Search results for "Sequencing"

showing 10 items of 1087 documents

Sequential transcriptome analysis of human liver cancer indicates late stage acquisition of malignant traits

2014

Background & Aims Human hepatocarcinogenesis is as a multi-step process starting from dysplastic lesions to early carcinomas (eHCC) that ultimately progress to HCC (pHCC). However, the sequential molecular alterations driving malignant transformation of the pre-neoplastic lesions are not clearly defined. This lack of information represents a major challenge in the clinical management of patients at risk. Methods We applied next-generation transcriptome sequencing to tumor-free surrounding liver (n=7), low- (n=4) and high-grade (n=9) dysplastic lesions, eHCC (n=5) and pHCC (n=3) from 8 HCC patients with hepatitis B infection. Integrative analyses of genetic and transcriptomic changes were pe…

AdultMaleHepatocarcinogenesisCarcinoma HepatocellularCarcinogenesisBiologyBioinformaticsmedicine.disease_causePolymorphism Single NucleotideArticleMalignant transformationTranscriptomeCarcinomamedicineTumor MicroenvironmentHumansMolecular pathogenesisRNA NeoplasmGeneAgedTumor microenvironmentHepatologyGene Expression ProfilingLiver NeoplasmsWnt signaling pathwayRNA sequencingMiddle Agedmedicine.diseaseGene expression profilingCell Transformation NeoplasticMutationCancer researchDisease ProgressionFemaleCarcinogenesis
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Truncating mutations in the last exon of NOTCH2 cause a rare skeletal disorder with osteoporosis.

2010

Hajdu-Cheney syndrome is a rare autosomal dominant skeletal disorder with facial anomalies, osteoporosis and acro-osteolysis. We sequenced the exomes of six unrelated individuals with this syndrome and identified heterozygous nonsense and frameshift mutations in NOTCH2 in five of them. All mutations cluster to the last coding exon of the gene, suggesting that the mutant mRNA products escape nonsense-mediated decay and that the resulting truncated NOTCH2 proteins act in a gain-of-function manner.

AdultMaleHeterozygoteHajdu–Cheney syndromeAdolescentmedia_common.quotation_subjectNonsenseMolecular Sequence DataBiologymedicine.disease_causeHajdu-Cheney SyndromeFrameshift mutationExonYoung AdultRare DiseasesSkeletal disorderGeneticsmedicineHumansAmino Acid SequenceReceptor Notch2Frameshift MutationGeneExome sequencingmedia_commonGeneticsMutationBase SequenceDNAExonsMiddle Agedmedicine.diseasePedigreeCodon NonsenseChild PreschoolMutationFemaleSignal TransductionNature genetics
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Prominence vs. aboutness in sequencing: a functional distinction within the left inferior frontal gyrus

2009

Prior research on the neural bases of syntactic comprehension suggests that activation in the left inferior frontal gyrus (lIFG) correlates with the processing of word order variations. However, there are inconsistencies with respect to the specific subregion within the IFG that is implicated by these findings: the pars opercularisor the pars triangularis. Here, we examined the hypothesis that the dissociation between parsopercularis and pars triangularis activation may reflect functional differences between clause-medial and clause-initial word order permutations, respectively. To this end, we directly compared clause-medial and clause-initial object-before-subject orders in German in a wi…

AdultMaleLinguistics and LanguageDissociation (neuropsychology)Cognitive NeuroscienceExperimental and Cognitive Psychologyleft inferior frontal gyrusLeft inferior frontal gyrusFunctional LateralityLanguage and LinguisticsSpeech and HearingSuperior temporal gyrusHumansPrefrontal cortexaboutnessinformation structureLanguageBrain MappingLanguage TestsfMRICognitionsequencingGermanword orderMagnetic Resonance ImagingFrontal Lobesyntactic processingAboutnesssuperior temporal gyrusprominenceFemaleNerve NetComprehensionPsychologySentenceWord orderCognitive psychology
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Deciphering exome sequencing data: Bringing mitochondrial DNA variants to light

