Search results for "Exome"

showing 10 items of 202 documents

Association of Variants in the SPTLC1 Gene with Juvenile Amyotrophic Lateral Sclerosis

2021

Key Points Question What genetic variants are associated with juvenile amyotrophic lateral sclerosis (ALS)? Findings In this family-based genetic study, exome sequencing was performed in 3 patients diagnosed with juvenile ALS and failure to thrive; this identified de novo variants in SPTLC1 (p.Ala20Ser in 2 patients and p.Ser331Tyr in 1 patient). Variants in SPTLC1 are a known cause of hereditary sensory and autonomic neuropathy, type 1A, and these data extend the phenotype associated with this gene. Meaning De novo variants in the SPTLC1 gene are associated with juvenile ALS, a fatal neurological disorder.

Hereditary sensory neuropathy; L-serine; Mutations; Deoxysphingolipids; AccumulationEnzyme complexJuvenile amyotrophic lateral sclerosisSerine C-Palmitoyltransferase/dk/atira/pure/subjectarea/asjc/2700/2728Whole Exome Sequencing0302 clinical medicineMedicineFamily historyAmyotrophic lateral sclerosisChildIndex caseExome sequencingOriginal Investigation0303 health sciencesNeurosciences and neurology3. Good healthChild PreschoolFailure to thriveFemalemedicine.symptomLife Sciences & BiomedicineL-SERINECommentsHumanAdultmedicine.medical_specialtyAdolescent; Adult; Amyotrophic Lateral Sclerosis; Child; Child Preschool; Female; Genetic Predisposition to Disease; Humans; Mutation; Serine C-Palmitoyltransferase; Whole Exome Sequencing; Young AdultAdolescentClinical NeurologyNO03 medical and health sciencesYoung AdultDEOXYSPHINGOLIPIDSInternal medicineExome SequencingOnline FirstHumansJuvenileGenetic Predisposition to DiseasePreschool030304 developmental biologyACCUMULATIONScience & TechnologySPTLC1business.industryMUTATIONSResearchAmyotrophic Lateral Sclerosis3112 Neurosciencesmedicine.diseaseHEREDITARY SENSORY NEUROPATHYjuvenileMutation3111 BiomedicineNeurology (clinical)Neurosciences & NeurologyALSgeneticbusiness030217 neurology & neurosurgeryAmyotrophic Lateral Sclerosi
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An Unexplained Congenital Disorder of Glycosylation-II in a Child with Neurohepatic Involvement, Hypercholesterolemia and Hypoceruloplasminemia

2017

We report on a 12-year-old adopted boy with psychomotor disability, absence seizures, and normal brain MRI. He showed increased (but initially, at 5 months, normal) serum cholesterol, increased alkaline phosphatases, transiently increased transaminases and hypoceruloplasminemia with normal serum and urinary copper. Blood levels of immunoglobulins, haptoglobin, antithrombin, and factor XI were normal. A type 2 serum transferrin isoelectrofocusing and hypoglycosylation of apoCIII pointed to a combined N- and O-glycosylation defect. Neither CDG panel analysis with 79 CDG-related genes, nor whole exome sequencing revealed the cause of this CDG. Whole genome sequencing was not performed since th…

Hypoceruloplasminemiacongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtySettore MED/09 - Medicina InternaUrinary systemHypercholesterolemiaArticleInternal medicineNeurohepatic involvementmedicineCDG-IIGlycomicsExome sequencingWhole genome sequencingchemistry.chemical_classificationbiologybusiness.industryHaptoglobinAntithrombinmedicine.diseaseDisorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]EndocrinologyMALDI TOFchemistryTransferrinbiology.proteinCDGAntibodybusinessCongenital disorder of glycosylationmedicine.drug
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Mutations in the MORC2 gene cause axonal Charcot-Marie-Tooth disease

2016

Charcot-Marie-Tooth disease (CMT) is a complex disorder with wide genetic heterogeneity. Here we present a new axonal Charcot-Marie-Tooth disease form, associated with the gene microrchidia family CW-type zinc finger 2 (MORC2). Whole-exome sequencing in a family with autosomal dominant segregation identified the novel MORC2 p. R190W change in four patients. Further mutational screening in our axonal Charcot-Marie-Tooth disease clinical series detected two additional sporadic cases, one patient who also carried the same MORC2 p. R190W mutation and another patient that harboured a MORC2 p. S25L mutation. Genetic and in silico studies strongly supported the pathogenicity of these sequence vari…

MORC2 genewhole-exome sequencingCharcot-Marie-Tooth diseaseaxonal degenerationSchwann cell
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TBL1XR1 mutations in Pierpont syndrome are not restricted to the recurrent p.Tyr446Cys mutation

