Search results for " Exome"

showing 10 items of 36 documents

Are mutations in the dhrs9 gene causally linked to epilepsy? A case report

2020

The DHRS9 gene is involved in several pathways including the synthesis of allopregnanolone from progesterone. Allopregnanolone is a positive modulator of gamma aminobutyric acid (GABA) action and plays a role in the control of neuronal excitability and seizures. Whole-exome sequencing performed on a girl with an early onset epilepsy revealed that she was a compound heterozygote for two novel missense mutations of the DHRS9 gene likely to disrupt protein function. No previous studies have reported the implication of this gene in epilepsy. We discuss a new potential pathogenic mechanism underlying epilepsy in a child, due to a defective progesterone pathway.

0301 basic medicineCase ReportCompound heterozygosityBioinformaticsAllopregnanolone DHRS9 Exome GABA NGS Temporal lobe epilepsygamma-Aminobutyric acid03 medical and health scienceschemistry.chemical_compoundEpilepsyGABA0302 clinical medicinemedicineMissense mutationGeneExomelcsh:R5-920business.industryMechanism (biology)DHRS9AllopregnanoloneallopregnanoloneGeneral Medicinetemporal lobe epilepsymedicine.disease030104 developmental biologychemistryNGSlcsh:Medicine (General)business030217 neurology & neurosurgeryexomemedicine.drug
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Exome-Wide Association Study on Alanine Aminotransferase Identifies Sequence Variants in the GPAM and APOE Associated With Fatty Liver Disease.

2021

BACKGROUND & AIMS: Fatty liver disease (FLD) is a growing epidemic that is expected to be the leading cause of end-stage liver disease within the next decade. Both environmental and genetic factors contribute to the susceptibility of FLD. Several genetic variants contributing to FLD have been identified in exome-wide association studies. However, there is still a missing hereditability indicating that other genetic variants are yet to be discovered. METHODS: To find genes involved in FLD, we first examined the association of missense and nonsense variants with alanine amino transferase at an exome-wide level in 425,671 participants from the UK Biobank. We then validated genetic variants wit…

0301 basic medicineGenome-wide association studyLiver disease0302 clinical medicineENRICHMENT ANALYSISNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseExomeCONFERS SUSCEPTIBILITYGeneticsINSULIN-RESISTANCEmedicine.diagnostic_testFatty liverGastroenterologyAlanine Transaminase1-Acylglycerol-3-Phosphate O-Acyltransferase3. Good healthGENOMEEuropePhenotypeLiver biopsy030211 gastroenterology & hepatologyNonalcoholic Fatty Liver DiseaseMAFLDSingle-nucleotide polymorphismBiologyTransaminaseRisk Assessment03 medical and health sciencesApolipoproteins ENAFLDmedicineGenetic predispositionHumansGenetic Predisposition to DiseaseHEPATIC STEATOSISGenetic associationMAFLD Phenotype Reproducibility of Results Risk Assessment Risk Factors Transcriptome Genetic Variation Metabolic Associated Fatty Liver Disease Nonalcoholic Fatty Liver Disease Transaminase 1-Acylglycerol-3-Phosphate O-Acyltransferase Alanine Transaminase Apolipoproteins E Biomarkers Europe Exome Gene Expression Profiling Genetic Predisposition to Disease Genome-Wide Association Study Humans Non-alcoholic Fatty Liver DiseaseHepatologyMUTATIONSGene Expression ProfilingGenetic VariationReproducibility of Resultsmedicine.diseaseX-RECEPTORGENE030104 developmental biology3121 General medicine internal medicine and other clinical medicineMetabolic Associated Fatty Liver DiseaseRNA-SEQ DATATranscriptomePATHOGENICITYBiomarkersGenome-Wide Association StudyGastroenterology
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Machine Learning-Based Approach Highlights the Use of a Genomic Variant Profile for Precision Medicine in Ovarian Failure

