Search results for "030105 genetics & heredity"

showing 9 items of 119 documents

First report of X-linked hypohidrotic ectodermal dysplasia with a hemizygous c.1142G > C in the EDA gene: variant of uncertain significance or new pa…

2021

AbstractBackgroundHypohidrotic Ectodermal Dysplasia (HED) is a genetic disorder which affects structures of ectodermal origin. X-linked hypohidrotic ectodermal dysplasia (XLHED) is the most common form of disease. XLHED is characterized by hypotrichosis, hypohydrosis and hypodontia. The cardinal features of classic HED become obvious during childhood.Identification of a hemizygous EDA pathogenic variant in an affected male confirms the diagnosis.Case presentationWe report on a male newborn with the main clinical characteristics of the X-linked HED including hypotrichosis, hypodontia and hypohidrosis. Gene panel sequencing identified a new hemizygous missense variant of uncertain significanc…

Male0301 basic medicineProbandMutation MissenseVariants of uncertain significance (VUS)Case ReportX-linked.030105 genetics & heredityPediatricsRJ1-57003 medical and health sciencesEDA geneHumansMedicineMissense mutationHypohidrotic ectodermal dysplasiaX chromosomeHemizygoteGeneticsX-linkedChromosomes Human XEctodermal Dysplasia 1 Anhidroticbusiness.industryInfant NewbornGenetic disorderGeneral MedicineEctodysplasinsmedicine.diseaseHypoidrotic ectodermal dysplasiaHypodontia030104 developmental biologyHypotrichosisEctodysplasin AbusinessItalian Journal of Pediatrics
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Expanding the β-III Spectrin-Associated Phenotypes toward Non-Progressive Congenital Ataxias with Neurodegeneration

2021

(1) Background: A non-progressive congenital ataxia (NPCA) phenotype caused by b-III spectrin (SPTBN2) mutations has emerged, mimicking spinocerebellar ataxia, autosomal recessive type 14 (SCAR14). The pattern of inheritance, however, resembles that of autosomal dominant classical spinocerebellar ataxia type 5 (SCA5). (2) Methods: In-depth phenotyping of two boys studied by a customized gene panel. Candidate variants were sought by structural modeling and protein expression. An extensive review of the literature was conducted in order to better characterize the SPTBN2-associated NPCA. (3) Results: Patients exhibited an NPCA with hypotonia, developmental delay, cerebellar syndrome, and cogni…

Male0301 basic medicineProbandPathologyProtein ConformationSequence Homology<i>SPTBN2 </i>geneb-III spectrin030105 genetics & heredityFluid-attenuated inversion recoveryCohort Studieslcsh:ChemistryNon-progressive congenital ataxia0302 clinical medicineβ-III spectrinSpectrin:enfermedades del sistema nervioso::enfermedades neurodegenerativas [ENFERMEDADES]Age of OnsetChildlcsh:QH301-705.5Spectroscopy:Otros calificadores::Otros calificadores::/genética [Otros calificadores]NeurodegenerationneurodegenerationNeurodegenerative Diseasesnon-progressive congenital ataxiaSyndromeGeneral MedicinePhenotypeHypotoniaComputer Science ApplicationsPhenotype:Nervous System Diseases::Neurodegenerative Diseases [DISEASES]Spinocerebellar ataxiamedicine.symptomSPTBN2 genemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesCerebellar AtaxiaNeuroimagingBiologyCatalysisArticleInorganic Chemistry03 medical and health sciences:Nervous System Diseases::Central Nervous System Diseases::Brain Diseases::Cerebellar Diseases::Cerebellar Ataxia [DISEASES]:Other subheadings::Other subheadings::/genetics [Other subheadings]medicineHumansAmino Acid SequencePhysical and Theoretical ChemistryNeurodegenerationMolecular BiologyGenetic Association StudiesOrganic ChemistrySpectrinmedicine.diseaseHyperintensitySistema nerviós - Degeneració - Aspectes genèticslcsh:Biology (General)lcsh:QD1-999:enfermedades del sistema nervioso::enfermedades del sistema nervioso central::enfermedades cerebrales::enfermedades cerebelosas::ataxia cerebelosa [ENFERMEDADES]Mutation030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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Skraban‐Deardorff syndrome: Six new cases of WDR 26 ‐related disease and expansion of the clinical phenotype

