinaseCell DeathAnimalhypoxiaKinaseReceptors Purinergic P1RhoACell BiologyPhosphatidic acidAdenosineCell HypoxiaRatsCell biologyEndocrinologychemistryHepatocytesRatrhoA GTP-Binding Proteinmedicine.drugCell Death & Differentiation
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Alternating Hemiplegia of Childhood: neurological comorbidities and intrafamilial variability.

2022

Abstract Background Alternating of Childhood (AHC) is an uncommon and complex disorder characterized by age of onset before 18 months with recurrent hemiplegia of one or either sides of the body or quadriplegia. The disorder is mainly caused by mutations in ATP1A3 gene, and to a lesser extent in ATP1A2 gene. In AHC neurological co-morbidities are various and frequently reported including developmental delay, epilepsy, tonic or dystonic spells, nystagmus,autonomic manifestations with intrafamilial variability. Case presentation Clinical and genetic findings of a couple of twins (Family 1: Case 1 and Case 2) and a couple of siblings (Family 2: Case 3 and Case 4) coming from two different Ital…

MaleEpilepsyAlternating hemiplegia of childhood (AHC)Alternating hemiplegia of childhood (AHC) Case report Comorbidities Epilepsy GRIN2AMutation MissenseInfantHemiplegiaNeurology Behaviour and DevelopmentGRIN2AComorbiditiesCase reportMutationHumansSodium-Potassium-Exchanging ATPaseChildItalian journal of pediatrics
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Exploring by whole exome sequencing patients with initial diagnosis of Rubinstein-Taybi syndrome: the interconnections of epigenetic machinery disord…

2019

Rubinstein–Taybi syndrome (RSTS) is an autosomal-dominant neurodevelopmental disease affecting 1:125,000 newborns characterized by intellectual disability, growth retardation, facial dysmorphisms and skeletal abnormalities. RSTS is caused by mutations in genes encoding for writers of the epigenetic machinery: CREBBP (~ 60%) or its homologous EP300 (~ 10%). No causative mutation is identified in up to 30% of patients. We performed whole-exome sequencing (WES) on eight RSTS-like individuals who had normal high-resolution array CGH testing and were CREBBP- and EP300-mutation -negative, to identify the molecular cause. In four cases, we identified putatively causal variants in three genes (ASXL…

MaleGenetic Association StudieCompound heterozygosityWhole Exome SequencingArticleEpigenesis Genetic03 medical and health scienceswhole exome sequencing Rubinstein–Taybi syndrome epigenetic mutationsExome SequencingGeneticsmedicineHumansEpigeneticsEP300ChildGenetics (clinical)Exome sequencingGenetic Association Studies030304 developmental biologyGeneticsRubinstein-Taybi Syndrome0303 health sciencesComparative Genomic HybridizationbiologyRubinstein–Taybi syndrome030305 genetics & heredityInfant NewbornFaciesInfantmedicine.diseaseFacieCREB-Binding ProteinHuman geneticsRSTSKMT2APhenotypeChild PreschoolMutationbiology.proteinNeurodegenerative disordersFemaleHaploinsufficiencyE1A-Associated p300 ProteinHumanHuman genetics
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Add-on peginterferon alfa-2a to nucleos(t)ide analogue therapy for Caucasian patients with hepatitis B ‘e’ antigen-negative chronic hepatitis B genot…

2019

Nucleos(t)ide analogues (NAs) and peginterferon have complementary effects in chronic hepatitis B, but it is unclear whether combination therapy improves responses in genotype D-infected patients. We conducted an open-label study of peginterferon alfa-2a 180 μg/week added to ongoing NA therapy in hepatitis B e antigen (HBeAg)-negative, genotype D-infected patients with HBV DNA <20 IU/mL. The primary endpoint was proportion of patients with ≥50% decline in serum HBsAg by the end of the 48-week add-on phase. Seventy patients received treatment, 11 were withdrawn at week 24 for no decrease in HBsAg, and 14 withdrew for other reasons. Response rate (per-protocol population) was 67.4% (29/43) at…

MaleHBsAgGastroenterologyPolyethylene Glycolschronic hepatitis B; HBeAg-negative; nucleos(t)ide analogues; peginterferon; treatment; Hepatology; Infectious Diseases; Virology0302 clinical medicineInterferonGenotypeHBVHepatitis B e Antigenspeginterferonchronic hepatitis b; hbeag-negative; nucleos(t)ide analogues; peginterferon; treatment; adult; antiviral agents; drug administration schedule; drug therapy combination; female; genotype; hepatitis b e antigens; hepatitis b virus; hepatitis b chronic; humans; interferon-alpha; male; middle aged; nucleosides; polyethylene glycols; recombinant proteins; treatment outcomeeducation.field_of_studytreatmentnucleos(t)ide analoguesvirus diseasesNucleosidesMiddle AgedRecombinant ProteinsTreatment OutcomeInfectious Diseasesnucleos(t)ide analogueHBeAg030220 oncology & carcinogenesisDrug Therapy CombinationFemale030211 gastroenterology & hepatologyPeginterferon alfa-2amedicine.drugAdultHepatitis B virusmedicine.medical_specialtyGenotypeCombination therapyPopulationHBeAg-negativeInfectious DiseaseHBeAg-negative; chronic hepatitis B; nucleos(t)ide analogues; peginterferon; treatmentchronic hepatitis B; HBeAg-negative; nucleos(t)ide analogues; peginterferon; treatmentAntiviral AgentsDrug Administration Schedule03 medical and health sciencesHepatitis B ChronicInternal medicineVirologymedicineHumanschronic hepatitis BeducationHepatologybusiness.industryInterferon-alphaConfidence intervalbusiness
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Sequence variants at CHRNB3-CHRNA6 and CYP2A6 affect smoking behavior

2010

Contains fulltext : 89305.pdf (Publisher’s version ) (Closed access) Smoking is a common risk factor for many diseases. We conducted genome-wide association meta-analyses for the number of cigarettes smoked per day (CPD) in smokers (n = 31,266) and smoking initiation (n = 46,481) using samples from the ENGAGE Consortium. In a second stage, we tested selected SNPs with in silico replication in the Tobacco and Genetics (TAG) and Glaxo Smith Kline (Ox-GSK) consortia cohorts (n = 45,691 smokers) and assessed some of those in a third sample of European ancestry (n = 9,040). Variants in three genomic regions associated with CPD (P < 5 x 10(-8)), including previously identified SNPs at 15q25 repre…

MaleNetherlands Twin Register (NTR)Lung NeoplasmsSingle-nucleotide polymorphismGenome-wide association studyAetiology screening and detection [ONCOL 5]Receptors NicotinicGenetic analysisArticleMolecular epidemiology [NCEBP 1]Cohort Studies03 medical and health sciences0302 clinical medicineSDG 3 - Good Health and Well-beingOdds RatioGeneticsmedicine/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_HumansCYP2A6Lung cancerAlleles030304 developmental biologyGenetics0303 health sciencesbiologyCHRNA6CHRNA5Hormonal regulation [IGMD 6]SmokingGenetic VariationGenomicsTobacco Use DisorderOdds ratiomedicine.disease3. Good healthPhenotypeEvaluation of complex medical interventions [NCEBP 2]genome-wide association nicotinic acetylcholine-receptors lung-cancer susceptibility locus molecular-genetics heavy smoking adult twins dependence genes snpsbiology.protein/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleAryl Hydrocarbon Hydroxylases030217 neurology & neurosurgeryGenome-Wide Association Study
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