2021

Ovarian failure (OF) is a common cause of infertility usually diagnosed as idiopathic, with genetic causes accounting for 10–25% of cases. Whole-exome sequencing (WES) may enable identifying contributing genes and variant profiles to stratify the population into subtypes of OF. This study sought to identify a blood-based gene variant profile using accumulation of rare variants to promote precision medicine in fertility preservation programs. A case–control (n = 118, n = 32, respectively) WES study was performed in which only non-synonymous rare variants &lt

0301 basic medicineInfertilityOncologygenomic taxonomymedicine.medical_specialtyprecision medicineovarian failurePopulationMedicine (miscellaneous)BiologyGenoma humàArticlewhole exome sequencing03 medical and health sciences0302 clinical medicineInternal medicinemedicinesingle nucleotide variantFertility preservationeducationGeneExome sequencingeducation.field_of_study030219 obstetrics & reproductive medicinebusiness.industryRpersonalized medicinePrecision medicinemedicine.diseaseprediction modelMinor allele frequency030104 developmental biologyGinecologiaMedicineovaryPersonalized medicineinfertilitybusinessgenome variant profileJournal of Personalized Medicine
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Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

2017

International audience; We identified rare coding variants associated with Alzheimer's disease in a three-stage case-control study of 85,133 subjects. In stage 1, we genotyped 34,174 samples using a whole-exome microarray. In stage 2, we tested associated variants (P < 1 × 10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, we used an additional 14,997 samples to test the most significant stage 2 associations (P < 5 × 10-8) using imputed genotypes. We observed three new genome-wide significant nonsynonymous variants associated with Alzheimer's disease: a protective variant in PLCG2 (rs72824905: p.Pro522Arg, P = 5.38 × 10-10, odds ratio (OR) = 0.68…

0301 basic medicineLinkage disequilibrium[SDV]Life Sciences [q-bio]MedizinSequence HomologyGenome-wide association studygenetics [Alzheimer Disease]metabolism [Microglia]Linkage Disequilibrium0302 clinical medicinegenetics [Protein Interaction Maps]genetics [Membrane Glycoproteins]Gene FrequencyImmunologicgenetics [Adaptor Proteins Signal Transducing]Receptorsgenetics [Exome]Odds RatioInnategenetics [Receptors Immunologic]ExomeProtein Interaction Mapsgenetics [Genetic Predisposition to Disease]Receptors ImmunologicABI3 protein humanGeneticsAdaptor Proteins Signal Transducing; Alzheimer Disease; Amino Acid Sequence; Case-Control Studies; Exome; Gene Expression Profiling; Gene Frequency; Genetic Predisposition to Disease; Genotype; Humans; Immunity Innate; Linkage Disequilibrium; Membrane Glycoproteins; Microglia; Odds Ratio; Phospholipase C gamma; Protein Interaction Maps; Receptors Immunologic; Sequence Homology Amino Acid; Polymorphism Single Nucleotide; GeneticsMembrane GlycoproteinsAdaptor ProteinsSingle NucleotideAdaptor Proteins Signal Transducing; Alzheimer Disease; Amino Acid Sequence; Case-Control Studies; Exome; Gene Expression Profiling; Gene Frequency; Genetic Predisposition to Disease; Genotype; Humans; Immunity Innate; Linkage Disequilibrium; Membrane Glycoproteins; Microglia; Odds Ratio; Phospholipase C gamma; Protein Interaction Maps; Receptors Immunologic; Sequence Homology Amino Acid; Polymorphism Single Nucleotide3. Good health[SDV] Life Sciences [q-bio]Amino AcidSettore MED/26 - NEUROLOGIAgenetics [Phospholipase C gamma][SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]MicrogliaAlzheimer's diseaseCommon disease-common variantGenotypeBiologyPolymorphism Single NucleotideArticle03 medical and health sciencesAlzheimer Diseaseddc:570medicineJournal ArticleGeneticsHumansGenetic Predisposition to Disease[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Amino Acid SequencePolymorphismAllele frequencyAdaptor Proteins Signal TransducingTREM2 protein humanSequence Homology Amino AcidTREM2Phospholipase C gammaGene Expression ProfilingCase-control studySignal TransducingImmunitymedicine.diseaseR1Immunity InnateMinor allele frequencygenetics [Immunity Innate]030104 developmental biologyCase-Control StudiesHuman medicine030217 neurology & neurosurgery
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De novo mutations in the X-linked TFE3 gene cause intellectual disability with pigmentary mosaicism and storage disorder-like features