2021

International audience; Skraban-Deardorff syndrome (a disease related to variations in the WDR26 gene; OMIM #617616) was first described in a cohort of 15 individuals in 2017. The syndrome comprises intellectual deficiency, severe speech impairment, ataxic gait, seizures, mild hypotonia with feeding difficulties during infancy, and dysmorphic features. Here, we report on six novel heterozygous de novo pathogenic variants in WDR26 in six probands. The patients’ phenotypes were consistent with original publication. One patient displayed marked hypotonia with an abnormal muscle biopsy; this finding warrants further investigation. Gait must be closely monitored, in order to highlight any muscul…

Male0301 basic medicineProbandPediatricsmedicine.medical_specialtyAdolescent[SDV]Life Sciences [q-bio]Developmental DisabilitiesSkraban-Deardorff syndromeDisease030105 genetics & heredityYoung Adult03 medical and health sciencesIntellectual disabilityGeneticsmedicineWDR26HumansAbnormalities MultiplehypotoniaAtaxic GaitChildGenetics (clinical)Adaptor Proteins Signal Transducing[SDV.GEN]Life Sciences [q-bio]/GeneticsMuscle biopsymedicine.diagnostic_testbusiness.industryInfantSyndromemedicine.diseaseGaitHypotonia3. Good health[SDV] Life Sciences [q-bio]Phenotype030104 developmental biologyspeech therapyintellectual disabilityChild PreschoolMutationCohortlanguage development disordersFemalemedicine.symptombusinessClinical Genetics
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Angioedema due to acquired C1-inhibitor deficiency: spectrum and treatment with C1-inhibitor concentrate

2018

Abstract Background Acquired angioedema due to C1-inhibitor (C1-INH) deficiency (AAE-C1-INH) is a serious condition that may result in life-threatening asphyxiation due to laryngeal edema. It is associated with malignant B-cell lymphoma and other disorders. The purpose of this study was to describe the characteristics and associated disorders of patients with AAE-C1-INH and assess the efficacy of plasma-derived C1-INH concentrate (pdC1-INH) in the treatment of AAE-C1-INH. Forty-four patients with AAE-C1-INH from the Angioedema Outpatient Service of Mainz were assessed for associated disorders. In 32 of these patients, the duration of swelling attacks was measured before and after treatment …

Male0301 basic medicinelcsh:Medicine030105 genetics & heredityGastroenterologyAcquired angioedemaC1-inhibitor0302 clinical medicineGermanyImmunology and Allergyheterocyclic compoundsPharmacology (medical)Genetics (clinical)Non-Hodgkin lymphomaAged 80 and overC1-inhibitor deficiencybiologyGeneral MedicineMiddle Agedrespiratory systemTreatment OutcomeC1-inhibitor concentrate C1-inhibitor antibodiesFemalemedicine.symptomComplement C1 Inhibitor ProteinAdultmedicine.medical_specialtyC1 inhibitor deficiencyImmunologyMalignancyLaryngeal Edema03 medical and health sciencesInternal medicinemedicineHumansAngioedemaAgedRetrospective StudiesAngioedemabusiness.industryResearchlcsh:RAngioedemas HereditaryAutoantibodybiochemical phenomena metabolism and nutritionbacterial infections and mycosesmedicine.diseaserespiratory tract diseasesLymphomabiology.proteinbusiness030217 neurology & neurosurgeryMonoclonal gammopathy of undetermined significanceOrphanet Journal of Rare Diseases
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Bainbridge-Ropers syndrome caused by loss-of-function variants in ASXL3: a recognizable condition

2016

International audience; Truncating ASXL3 mutations were first identified in 2013 by Bainbridge et al. as a cause of syndromic intellectual disability in four children with similar phenotypes using whole-exome sequencing. The clinical features - postulated by Bainbridge et al. to be overlapping with Bohring-Opitz syndrome - were developmental delay, severe feeding difficulties, failure to thrive and neurological abnormalities. This condition was included in OMIM as 'Bainbridge-Ropers syndrome' (BRPS, #615485). To date, a total of nine individuals with BRPS have been published in the literature in four reports (Bainbridge et al., Dinwiddie et al, Srivastava et al. and Hori et al.). In this re…

