Search results for "heredity"

showing 10 items of 247 documents

Should Vanishing Twin Pregnancies Be Systematically Excluded From Cell-Free Fetal DNA Testing?

2020

Objective To demonstrate the feasibility of cell-free DNA (cfDNA) testing in vanishing twin (VT) pregnancies in routine clinical practice. Methods Our study included 24 874 singleton and 206 VT consecutive pregnancies. Cell-free DNA was analyzed by massively parallel sequencing. Both aneuploidy analysis (chromosomes 13,18, 21, X, and Y) and fetal fraction estimation were performed according to an Illumina algorithm. Contaminant DNA contribution from the demised co-twin was studied in detail. Results VT pregnancies exhibited a higher prevalence of screen-positive cases (5.8% vs 2.5%), sex discrepancies (10.2% vs 0.05%), and false positive rates (FPR) (2.6% vs 0.3%) than singleton pregnancies…

Adult0301 basic medicinemedicine.medical_specialtyAneuploidy030105 genetics & heredity03 medical and health sciences0302 clinical medicinePregnancyPrenatal DiagnosisHumansMedicineGenetics (clinical)Retrospective StudiesVanishing twinFetusPregnancy030219 obstetrics & reproductive medicinebusiness.industryObstetricsSingletonIncidence (epidemiology)Obstetrics and GynecologyGeneral Medicinemedicine.diseaseCell-free fetal DNAPregnancy TwinFemalebusinessTrisomyCell-Free Nucleic AcidsObstetrical & Gynecological Survey
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Risk Perception and Psychological Distress in Genetic Counselling for Hereditary Breast and/or Ovarian Cancer

2017

International audience; Oncological Genetic Counselling (CGO) allows the identification of a genetic component that increases the risk of developing a cancer. Individuals' psychological reactions are influenced by both the content of the received information and the subjective perception of their own risk of becoming ill or being a carrier of a genetic mutation. This study included 120 participants who underwent genetic counselling for breast and/or ovarian cancer. The aim of the study was to examine the relation between their cancer risk perception and the genetic risk during CGO before receiving genetic test results, considering the influence of some psychological variables, in particular…

Adult0301 basic medicinemedicine.medical_specialtygenetic structuresmedia_common.quotation_subjectGenetic counseling[SHS.PSY]Humanities and Social Sciences/PsychologyBreast NeoplasmsGenetic CounselingAnxiety030105 genetics & heredityHospital Anxiety and Depression Scale[SHS]Humanities and Social Sciences[SHS.PSY] Humanities and Social Sciences/Psychology03 medical and health sciences0302 clinical medicineRisk FactorsPerceptionmedicineHumansGenetic Predisposition to DiseaseDistrePsychiatryGenetics (clinical)Depression (differential diagnoses)BRCA 1/2media_commonOvarian NeoplasmsGenetic counsellingDistressCancerMiddle Agedmedicine.diseaseCancer risk perception3. Good healthRisk perceptionDistress030220 oncology & carcinogenesisMutationAnxietyFemalePerception[SHS] Humanities and Social SciencesGenetic risk perceptionmedicine.symptomPsychologyStress PsychologicalClinical psychology
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Search for a gene responsible for Floating-Harbor syndrome on chromosome 12q15q21.1.

2012

International audience; Floating-Harbor syndrome (FHS) is characterized by characteristic facial dysmorphism, short stature with delayed bone age, and expressive language delay. To date, the gene(s) responsible for FHS is (are) unknown and the diagnosis is only made on the basis of the clinical phenotype. The majority of cases appeared to be sporadic but rare cases following autosomal dominant inheritance have been reported. We identified a 4.7 Mb de novo 12q15-q21.1 microdeletion in a patient with FHS and intellectual deficiency. Pangenomic 244K array-CGH performed in a series of 12 patients with FHS failed to identify overlapping deletions. We hypothesized that FHS is caused by haploinsuf…

AdultHeart Septal Defects VentricularMaleCandidate geneFloating Harbor syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsHaploinsufficiencyBiologyBioinformaticsShort statureCraniofacial Abnormalities03 medical and health sciences12q15q21.1 microdeletion[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to Disease[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyChild[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Growth Disorders030304 developmental biologySequence DeletionPhenocopyGenetics0303 health sciencesComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsChromosomes Human Pair 12Genetic heterogeneity030305 genetics & heredityChromosomeHigh-Throughput Nucleotide Sequencinghigh-throughput sequencingmedicine.disease3. Good healthPhenotypeFloating–Harbor syndromeChild PreschoolMutation (genetic algorithm)Femalemedicine.symptomHaploinsufficiency[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Not All Floating-Harbor Syndrome Cases are Due to Mutations in Exon 34 of SRCAP

2013

International audience; Floating-Harbor syndrome (FHS) is a rare disorder characterized by short stature, delayed bone age, speech delay, and dysmorphic facial features. We report here the molecular analysis of nine cases, fulfilling the diagnostic criteria for FHS. Using exome sequencing, we identified SRCAP as the disease gene in two cases and subsequently found SRCAP truncating mutations in 6/9 cases. All mutations occurred de novo and were located in exon 34, in accordance with the recent report of Hood et al. However, the absence of SRCAP mutations in 3/9 cases supported genetic heterogeneity of FH syndrome. Importantly, no major clinical differences were observed supporting clinical h…

