Search results for "exome"

showing 10 items of 202 documents

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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Haplotype reference consortium panel: Practical implications of imputations with large reference panels.

2017

Contains fulltext : 177754.pdf (Publisher’s version ) (Open Access) Recently, the Haplotype Reference Consortium (HRC) released a large imputation panel that allows more accurate imputation of genetic variants. In this study, we compared a set of directly assayed common and rare variants from an exome array to imputed genotypes, that is, 1000 genomes project (1000GP) and HRC. We showed that imputation using the HRC panel improved the concordance between assayed and imputed genotypes at common, and especially, low-frequency variants. Furthermore, we performed a genome-wide association meta-analysis of vertical cup-disc ratio, a highly heritable endophenotype of glaucoma, in four cohorts usin…

0301 basic medicineGenotypeConcordanceGenome-wide association study610 Medicine & healthBiologyPolymorphism Single NucleotideSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]03 medical and health sciencesGene FrequencyGeneticsAssociation studies Imputation 1000 Genomes Project reference Panel Haplotype Reference Consortium Vertical cup-disc ratioHumansExome1000 Genomes Project610 Medicine & healthExomeAllele frequencyGenetics (clinical)Genetic associationGeneticsGenome HumanHaplotypeGenetic Variation030104 developmental biologyHaplotypesImputation (genetics)Genome-Wide Association Study
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Integrative Genome-Scale DNA Methylation Analysis of a Large and Unselected Cohort Reveals 5 Distinct Subtypes of Colorectal Adenocarcinomas

2019

BACKGROUND & AIMS: Colorectal cancer is an epigenetically heterogeneous disease, however, the extent and spectrum of the CpG island methylator phenotype (CIMP) is not clear. METHODS: Genome-scale methylation and transcript expression were measured by DNA Methylation and RNA expression microarray in 216 unselected colorectal cancers, and findings were validated using The Cancer Genome Atlas 450K and RNA sequencing data. Mutations in epigenetic regulators were assessed using CIMP-subtyped Cancer Genome Atlas exomes. RESULTS: CIMP-high cancers dichotomized into CIMP-H1 and CIMP-H2 based on methylation profile. KRAS mutation was associated significantly with CIMP-H2 cancers, but not CIMP-H1 can…

0301 basic medicineHepatologyCpG Island Methylator PhenotypeColorectal cancerGastroenterologyMethylationBiologymedicine.disease_causemedicine.diseasedigestive system diseases3. Good health03 medical and health sciences030104 developmental biology0302 clinical medicineDNA methylationCancer researchmedicinelcsh:Diseases of the digestive system. Gastroenterology030211 gastroenterology & hepatologyKRASEpigeneticslcsh:RC799-869neoplasmsGeneExome sequencingCellular and Molecular Gastroenterology and Hepatology
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Wiedemann-Steiner syndrome as a major cause of syndromic intellectual disability: A study of 33 French cases.

2018

International audience; Wiedemann-Steiner syndrome (WSS) is a rare syndromic condition in which intellectual disability (ID) is associated with hypertrichosis cubiti, short stature, and characteristic facies. Following the identification of the causative gene (KMT2A) in 2012, only 31 cases of WSS have been described precisely in the literature. We report on 33 French individuals with a KMT2A mutation confirmed by targeted gene sequencing, high-throughput sequencing or exome sequencing. Patients' molecular and clinical features were recorded and compared with the literature data. On the molecular level, we found 29 novel mutations. We observed autosomal dominant transmission of WSS in 3 fami…