2020

IntroductionPigmentary mosaicism (PM) manifests by pigmentation anomalies along Blaschko’s lines and represents a clue toward the molecular diagnosis of syndromic intellectual disability (ID). Together with new insights on the role for lysosomal signalling in embryonic stem cell differentiation, mutations in the X-linked transcription factor 3 (TFE3) have recently been reported in five patients. Functional analysis suggested these mutations to result in ectopic nuclear gain of functions.Materials and methodsSubsequent data sharing allowed the clustering of de novo TFE3 variants identified by exome sequencing on DNA extracted from leucocytes in patients referred for syndromic ID with or with…

0301 basic medicineMESH: Basic Helix-Loop-Helix Leucine Zipper Transcription Factors[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyIntellectual disabilityTFE3Biology[SDV.GEN.GH] Life Sciences [q-bio]/Genetics/Human geneticsMESH: Intellectual Disability03 medical and health sciencesExon0302 clinical medicineMESH: Whole Exome SequencingMESH: ChildIntellectual disabilityGeneticsmedicineMissense mutationGeneGenetics (clinical)Exome sequencingPigmentary mosaicismMESH: Pathology MolecularGeneticsMESH: AdolescentMESH: HumansAlternative splicingLysosomal metabolismMESH: Child Preschool[SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/NeurobiologyMESH: Adultmedicine.diseasePhenotypeMESH: InfantMESH: MaleTFE3Storage disorder030104 developmental biologyMESH: Genes X-Linked[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMESH: Young AdultMESH: EpilepsyMESH: MosaicismMESH: Pigmentation DisordersMESH: Female030217 neurology & neurosurgery
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Further delineation of the clinical spectrum of de novo TRIM8 truncating mutations.

2018

IF 2.264; International audience; De novo mutations of the TRIM8 gene, which codes for a tripartite motif protein, have been identified using whole exome sequencing (WES) in two patients with epileptic encephalopathy (EE), but these reports were not sufficient to conclude that TRIM8 was a novel gene responsible for EE. Here we report four additional patients presenting with EE and de novo truncating mutations of TRIM8 detected by WES, and give further details of the patient previously reported by the Epi4K consortium. Epilepsy of variable severity was diagnosed in children aged 2 months to 3.5 years of age. All patients had developmental delay of variable severity with no or very limited la…

0301 basic medicineMaleAdolescentNerve Tissue ProteinsBioinformaticswhole exome sequencing03 medical and health sciencesEpilepsyTripartite MotifGeneticsmedicineHumansTRIM8Amino Acid SequenceChildGeneGenetics (clinical)De novo mutationsExome sequencingbusiness.industrynephrotic syndromeEpileptic encephalopathyInfant NewbornInfantmedicine.diseasePhenotype3. Good health030104 developmental biologyepileptic encephalopathy[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolMutationFemalebusinessCarrier ProteinsNephrotic syndromeAmerican journal of medical genetics. Part A
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The oculoauriculofrontonasal syndrome: Further clinical characterization and additional evidence suggesting a nontraditional mode of inheritance

2018

IF 2.264; International audience; The oculoauriculofrontonasal syndrome (OAFNS) is a rare disorder characterized by the association of frontonasal dysplasia (widely spaced eyes, facial cleft, and nose abnormalities) and oculo-auriculo-vertebral spectrum (OAVS)-associated features, such as preauricular ear tags, ear dysplasia, mandibular asymmetry, epibulbar dermoids, eyelid coloboma, and costovertebral anomalies. The etiology is unknown so far. This work aimed to identify molecular bases for the OAFNS. Among a cohort of 130 patients with frontonasal dysplasia, accurate phenotyping identified 18 individuals with OAFNS. We describe their clinical spectrum, including the report of new features…