AdultHeart Septal Defects VentricularMaleDNA Mutational AnalysisBiologyShort statureCraniofacial Abnormalitiesgenetic heterogeneity03 medical and health sciencesExonGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to DiseaseChildFloating-Harbor syndromeGenetics (clinical)Exome sequencingGrowth Disorders030304 developmental biologyDisease geneGeneticsAdenosine Triphosphatases0303 health sciences[SDV.GEN]Life Sciences [q-bio]/GeneticsGenetic heterogeneity030305 genetics & heredityBone ageExonsmedicine.diseaseSRCAP3. Good healthFloating–Harbor syndromeSpeech delayMutationFemalemedicine.symptom[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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Homozygous variants in the gene SCAPER cause syndromic intellectual disability

2019

The S-Phase Cyclin A Associated Protein In The ER (SCAPER) gene is a ubiquitously expressed gene with unknown function in the brain. Recently, biallelic SCAPER variants were described in four patients from three families with retinitis pigmentosa (RP) and intellectual disability (ID). Here, we expand the spectrum of pathogenic variants in SCAPER and report on 10 further patients from four families with ID, RP, and additional dysmorphic features carrying homozygous variants in SCAPER. The variants found comprise frameshift, nonsense, and missense variants as well as an intragenic homozygous deletion, which spans SCAPER exons 15 and 16 and introduces a frameshift and a premature stop codon. A…

AdultMale0301 basic medicineAdolescentmedia_common.quotation_subjectCyclin ANonsenseGene Expression030105 genetics & heredityFrameshift mutationConsanguinityMice03 medical and health sciencesExonNeural Stem CellsIntellectual DisabilityRetinitis pigmentosaGene expressionGeneticsmedicineAnimalsHumansMissense mutationFamilyChildGeneGenetics (clinical)media_commonCerebral CortexNeuronsGeneticsbiologyHomozygoteSyndromemedicine.diseasePedigree030104 developmental biologyMutationbiology.proteinFemaleCarrier ProteinsRetinitis PigmentosaAmerican Journal of Medical Genetics Part A
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Whole genome paired-end sequencing elucidates functional and phenotypic consequences of balanced chromosomal rearrangement in patients with developme…

2019

BackgroundBalanced chromosomal rearrangements associated with abnormal phenotype are rare events, but may be challenging for genetic counselling, since molecular characterisation of breakpoints is not performed routinely. We used next-generation sequencing to characterise breakpoints of balanced chromosomal rearrangements at the molecular level in patients with intellectual disability and/or congenital anomalies.MethodsBreakpoints were characterised by a paired-end low depth whole genome sequencing (WGS) strategy and validated by Sanger sequencing. Expression study of disrupted and neighbouring genes was performed by RT-qPCR from blood or lymphoblastoid cell line RNA.ResultsAmong the 55 pat…

AdultMale0301 basic medicineCandidate geneAdolescentDNA Copy Number VariationsDevelopmental Disabilities030105 genetics & heredityGenomeTranslocation GeneticStructural variationChromosome BreakpointsStructure-Activity RelationshipYoung Adult03 medical and health sciencessymbols.namesakeposition effectGeneticsHumansChildGeneGenetic Association StudiesGenetics (clinical)Paired-end tagComputingMilieux_MISCELLANEOUSchromosomal rearrangementsChromosome AberrationsGene RearrangementWhole genome sequencingGeneticsSanger sequencingwhole genome sequencingbiologystructural variationInfantNFIXPhenotype030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsintellectual disabilityChild Preschoolbiology.proteinsymbolsFemaleBiomarkers
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Cholelithiasis in Patients with Gaucher Disease type 1: Risk Factors and the Role of ABCG5/ABCG8 Gene Variants

2016

Background & Aim: Patients with Gaucher disease type 1 (GD1) show an altered lipid profile and a certain degree of insulin resistance, which might contribute to cholelithiasis (CL) and could possibly be associated with ABCG5/ABCG8 gene variants. We aimed to investigate the prevalence of CL in Caucasian adult patients with GD1 and the possible risk factors, including gene variants of the ABCG5/ABCG8 genes.
 Methods: 61 Caucasian patients with GD1 (38 female/23male), aged 18-62 years and 61 healthy subjects matched for age, gender and BMI, without CL, for comparison of lipid profiles. Data before start of enzyme replacement therapy (ERT) were recorded: clinical, haematological, sever…