Male0301 basic medicinemedicine.medical_specialtyMicrocephalyfamilyAdolescentphenotypeDevelopmental DisabilitiesSevere muscular hypotoniaMedizinTrigonocephaly030105 genetics & heredityBiologyArticle03 medical and health sciencesIntellectual disabilityGeneticsmedicineHumansCraniofacial[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsnovo frameshift mutationgenedisordersGenetics (clinical)GeneticsInfantSyndromemedicine.diseaseDermatologyFailure to Thrive030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsintellectual disabilityChild Preschoolbohring-opitz syndromeMutationFailure to thriveMedical geneticsFemalemedicine.symptomBohring–Opitz syndromeTranscription Factors
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Associations between cognitive performance and the rehabilitation, medical care and social support provided to French children with Prader-Willi synd…

2020

International audience; Prader-Willi syndrome (PWS) is a rare genetic neurodevelopmental disorder with a characteristic behavioural phenotype. A multidisciplinary approach to care is required to prevent multiple medical complications in individuals affected by PWS. The aim of this study was to describe the rehabilitation, medical care, educational and social support provided to school-aged French PWS patients with varying neuropsychological profiles. Data were obtained from a French multicentre study that included patients aged 4-20 years with diverse genetic syndromes. Nineteen PWS subjects with a mean age of 9.2 years were included. The mean full-scale intellectual quotient (IQ) was 58 (W…

Male0301 basic medicinemedicine.medical_treatmentIntellectual disabilityMESH: CognitionCBCL030105 genetics & heredityCognitionMultidisciplinary approachMESH: ChildIntellectual disabilityMedicineChildGenetics (clinical)RehabilitationMESH: Hormone Replacement TherapyNeurological RehabilitationNeuropsychologyWechsler Adult Intelligence ScaleGeneral Medicine3. Good healthMESH: Young AdultChild PreschoolEducation SpecialFemaleFrancePrader-Willi SyndromeOccupational therapymedicine.medical_specialtyAdolescentHormone Replacement TherapyMESH: Social Support[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsYoung Adult03 medical and health sciencesSocial supportMESH: Neurological RehabilitationGeneticsHumansPsychiatryMESH: AdolescentMESH: Humansbusiness.industryMESH: Child PreschoolSocial Supportmedicine.diseaseMESH: MaleMESH: FrancePatient care management030104 developmental biologyMESH: Education Special[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMESH: Prader-Willi SyndromebusinessMESH: FemaleEuropean Journal of Medical Genetics
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Rare variants in the genetic background modulate cognitive and developmental phenotypes in individuals carrying disease-associated variants

2019

Purpose: To assess the contribution of rare variants in the genetic background toward variability of neurodevelopmental phenotypes in individuals with rare copy-number variants (CNVs) and gene-disruptive variants. Methods: We analyzed quantitative clinical information, exome sequencing, and microarray data from 757 probands and 233 parents and siblings who carry disease-associated variants. Results: The number of rare likely deleterious variants in functionally intolerant genes (“other hits”) correlated with expression of neurodevelopmental phenotypes in probands with 16p12.1 deletion (n=23, p=0.004) and in autism probands carrying gene-disruptive variants (n=184, p=0.03) compared with thei…

MaleParents0301 basic medicineProbandNeuronalGenetic Carrier Screening16p11.2 deletion030105 genetics & heredityCognitionFamily historyNeural Cell Adhesion MoleculesGenetics (clinical)Exome sequencingSequence DeletionGeneticsGenetic Carrier ScreeningPhenotypePenetrancePedigreePhenotypeAutistic Disorder/genetics; Autistic Disorder/physiopathology; Cell Adhesion Molecules Neuronal/genetics; Chromosomes Human Pair 16/genetics; Cognition/physiology; DNA Copy Number Variations/genetics; Female; Gene Expression Regulation/genetics; Genetic Background; Genetic Carrier Screening; Humans; Male; Methyltransferases/genetics; Nerve Tissue Proteins/genetics; Parents; Pedigree; Phenotype; Proteins/genetics; Sequence Deletion/genetics; Siblings; 16p11.2 deletion; CNV; autism; modifier; phenotypic variabilityFemaleGenetic BackgroundHumanDNA Copy Number VariationsCell Adhesion Molecules NeuronalCNVautismNerve Tissue ProteinsBiologyChromosomesArticle03 medical and health sciencesmental disordersmedicineHumansAutistic DisorderBiologyGenemodifierPair 16SiblingsCalcium-Binding ProteinsProteinsMethyltransferasesmedicine.disease16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Genetics (clinical)Cytoskeletal Proteins030104 developmental biologyGene Expression Regulation[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutismphenotypic variabilityHuman medicine16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Autistic Disorder; Cell Adhesion Molecules Neuronal; Chromosomes Human Pair 16; Cognition; DNA Copy Number Variations; Female; Gene Expression Regulation; Genetic Background; Humans; Male; Methyltransferases; Nerve Tissue Proteins; Parents; Pedigree; Phenotype; Proteins; Sequence Deletion; Siblings; Genetic Carrier ScreeningCell Adhesion MoleculesChromosomes Human Pair 16Transcription FactorsGenetics in Medicine
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Overlapping phenotypes between SHORT and Noonan syndromes in patients with PTPN11 pathogenic variants