2018

IF 2.264; International audience; Pierpont syndrome is a rare and sporadic syndrome, including developmental delay, facial characteristics, and abnormal extremities. Recently, a recurrent de novo TBL1XR1 variant (c.1337A > G; p.Tyr446Cys) has been identified in eight patients by whole‐exome sequencing. A dominant‐negative effect of this mutation is strongly suspected, since patients with TBL1XR1 deletion and other variants predicting loss of function do not share the same phenotype. We report two patients with typical Pierpont‐like syndrome features. Exome sequencing allowed identifying a de novo heterozygous missense TBL1XR1 variant in both patients, different from those already reported: …

Male0301 basic medicineAdolescentGenotypeReceptors Cytoplasmic and NuclearBiology03 medical and health sciences0302 clinical medicinePIERPONT SYNDROMEGeneticsHumansTBL1XR1Missense mutationAbnormalities MultipleRecurrent mutationGenetic TestingAllelesGenetics (clinical)Exome sequencingLoss functionUltrasonographyGeneticsComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsBrainFaciesNuclear ProteinsSyndromeMagnetic Resonance ImagingPhenotype3. Good healthRepressor ProteinsPhenotype030104 developmental biologyAmino Acid Substitution030220 oncology & carcinogenesisMutationMutation (genetic algorithm)Pierpont syndromeAmerican Journal of Medical Genetics Part A
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De Novo Mutations in SLC25A24 Cause a Disorder Characterized by Early Aging, Bone Dysplasia, Characteristic Face, and Early Demise

2017

International audience; A series of simplex cases have been reported under various diagnoses sharing early aging, especially evident in congenitally decreased subcutaneous fat tissue and sparse hair, bone dysplasia of the skull and fingers, a distinctive facial gestalt, and prenatal and postnatal growth retardation. For historical reasons, we suggest naming the entity Fontaine syndrome. Exome sequencing of four unrelated affected individuals showed that all carried the de novo missense variant c.649C>T (p.Arg217Cys) or c.650G>A (p.Arg217His) in SLC25A24, a solute carrier 25 family member coding for calcium-binding mitochondrial carrier protein (SCaMC-1, also known as SLC25A24). SLC25A24 all…

Male0301 basic medicineAgingMitochondrionPetty syndromeAntiportersATP-Mg/Pi carriersAdenosine TriphosphateCytosol0302 clinical medicineAdenine nucleotideMissense mutation[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)Exome sequencingMembrane Potential MitochondrialGeneticsProgeriaATP synthaseSCaMC-1SyndromeMitochondria3. Good healthFemalemedicine.medical_specialtylipodystrophyMolecular Dynamics SimulationBiologyPhosphatesMitochondrial Proteins03 medical and health sciencesReportInternal medicineGeneticsmedicineHumansFetal DeathBone Diseases DevelopmentalAdenineSLC25A24Calcium-Binding ProteinsagingInfant NewbornInfantprogeriaFibroblastsmedicine.diseaseMitochondrial carrierSolute carrier familyOxygenprogeroid disorder030104 developmental biologyEndocrinology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMutationbiology.protein030217 neurology & neurosurgery
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Exome Analysis Reveals Genomic Markers Associated with Better Efficacy of Nivolumab in Lung Cancer Patients

2019

Abstract Purpose: Immune checkpoint inhibitors revolutionized the treatment of non-small cell lung cancer (NSCLC). However, only one-quarter of patients benefit from these new therapies. PD-L1 assessment and tumor mutational burden (TMB) are available tools to optimize use of checkpoint inhibitors but novel tools are needed. Exome sequencing could generate many variables but their role in identifying predictors of response is unknown. Experimental Design: We performed somatic and constitutional exome analyses for 77 patients with NSCLC treated with nivolumab. We studied: one-tumor-related characteristics: aneuploidy, CNA clonality, mutational signatures, TMB, mutations in WNT, AKT, MAPK, an…

Male0301 basic medicineCancer ResearchLung NeoplasmsDNA repairAntineoplastic AgentsPembrolizumabAntibodies Monoclonal HumanizedB7-H1 AntigenDisease-Free Survival03 medical and health sciencesAntineoplastic Agents Immunological0302 clinical medicineCarcinoma Non-Small-Cell LungExome SequencingBiomarkers TumorHumansMedicineCTLA-4 AntigenLung cancerExomeExome sequencingAgedRetrospective StudiesAged 80 and overbusiness.industryGenomicsMiddle Agedmedicine.diseaseIpilimumabNivolumabTreatment Outcome030104 developmental biologyOncology030220 oncology & carcinogenesisMutationMonoclonalCancer researchBiomarker (medicine)FemaleNivolumabbusinessClinical Cancer Research
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Variant recurrence in neurodevelopmental disorders: the use of publicly available genomic data identifies clinically relevant pathogenic missense var…

