Search results for "DELETION"

showing 10 items of 383 documents

Heterozygous HMGB1 loss-of-function variants are associated with developmental delay and microcephaly

2021

International audience; 13q12.3 microdeletion syndrome is a rare cause of syndromic intellectual disability. Identification and genetic characterization of patients with 13q12.3 microdeletion syndrome continues to expand the phenotypic spectrum associated with it. Previous studies identified four genes within the approximately 300 Kb minimal critical region including two candidate protein coding genes: KATNAL1 and HMGB1. To date, no patients carrying a sequence-level variant or a single gene deletion in HMGB1 or KATNAL1 have been described. Here we report six patients with loss-of-function variants involving HMGB1 and who had phenotypic features similar to the previously described 13q12.3 m…

Male0301 basic medicineHeterozygoteMicrocephalyAdolescentDNA Copy Number VariationsLanguage delay[SDV]Life Sciences [q-bio]KaryotypeInheritance Patternschemical and pharmacologic phenomena030105 genetics & heredityBiologydysmorphic featuresloss of function mutation03 medical and health sciencesExome SequencingIntellectual disabilityGeneticsmedicineHumansGenetic Predisposition to DiseaseHMGB1 ProteinChildGeneGenetic Association StudiesIn Situ Hybridization FluorescenceGenetics (clinical)Loss functionGeneticsHMGB1FaciesExonsdevelopmental disabilitiesMicrodeletion syndromemedicine.diseasePhenotypePhenotype030104 developmental biologyChild PreschoolMicrocephalyFemaleHaploinsufficiency
researchProduct

A new family with an SLC9A6 mutation expanding the phenotypic spectrum of Christianson syndrome

2016

Using targeted next generation sequencing, we have identified a splicing mutation (c.526-9_526-5del) in the SLC9A6 gene in a 9-year-old boy with mild intellectual disability (ID), microcephaly, and social interaction disabilities. This intronic microdeletion leads to the skipping of exon 3 and to an in-frame deletion of 26 amino acids in the TM4 domain. It segregates with cognitive impairment or learning difficulties in other members of the family. Mutations in SLC9A6 have been reported in X-linked Christianson syndrome associating severe to profound intellectual deficiency and an Angelman-like phenotype with microcephaly, absent speech, ataxia with progressive cerebellar atrophy, ophthalmo…

Male0301 basic medicineProbandMicrocephalyDNA Mutational Analysisx-chromosome inactivationSLC9A6Gene mutationexchangerEpilepsyOcular Motility Disorders0302 clinical medicineangelman-syndromeX Chromosome InactivationIntellectual disabilitymicrocephalyChild10. No inequalityGenetics (clinical)Sequence DeletionGeneticsBrainGenetic Diseases X-LinkedtoolMagnetic Resonance ImagingPedigree3. Good healthPhenotypeFemaleCerebellar atrophyChristianson syndromemedicine.symptomAdultHeterozygoteSodium-Hydrogen ExchangersAtaxiaAdolescentlearning disabilities linked mental-retardation03 medical and health sciencescerebellar atrophyIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyAngelman syndromeGeneticsmedicineHumansFamilygeneGenetic Association Studiesbusiness.industryFaciesmedicine.disease030104 developmental biologysplicing signalsMutationepilepsyAtaxiaRNA Splice Sitesbusiness030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
researchProduct

A de novo microdeletion of SEMA5A in a boy with autism spectrum disorder and intellectual disability.

2016

AbstractSemaphorins are a large family of secreted and membrane-associated proteins necessary for wiring of the brain. Semaphorin 5A (SEMA5A) acts as a bifunctional guidance cue, exerting both attractive and inhibitory effects on developing axons. Previous studies have suggested that SEMA5A could be a susceptibility gene for autism spectrum disorders (ASDs). We first identified a de novo translocation t(5;22)(p15.3;q11.21) in a patient with ASD and intellectual disability (ID). At the translocation breakpoint on chromosome 5, we observed a 861-kb deletion encompassing the end of the SEMA5A gene. We delineated the breakpoint by NGS and observed that no gene was disrupted on chromosome 22. We…

Male0301 basic medicinemedicine.medical_specialtyAutism Spectrum DisorderChromosomes Human Pair 22Translocation BreakpointNerve Tissue ProteinsSemaphorinsBiology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsBioinformaticsArticleTranslocation GeneticautismeChromosome Breakpoints03 medical and health sciencesSemaphorin[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyIntellectual Disabilitymental disordersIntellectual disabilityGeneticsmedicineHumans[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsChildGenetics (clinical)Genetics[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyNeurosciencesMembrane Proteinsmedicine.disease030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderNeurons and CognitionPaternal InheritancecerveauChromosomes Human Pair 5AutismMedical geneticsChromosome DeletionmicrodélétionhumainChromosome 22[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenetic screen
researchProduct