2020

Overlapping syndromes such as Noonan, Cardio-Facio-Cutaneous, Noonan syndrome (NS) with multiple lentigines and Costello syndromes are genetically heterogeneous conditions sharing a dysregulation of the RAS/mitogen-activated protein kinase (MAPK) pathway and are known collectively as the RASopathies. PTPN11 was the first disease-causing gene identified in NS and remains the more prevalent. We report seven patients from three families presenting heterozygous missense variants in PTPN11 probably responsible for a disease phenotype distinct from the classical Noonan syndrome. The clinical presentation and common features of these seven cases overlap with the SHORT syndrome. The latter is the c…

Malemusculoskeletal diseases0301 basic medicineMAPK/ERK pathwaycongenital hereditary and neonatal diseases and abnormalitiesMAP Kinase Signaling SystemProtein Tyrosine Phosphatase Non-Receptor Type 11030105 genetics & heredityBiologyGene productPhosphatidylinositol 3-Kinases03 medical and health sciencesMetabolic DiseasesGeneticsmedicineHumansMissense mutationskin and connective tissue diseasesProtein kinase BGrowth DisordersGenetics (clinical)GeneticsGenetic heterogeneityNoonan SyndromeGenetic Variationmedicine.diseasePTPN11NephrocalcinosisPhenotype030104 developmental biologySHORT syndromeHypercalcemiaNoonan syndromeFemaleMitogen-Activated Protein KinasesSignal TransductionClinical Genetics
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Comparison of HapMap and 1000 genomes reference panels in a large-scale genome-wide association study

2017

An increasing number of genome-wide association (GWA) studies are now using the higher resolution 1000 Genomes Project reference panel (1000G) for imputation, with the expectation that 1000G imputation will lead to the discovery of additional associated loci when compared to HapMap imputation. In order to assess the improvement of 1000G over HapMap imputation in identifying associated loci, we compared the results of GWA studies of circulating fibrinogen based on the two reference panels. Using both HapMap and 1000G imputation we performed a meta-analysis of 22 studies comprising the same 91,953 individuals. We identified six additional signals using 1000G imputation, while 29 loci were ass…

Netherlands Twin Register (NTR)0301 basic medicineGlycobiologySocial Scienceslcsh:MedicineGenome-wide association study030105 genetics & heredityBiochemistryMathematical and Statistical TechniquesSociologyCell SignalingConsortiaGENETIC-VARIANTSMedicine and Health SciencesIMPUTATIONInternational HapMap Projectlcsh:ScienceGeneticsMultidisciplinaryCOMMON VARIANTSGenomicsMultidisciplinary SciencesINSIGHTSCARDIOVASCULAR-DISEASEPhysical SciencessymbolsScience & Technology - Other TopicsHealth Services ResearchGenomic Signal ProcessingStatistics (Mathematics)Research ArticleSignal TransductionGenotypingSUSCEPTIBILITY LOCIGeneral Science & TechnologyBIOLOGYSingle-nucleotide polymorphismGenomicsHapMap ProjectComputational biologyPRESSUREBiologyResearch and Analysis Methods03 medical and health sciencessymbols.namesakeMD MultidisciplinaryGenome-Wide Association StudiesGeneticsJournal Article/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_HumansStatistical Methods1000 Genomes ProjectMolecular Biology TechniquesMolecular BiologyMETAANALYSISGlycoproteinsScience & Technologylcsh:RHuman GenomeCONSORTIUMBiology and Life SciencesComputational BiologyFibrinogenHuman GeneticsCell BiologyComparative GenomicsGenome AnalysisHealth Care030104 developmental biologyBonferroni correctionlcsh:QHaplotype estimationMathematicsImputation (genetics)Meta-AnalysisGenome-Wide Association Study
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