0301 basic medicineMaleInheritance Patterns030105 genetics & heredityfrontonasal dysplasiawhole exome sequencingCraniofacial Abnormalities0302 clinical medicinePolymicrogyriaEye AbnormalitiesEar External10. No inequalityChildGenetics (clinical)Exome sequencingwhole genome sequencingThyroid agenesisHypoplasiaDNA-Binding ProteinsPhenotypeChild PreschoolFemaleRespiratory System Abnormalitiesmedicine.medical_specialtyAdolescentQuantitative Trait LociOculoauriculofrontonasal syndrome03 medical and health sciencesExome SequencingGeneticsmedicineHumansGenetic Predisposition to DiseaseFrontonasal dysplasiaGenetic Association StudiesWhole genome sequencingHomeodomain Proteinsbusiness.industryFacial cleftSkullInfant NewbornFaciesInfant030206 dentistrymedicine.diseaseDermatologySpine[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsDysplasiabusinessTomography Spiral ComputedTranscription Factors
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Dominant variants in the splicing factor PUF60 cause a recognizable syndrome with intellectual disability, heart defects and short stature

2016

Item does not contain fulltext Verheij syndrome, also called 8q24.3 microdeletion syndrome, is a rare condition characterized by ante- and postnatal growth retardation, microcephaly, vertebral anomalies, joint laxity/dislocation, developmental delay (DD), cardiac and renal defects and dysmorphic features. Recently, PUF60 (Poly-U Binding Splicing Factor 60 kDa), which encodes a component of the spliceosome, has been discussed as the best candidate gene for the Verheij syndrome phenotype, regarding the cardiac and short stature phenotype. To date, only one patient has been reported with a de novo variant in PUF60 that probably affects function (c.505C>T leading to p.(His169Tyr)) associated wi…

0301 basic medicineMaleMESH: Heart Defects Congenital / physiopathologyMicrocephalyPathologyMESH: Heart Defects Congenital / geneticsMESH: Exome / genetics030105 genetics & heredityMESH: RNA Splicing / geneticsMicrophthalmia[SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseasesMESH: ChildExomeMESH: RNA Splicing Factors / geneticsChildFrameshift MutationMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingColobomaMESH: Frameshift MutationHigh-Throughput Nucleotide SequencingMicrodeletion syndromeMicrocephaly Verheij syndrome PUF60ChemistryPhenotypeChild PreschoolDISEASESMicrocephalyMedical geneticsFemaleRNA Splicing Factorsmedicine.symptomChromosome DeletionChromosomes Human Pair 8MESH: Dwarfism / genetics*Heart Defects Congenitalmedicine.medical_specialtyGENESAdolescentRNA SplicingMESH: Chromosome DeletionDwarfismBiologyMESH: PhenotypeShort statureArticlePUF6003 medical and health sciencesInternal medicineIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyGeneticsmedicineHumansCraniofacialBiologyMESH: AdolescentNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]MESH: HumansMESH: Child Preschoolmedicine.diseaseMESH: Repressor Proteins / geneticsMESH: MaleRepressor Proteins030104 developmental biologyEndocrinologyMESH: Chromosomes Human Pair 8 / geneticsMESH: Dwarfism / physiopathologyMESH: Intellectual Disability / physiopathologyHuman medicineMESH: Intellectual Disability / geneticsVerheij syndromeMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Intersociety policy statement on the use of whole-exome sequencing in the critically ill newborn infant.