SARS CoV2 infection _The longevity study perspectives

2021

Graphical abstract

MaleAgingssRNA single-stranded RNARFLP restriction fragment length polymorphismHSPs heat shock proteinsReviewPTMs post-translational modificationsSevere Acute Respiratory SyndromeBiochemistryHIV-1 human immunodeficiency virus-1TNF-α tumor necrosis factor-αEC endothelial cells0302 clinical medicineFluAV influenza A virusI insertionMedicineIFN-γ interferon-γDIC disseminated intravascular coagulationPCR Polymerase Chain Reactionmedia_commonAged 80 and overLongevityRBD receptor-binding domainNeurologyLongevity modelMI myocardial infarctionNK natural killerhPIV2 human parainfluenza virus type 2media_common.quotation_subjectResearching genetic basis of resistance and potential pharmacological targetsLongevityDBP diastolic blood pressureNF-Kb nuclear transcription factor kBRANTES regulated upon activation normal T cell expressed and secretedMphi human macrophages03 medical and health sciencesCox 2 cyclooxygenase 2ORF open reading framePT prothrombin timeSettore MED/05 - Patologia ClinicaHumansMolecular BiologyInflammatory genesARDS acute respiratory distress syndromeNO nitric oxideD deletionCpGIs CpG islandsT2DM type 2 diabetes mellitusmedicine.diseaseFDP fibrin degradation products030104 developmental biologySARS CoV2 severe acute respiratory syndrome Coronavirus 2 virusImmunologyBMI body max indexItalian nonagenarians/centenariansRSV respiratory syncytial virusComplication030217 neurology & neurosurgeryMAPK mitogen-activated protein kinaseIP-10 IFN-γ -Inducible Protein 1040301 basic medicineAT1R activity of angiotensin 1 receptorsDCs dentritic cellsSSCP single strand conformation polymorphismACE/DD polymorphism of the angiotensin converting enzymeFGF21 fibroblast growth factor 21TLR4 toll-like receptor 4NAD nicotinamide adenine dinucleotideACE angiotensin-I converting enzymeAT2R activity of angiotensin 2 receptorsCOVID-19 Coronavirus disease 2019Respiratory distressACE2 angiotensin converting enzyme 2MKP-1 mitogen-activated protein kinase phosphatase-1 ()PD protease domainSNP single nucleotide polymorphismEH essential hypertensionTNFR tumor necrosis factor receptorINR international normalized ratio of the prothrombin timePAI-1 plasminogen activator inhibitor-1Ang angiotensinLPS lipopolysaccharideMCP1 monocyte chemoattractant protein-1medicine.symptomaPTT partial thromboplastin timeBiotechnologyDUSP1 dual specificity phosphatase 1Coronavirus disease 2019 (COVID-19)PC prostate cancerRAS renin-angiotensin aldosterone systemCCR5Δ32 genetic variant of chemokine receptorCOVID-19 Researching genetic basis of resistance and potential pharmacological targets Italian nonagenarians/centenarians Longevity modelAsymptomaticSARS-1 severe acute respiratory syndrome virus 1SIRT-1 Sirtuin 1Th1 t-helper lymphocyte type 1Immune systemROS reactive oxygen speciesTGF-β transforming growth factor betaET-1 endothelin-1ComputingMethodologies_COMPUTERGRAPHICSADAM-17 metallopeptidase domain 17business.industrySARS-CoV-2SBP systolic blood pressureCOVID-19HDACs histone deacetylasesComorbidityImmune Systembusiness5-LO lipoxygenase 5Ageing Research Reviews
researchProduct

Allogeneic Stem Cell Transplantation for Myelodysplastic Syndrome Patients with a 5q Deletion

2018

The deletion (5q) karyotype (del [5q]) in patients with myelodysplastic syndrome (MDS) is the most common karyotypic abnormality in de novo MDS. An increased number of blasts and additional karyotypic abnormalities (del [5q]+) are associated with a poor outcome. We analyzed the outcome of allogeneic hematopoietic cell transplants (HCT) in patients suffering from MDS with only del (5q) or del (5q)+ . A total of 162 patients, of median age 54 years (range, 9 to 73), having MDS and del (5q) abnormalities received HCT from identical siblings (n = 87) or unrelated donors (n = 75). The cumulative incidence of nonrelapse mortality and relapse incidence at 4 years was 29% (95% CI, 22 to 36) and 46%…

MaleBLOODDatabases FactualIMPACTCHROMOSOMECancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2]medicine.medical_treatment[SDV]Life Sciences [q-bio]MedizinHematopoietic stem cell transplantationPROGNOSTIC SCORING SYSTEMGastroenterology0302 clinical medicineRecurrencehemic and lymphatic diseasesMDSCumulative incidenceLENALIDOMIDEIncidenceIncidence (epidemiology)Hazard ratioHematopoietic Stem Cell TransplantationHematologyMiddle AgedAllograftsTP53 MUTATIONSEUROPEAN-SOCIETY3. Good healthSurvival Rate030220 oncology & carcinogenesisWORKING PARTYChromosomes Human Pair 5FemaleChromosome DeletionLife Sciences & BiomedicineDEL(5Q)del (5q)medicine.drugAdultmedicine.medical_specialtyImmunology3122 CancersDisease-Free SurvivalSettore MED/01 - Statistica Medica03 medical and health sciencesSex FactorsAll institutes and research themes of the Radboud University Medical CenterInternal medicinemedicineHumansMARROW-TRANSPLANTATIONSurvival rateLenalidomideTransplantationScience & Technologybusiness.industryMyelodysplastic syndromesmedicine.diseaseAllogeneic stem cell transplantationTransplantationMyelodysplastic Syndromesbusiness030215 immunology
researchProduct

4843delC of the BRCA1 gene is a possible founder mutation in Southern Italy (Sicily).