2019

Next-generation sequencing has revealed the major impact of de novo variants (DNVs) in developmental disorders (DD) such as intellectual disability, autism, and epilepsy. However, a substantial fraction of these predicted pathogenic DNVs remains challenging to distinguish from background DNVs, notably the missense variants acting via nonhaploinsufficient mechanisms on specific amino acid residues. We hypothesized that the detection of the same missense variation in at least two unrelated individuals presenting with a similar phenotype could be a powerful approach to reveal novel pathogenic variants. We looked for variations independently present in both our database of >1200 solo exomes and…

Male0301 basic medicineCandidate geneDevelopmental DisabilitiesMutation Missense030105 genetics & heredityBiology03 medical and health sciencesNeurodevelopmental disorderIntellectual DisabilityDatabases GeneticIntellectual disabilitymedicineHumansMissense mutationExomeGenetic Predisposition to DiseaseGenetic TestingAutistic DisorderGeneGenetics (clinical)Exome sequencingGeneticsComputational BiologyHigh-Throughput Nucleotide SequencingGenomicsSequence Analysis DNAmedicine.diseasePhenotype030104 developmental biologyNeurodevelopmental DisordersAutismFemaleTranscription FactorsGenetics in Medicine
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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
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Comprehensive Genomic and Transcriptomic Analysis of Three Synchronous Primary Tumours and a Recurrence from a Head and Neck Cancer Patient

2021

Synchronous primary malignancies occur in a small proportion of head and neck squamous cell carcinoma (HNSCC) patients. Here, we analysed three synchronous primaries and a recurrence from one patient by comparing the genomic and transcriptomic profiles among the tumour samples and determining the recurrence origin. We found remarkable levels of heterogeneity among the primary tumours, and through the patterns of shared mutations, we traced the origin of the recurrence. Interestingly, the patient carried germline variants that might have predisposed him to carcinogenesis, together with a history of alcohol and tobacco consumption. The mutational signature analysis confirmed the impact of alc…

Male0301 basic medicineOncologyAlcohol exposuremedicine.disease_causeGermlineNeoplasms Multiple PrimaryTranscriptomeFatal Outcome0302 clinical medicineMedicineBiology (General)Immune cell infiltrationSpectroscopysynchronous multiple primary malignanciesSmokersimmune cell infiltrationGenomicsGeneral MedicineComputer Science Applicationswhole exome sequencing (WES)Chemistrysomatic single nucleotide variantsHead and Neck Neoplasms030220 oncology & carcinogenesismedicine.medical_specialtyrecurrent head and neck squamous cell carcinoma (HNSCC)Alcohol DrinkingQH301-705.5ArticleCatalysisInorganic Chemistry03 medical and health sciencesInternal medicineHumansPhysical and Theoretical ChemistryQD1-999Molecular BiologyAgedNeoplasm Stagingbusiness.industryGene Expression ProfilingOrganic ChemistryHead and neck cancerRNA sequencing (RNA-seq)medicine.diseaseHead and neck squamous-cell carcinoma030104 developmental biologygermline variantsMutationClinical valueNeoplasm Recurrence LocalbusinessCarcinogenesisInternational Journal of Molecular Sciences
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Diagnostic strategy in segmentation defect of the vertebrae: a retrospective study of 73 patients

2018

BackgroundSegmentation defects of the vertebrae (SDV) are non-specific features found in various syndromes. The molecular bases of SDV are not fully elucidated due to the wide range of phenotypes and classification issues. The genes involved are in the Notch signalling pathway, which is a key system in somitogenesis. Here we report on mutations identified in a diagnosis cohort of SDV. We focused on spondylocostal dysostosis (SCD) and the phenotype of these patients in order to establish a diagnostic strategy when confronted with SDV.Patients and methodsWe used DNA samples from a cohort of 73 patients and performed targeted sequencing of the five known SCD-causing genes (DLL3,MESP2,LFNG,HES7…

Male0301 basic medicineOncologymedicine.medical_specialtyCandidate geneAdolescent030105 genetics & heredityspondylocostal dysostosisdiagnostic strategysegmentation defect of the vertebraewhole exome sequencingLFNG03 medical and health sciencesgene panelInternal medicineExome SequencingBasic Helix-Loop-Helix Transcription FactorsGeneticsmedicineHumansFLNBChildGenetics (clinical)Exome sequencingBone Diseases Developmentalbusiness.industryIntracellular Signaling Peptides and ProteinsGlycosyltransferasesInfantMembrane ProteinsRetrospective cohort studymedicine.diseasePhenotypeSpineSpondylocostal dysostosisPedigreePhenotype[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolMutationCohortFemaleT-Box Domain Proteinsbusiness
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