0301 basic medicineHypertrichosisMalePediatrics[SDV]Life Sciences [q-bio]MESH: Magnetic Resonance ImagingPathognomonicMESH: ChildIntellectual disabilityMESH: SyndromeChildMESH: High-Throughput Nucleotide SequencingGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSbiologyWiedemann-Steiner syndromeHigh-Throughput Nucleotide SequencingSyndromeKMT2AMESH: Amino Acid SubstitutionMagnetic Resonance Imaginghypertrichosis3. Good healthhairinessKMT2APhenotypeWiedemann-Steiner syndromeChild Preschoolcardiovascular systemFemaleDisease SusceptibilityFrancemedicine.symptomMESH: Tomography X-Ray ComputedMyeloid-Lymphoid Leukemia Proteinmedicine.medical_specialtyMESH: MutationAdolescentMESH: Disease SusceptibilityMESH: PhenotypeShort statureMESH: Intellectual Disability03 medical and health sciencesHypertrichosis cubitiIntellectual DisabilityGeneticsmedicineHumanshistone methylationMESH: Adolescent[SDV.GEN]Life Sciences [q-bio]/GeneticsMESH: Humansbusiness.industryMESH: Child PreschoolMESH: Histone-Lysine N-MethyltransferaseHistone-Lysine N-Methyltransferasemedicine.diseaseMESH: MaleMESH: France030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAmino Acid SubstitutionMESH: Myeloid-Lymphoid Leukemia ProteinMutationbiology.proteinbusinessTomography X-Ray ComputedMESH: FemaleClinical genetics
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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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Genome-wide profiling of non-smoking-related lung cancer cells reveals common RB1 rearrangements associated with histopathologic transformation in EG…

2020

The etiology and the molecular basis of lung adenocarcinomas (LuADs) in nonsmokers are currently unknown. Furthermore, the scarcity of available primary cultures continues to hamper our biological understanding of non-smoking-related lung adenocarcinomas (NSK-LuADs). We established patient-derived cancer cell (PDC) cultures from metastatic NSK-LuADs, including two pairs of matched EGFR-mutant PDCs before and after resistance to tyrosine kinase inhibitors (TKIs), and then performed whole-exome and RNA sequencing to delineate their genomic architecture. For validation, we analyzed independent cohorts of primary LuADs. In addition to known non-smoker-associated alterations (e.g. RET, ALK, EGFR…

0301 basic medicineLung NeoplasmsEGFRUbiquitin-Protein LigasesAdenocarcinoma of Lungmedicine.disease_cause03 medical and health sciences0302 clinical medicineGermline mutationtyrosine kinase inhibitorsmedicineGenetic predispositionHumanswhole-exome sequencingLung cancerGeneProtein Kinase InhibitorsExome sequencingMutationbusiness.industryEGFR RB1 lung adenocarcinoma nonsmokers tyrosine kinase inhibitors whole-exome sequencingHematologyrespiratory systemmedicine.diseaselung adenocarcinomadigestive system diseasesrespiratory tract diseasesErbB ReceptorsRetinoblastoma Binding Proteins030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisCancer cellMutationCancer researchbusinessRB1Tyrosine kinaseMicrotubule-Associated Proteinsnonsmokers
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Biallelic variants in LARS2 and KARS cause deafness and (ovario)leukodystrophy

2019

Supplemental Digital Content is available in the text.

0301 basic medicineLysine-tRNA LigaseMalePathologyMagnetic Resonance SpectroscopyMedizinmembrane proteins030204 cardiovascular system & hematologyMitochondrionDeafnessmedicine.disease_causeCompound heterozygosityCorrectionsLeukoencephalopathyMyelin0302 clinical medicineCytosolLeukoencephalopathies030212 general & internal medicineOvarian DiseasesTransfer RNA AminoacylationChildZebrafishMUTATIONExome sequencing10012MutationBrainMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]General MedicineMiddle AgedDisorders of movement Donders Center for Medical Neuroscience [Radboudumc 3]Magnetic Resonance ImagingMitochondriaProtein Transportendoplasmic reticulummedicine.anatomical_structureChild PreschoolTransfer RNAComputingMethodologies_DOCUMENTANDTEXTPROCESSING/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Biological AssayFemaleWRBRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Adultcardiomyopathiesmedicine.medical_specialtyMitochondrial diseaseAminoacylationMuscle disorderBiologyArticleMEDIATES INSERTIONAmino Acyl-tRNA Synthetases03 medical and health sciencesSDG 3 - Good Health and Well-beingmedicineAnimalsPoint MutationHumansAmino Acid SequenceAlleleAllelesCOMPLEXGenetic heterogeneitybusiness.industryArsenite Transporting ATPasesLeukodystrophyGenetic Variation10090Original ArticlesZebrafish Proteinsbiology.organism_classificationDILATED CARDIOMYOPATHYmedicine.diseasezebrafishGENEMolecular biologyDisease Models Animal030104 developmental biologyMembrane protein[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human genetics10084Neurology (clinical)Transfer RNA AminoacylationMEMBRANEbusinessSequence Alignment030217 neurology & neurosurgeryexomeNeurology
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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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