2007

Various studies have been published in Italy regarding the different BRCA1 mutations, but only the BRCA1-5083del19 mutation is recurrent and specific to individuals of Italian descent with a founder effect on the Calabrian population. In our previous study, BRCA1-5083del19 mutation carriers were found in four index cases of 106 Sicilian patients selected for familial and/or hereditary breast/ovarian cancers. The high frequency rate of this mutation identified in the Sicilian population led us to perform haplotype analysis in all family carriers. Five highly polymorphic microsatellite markers were used (D17S1320, D17S932, D17S1323, D17S1326, D17S1325) to establish whether or not all these fa…

MaleBRCA1 gene Founder mutation Haplotype analysis Hereditary breast and ovarian cancer Sicilian patientsSettore MED/06 - Oncologia MedicaGenetic counselingPopulationDNA Mutational AnalysisGenes BRCA1Single-nucleotide polymorphismBreast NeoplasmsBiologyBRCA1 geneHaplotype analysiHumansAlleleeducationAllelotypeFounder mutationSicilyGeneticsOvarian Neoplasmseducation.field_of_studyHaplotypeHematologylanguage.human_languageFounder EffectPedigreeOncologyHaplotypesHaplotype frequencylanguageFemaleSicilianGene DeletionFounder effectGenetic counselingMicrosatellite Repeats
researchProduct

Effects of Presynaptic Mutations on a Postsynaptic Cacna1s Calcium Channel Colocalized with mGluR6 at Mouse Photoreceptor Ribbon Synapses

2008

Purpose Photoreceptor ribbon synapses translate light-dependent changes of membrane potential into graded transmitter release via L-type voltage-dependent calcium channel (VDCC) activity. Functional abnormalities (e.g., a reduced electroretinogram b-wave), arising from mutations of presynaptic proteins, such as Bassoon and the VDCCalpha1 subunit Cacna1f, have been shown to altered transmitter release. L-type VDCCalpha1 subtype expression in wild-type and mutant mice was examined, to investigate the underlying pathologic mechanism. Methods Two antisera against Cacna1f, and a Cacna1f mouse mutant (Cacna1fDeltaEx14-17) were generated. Immunocytochemistry for L-type VDCCalpha1 subunits and addi…

MaleCalcium Channels L-TypeBlotting WesternPresynaptic TerminalsRibbon synapseBiologyReceptors Metabotropic GlutamateSynaptic TransmissionEpitopesMicePostsynaptic potentialAnimalsCalcium SignalingActive zoneFluorescent Antibody Technique IndirectMicroscopy ImmunoelectronSequence DeletionMembrane potentialSheepVoltage-dependent calcium channelReverse Transcriptase Polymerase Chain ReactionCalcium channelMetabotropic glutamate receptor 6ColocalizationAnatomyBlotting NorthernMice Mutant StrainsPeptide FragmentsCell biologyMice Inbred C57BLFemaleCalcium ChannelsRabbitssense organsPhotoreceptor Cells VertebrateInvestigative Opthalmology & Visual Science
researchProduct

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
researchProduct

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
researchProduct

Is BRCA1-5083del19, identified in breast cancer patients of Sicilian origin, a Calabrian founder mutation?

2007

Various studies have been published in Italy regarding the different BRCA1 mutations, but only the BRCA1-5083del19 mutation is recurrent and specific to individuals of Italian descent with a founder effect on the Calabrian population. In our previous study, BRCA1-5083del19 mutation carriers were found in four index cases of 106 Sicilian patients selected for familial and/or hereditary breast/ovarian cancers. The high frequency rate of this mutation identified in the Sicilian population led us to perform haplotype analysis in all family carriers. Five highly polymorphic microsatellite markers were used (D17S1320, D17S932, D17S1323, D17S1326, D17S1325) to establish whether or not all these fa…

MaleCancer ResearchSettore MED/06 - Oncologia MedicaPopulationBRCA1 breast cancerBreast NeoplasmsBiologyRisk AssessmentAllelotype AnalysisReference ValuesHumansAlleleeducationSicilySequence DeletionOvarian NeoplasmsGeneticseducation.field_of_studyBRCA1 ProteinHaplotypeFounder Effectlanguage.human_languagePedigreeOncologyMutationMutation (genetic algorithm)languageMicrosatelliteFemaleSicilianMicrosatellite RepeatsFounder effect
researchProduct