AdultMale0301 basic medicineHeterozygotemedicine.medical_specialtyAdolescentLipoproteinsmedicine.medical_treatmentSplenectomyABCG8030105 genetics & heredityGastroenterologyWhite PeopleYoung Adult03 medical and health sciencesInsulin resistanceGene FrequencyCholelithiasisRisk FactorsInternal medicineGenotypePrevalencemedicineHumansEnzyme Replacement TherapyGenetic Predisposition to DiseaseATP Binding Cassette Transporter Subfamily G Member 5Genetic Association StudiesGaucher Diseasemedicine.diagnostic_testRomaniabusiness.industryATP Binding Cassette Transporter Subfamily G Member 8HomozygoteGastroenterologyCase-control studyGenetic VariationEnzyme replacement therapyMiddle Agedmedicine.diseaseCross-Sectional StudiesPhenotypeCase-Control StudiesGlucosylceramidaseFemaleLipid profilebusinessDyslipidemiaJournal of Gastrointestinal and Liver Diseases
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Kosaki overgrowth syndrome: A novel pathogenic variant in PDGFRB and expansion of the phenotype including cerebrovascular complications

2020

Heterozygous activating variants in platelet-derived growth factor, beta (PDGFRB) are associated with phenotypes including Kosaki overgrowth syndrome (KOGS), Penttinen syndrome and infantile myofibromatosis (IM). Here, we present three new cases of KOGS, including a patient with a novel de novo variant c.1477A > T p.(Ser493Cys), and the oldest known individual age 53 years. The KOGS phenotype includes characteristic facial features, tall stature, scoliosis, hyperelastic thin skin, lipodystrophy, variable intellectual and neurological deterioration, and abnormalities on brain imaging. Long-term outcome is unknown. Our cases confirm the phenotypic spectrum includes progressive flexion contrac…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyInfantile myofibromatosisPDGFRBScoliosis030105 genetics & heredityCraniosynostosisReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesCamptodactylyGeneticsmedicineHumansJoint dislocationStrokeGrowth DisordersGenetics (clinical)business.industryGenetic VariationMiddle Agedmedicine.diseaseCerebrovascular DisordersPhenotype030104 developmental biologymedicine.symptomLipodystrophybusinessClinical Genetics
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Clinical and neuroimaging findings in 33 patients with MCAP syndrome: A survey to evaluate relevant endpoints for future clinical trials

2021

Megalencephaly-CApillary malformation-Polymicrogyria (MCAP) syndrome results from somatic mosaic gain-of-function variants in PIK3CA. Main features are macrocephaly, somatic overgrowth, cutaneous vascular malformations, connective tissue dysplasia, neurodevelopmental delay, and brain anomalies. The objectives of this study were to describe the clinical and radiological features of MCAP, to suggest relevant clinical endpoints applicable in future trials of targeted drug therapy. Based on a French collaboration, we collected clinical features of 33 patients (21 females, 12 males, median age of 9.9 years) with MCAP carrying mosaic PIK3CA pathogenic variants. MRI images were reviewed for 21 pat…

AdultMale0301 basic medicinePediatricsmedicine.medical_specialtyCutis marmorataAdolescentClass I Phosphatidylinositol 3-KinasesNeuroimagingContext (language use)Skin Diseases Vascular030105 genetics & heredityCohort StudiesYoung Adult03 medical and health sciencesGeneticsPolymicrogyriamedicineHumansPROSAbnormalities MultipleTelangiectasisMegalencephalyChildMCAP syndromeGenetics (clinical)Chiari malformationClinical Trials as Topicbusiness.industryMacrocephalyPIK3CAmedicine.diseaseMagnetic Resonance ImagingMegalencephaly3. Good healthClinical trial030104 developmental biologyChild PreschoolPostnatal macrocephalyFemalemedicine.symptombusiness[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyForecastingVentriculomegalyClinical Genetics
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Chromosome 15q BP3 to BP5 deletion is a likely locus for speech delay and language impairment: Report on a four‐member family and an unrelated boy

2020

Abstract Background Deletions in chromosome 15q13 have been reported both in healthy people and individuals with a wide range of behavioral and neuropsychiatric disturbances. Six main breakpoint (BP) subregions (BP1‐BP6) are mapped to the 15q13 region and three further embedded BP regions (BP3‐BP5). The deletion at BP4‐BP5 is the rearrangement most frequently observed compared to other known deletions in BP3‐BP5 and BP3‐BP4 regions. Deletions of each of these three regions have previously been implicated in a variable range of clinical phenotypes, including minor dysmorphism, developmental delay/intellectual disability, epilepsy, autism spectrum disorders, behavioral disturbances, and speec…

AdultMale0301 basic medicinespeech delayAdolescentlcsh:QH426-470BP3-BP5 deletionspeech delay.Chromosome DisordersLocus (genetics)030105 genetics & heredity03 medical and health sciencesEpilepsySettore MED/38 - Pediatria Generale E SpecialisticaSeizuresIntellectual DisabilityIntellectual disabilitychromosome 15 q13GeneticsmedicineHumansLanguage Development DisordersChildMolecular BiologyGenetics (clinical)GeneticsChromosomes Human Pair 15business.industryBreakpointlanguage impairmentOriginal Articlesmedicine.diseasePhenotypePedigreeBP3‐BP5 deletiondevelopmental delayLanguage developmentlcsh:GeneticsPhenotype030104 developmental biologyBP3-BP5 deletion; chromosome 15 q13; developmental delay; language impairment; speech delaySpeech delayAutismFemaleOriginal ArticleChromosome Deletionmedicine.symptombusinessMolecular Genetics & Genomic Medicine
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