2017

Abstract The rapid advancement of next-generation sequencing (NGS) technology and the decrease in costs for whole-exome sequencing (WES) and whole-genome sequening (WGS), has prompted its clinical application in several fields of medicine. Currently, there are no specific guidelines for the use of NGS in the field of neonatal medicine and in the diagnosis of genetic diseases in critically ill newborn infants. As a consequence, NGS may be underused with reduced diagnostic success rate, or overused, with increased costs for the healthcare system. Most genetic diseases may be already expressed during the neonatal age, but their identification may be complicated by nonspecific presentation, esp…

0301 basic medicineMaleNeonatal intensive care unitDiseaseReview030105 genetics & heredityPediatricsWhole Exome SequencingNeonateNeonatalOutcome Assessment Health CareDiagnosisPolicy MakingExome sequencingSanger sequencingGenomelcsh:RJ1-570Perinatology and Child HealthSettore MED/38Intensive Care UnitsItalyWhole-exome sequencingPractice Guidelines as TopicsymbolsWESFemaleHumanDiagnosiNICUmedicine.medical_specialtyMendelian03 medical and health sciencessymbols.namesakeOutcome Assessment (Health Care)Neonatal ScreeningNeonatal intensive care unitGeneticIntensive Care Units NeonatalExome SequencingmedicineDiagnosis; Genetic; Genome; Mendelian; Neonatal intensive care unit; Neonate; NICU; WES; WGS; Whole-exome sequencing; Pediatrics Perinatology and Child HealthHumansGenetic TestingIntensive care medicineSettore MED/06 - ONCOLOGIA MEDICAGenetic heterogeneityCritically illbusiness.industryGenome HumanInfant NewbornInfantlcsh:PediatricsNewbornInfant newborn030104 developmental biologyDiagnosis; Genetic; Genome; Mendelian; NICU; Neonatal intensive care unit; Neonate; WES; WGS; Whole-exome sequencing; Female; Genetic Testing; Genome Human; Humans; Infant; Infant Newborn; Intensive Care Units Neonatal; Italy; Male; Neonatal Screening; Outcome Assessment (Health Care); Policy Making; Whole Exome Sequencing; Practice Guidelines as TopicPediatrics Perinatology and Child HealthDifferential diagnosisbusinessWGS
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Comprehensive evaluation of coding region point mutations in microsatellite-unstable colorectal cancer

2018

Microsatellite instability (MSI) leads to accumulation of an excessive number of mutations in the genome, mostly small insertions and deletions. MSI colorectal cancers (CRCs), however, also contain more point mutations than microsatellite-stable (MSS) tumors, yet they have not been as comprehensively studied. To identify candidate driver genes affected by point mutations in MSI CRC, we ranked genes based on mutation significance while correcting for replication timing and gene expression utilizing an algorithm, MutSigCV. Somatic point mutation data from the exome kit-targeted area from 24 exome-sequenced sporadic MSI CRCs and respective normals, and 12 whole-genome-sequenced sporadic MSI CR…

0301 basic medicineMedicine (General)Candidate geneclinical evaluationgenetic identificationgenetic analysisQH426-470medicine.disease_causeChromatin Epigenetics Genomics & Functional Genomicswhole exome sequencingddc:590mutator genesingle nucleotide polymorphismddc:576.5Gene Regulatory NetworksExomeExome sequencingCancercancer cellGeneticsMutation1184 Genetics developmental biology physiology3. Good healthgenetic codesyöpägeenitpriority journalMolecular Medicinewild typepoint mutationSystems MedicineColorectal Neoplasmscongenital hereditary and neonatal diseases and abnormalitiesddc:025.063/5703122 Cancerscancer geneticsSingle-nucleotide polymorphismcolorectal cancerBiologygene frequencyta3111mikrosatelliititcolony formationR105W geneArticle03 medical and health sciencesR5-920Gene interactionReportGeneticsmedicineHumanscontrolled studyhumanneoplasmspaksusuolisyöpäPoint mutationgene interactionhuman celltumor-related geneMicrosatellite instabilityMolecular Sequence AnnotationSequence Analysis DNAmedicine.diseaseta3122digestive system diseaseshuman tissueSTK38L gene030104 developmental biologyvalidation processgene expressionSMARCB1 genemicrosatellite instability3111 Biomedicinegene replicationReports
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