2019

The expanding use of exome sequencing (ES) in diagnosis generates a huge amount of data, including untargeted mitochondrial DNA (mtDNA) sequences. We developed a strategy to deeply study ES data, focusing on the mtDNA genome on a large unspecific cohort to increase diagnostic yield. A targeted bioinformatics pipeline assembled mitochondrial genome from ES data to detect pathogenic mtDNA variants in parallel with the "in-house" nuclear exome pipeline. mtDNA data coming from off-target sequences (indirect sequencing) were extracted from the BAM files in 928 individuals with developmental and/or neurological anomalies. The mtDNA variants were filtered out based on database information, cohort …

AdultMaleMitochondrial DNAAtaxiaAdolescentDevelopmental Disabilities[SDV]Life Sciences [q-bio]BiologyDNA MitochondrialGenomeHaplogroupYoung Adult03 medical and health sciencesExome SequencingGeneticsmedicineHumansChildExomeGenetics (clinical)Exome sequencingComputingMilieux_MISCELLANEOUSAged030304 developmental biologyAged 80 and overGenetics0303 health sciences030305 genetics & heredityInfant NewbornComputational BiologyGenetic VariationInfantMiddle AgedPhenotypeEarly DiagnosisChild PreschoolFemaleNervous System Diseasesmedicine.symptom
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NDST1 missense mutations in autosomal recessive intellectual disability.

2014

NDST1 was recently proposed as a candidate gene for autosomal recessive intellectual disability in two families. It encodes a bifunctional GlcNAc N-deacetylase/N-sulfotransferase with important functions in heparan sulfate biosynthesis. In mice, Ndst1 is crucial for embryonic development and homozygous null mutations are perinatally lethal. We now report on two additional unrelated families with homozygous missense NDST1 mutations. All mutations described to date predict the substitution of conserved amino acids in the sulfotransferase domain, and mutation modeling predicts drastic alterations in the local protein conformation. Comparing the four families, we noticed significant overlap in …

AdultMaleModels MolecularCandidate geneAdolescentGenotypeProtein ConformationDNA Mutational AnalysisMutation MissenseGenes RecessiveBiologyBioinformaticsPolymorphism Single NucleotideAnimals Genetically ModifiedEpilepsyConsanguinityYoung AdultProtein structureIntellectual DisabilityIntellectual disabilityGeneticsmedicineMissense mutationAnimalsHumansChildGenetics (clinical)GeneticsGene knockdownMuscular hypotoniaBehavior AnimalComputational BiologyFaciesHigh-Throughput Nucleotide Sequencingmedicine.diseasePhenotypePedigreePhenotypeChild PreschoolGene Knockdown TechniquesDrosophilaFemaleSulfotransferasesGenome-Wide Association StudyAmerican journal of medical genetics. Part A
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IBD risk loci are enriched in multigenic regulatory modules encompassing putative causative genes

2018

GWAS have identified >200 risk loci for Inflammatory Bowel Disease (IBD). The majority of disease associations are known to be driven by regulatory variants. To identify the putative causative genes that are perturbed by these variants, we generate a large transcriptome data set (nine disease-relevant cell types) and identify 23,650 cis-eQTL. We show that these are determined by ∼9720 regulatory modules, of which ∼3000 operate in multiple tissues and ∼970 on multiple genes. We identify regulatory modules that drive the disease association for 63 of the 200 risk loci, and show that these are enriched in multigenic modules. Based on these analyses, we resequence 45 of the corresponding 100 ca…

AdultMaleMultifactorial InheritanceQUANTITATIVE TRAIT LOCUSGenotypeSEQUENCING DATAQuantitative Trait LociSUSCEPTIBILITYPolymorphism Single NucleotideArticleCohort StudiesCODING VARIANTSCrohn Disease80 and overJournal ArticleMedicine and Health SciencesLOCUSHumansGenetic Predisposition to DiseasePolymorphismGENOME-WIDE ASSOCIATIONGenetic Association StudiesAgedAged 80 and overScience & TechnologyAdult; Aged; Aged 80 and over; Cohort Studies; Crohn Disease; Female; Gene Expression Profiling; Genetic Association Studies; Genetic Predisposition to Disease; Genotype; Humans; Inflammatory Bowel Diseases; Male; Middle Aged; Polymorphism Single Nucleotide; Quantitative Trait Loci; Sequence Analysis DNA; Multifactorial InheritanceGene Expression ProfilingCOMPLEX TRAITSBiology and Life SciencesSequence Analysis DNASingle NucleotideDNAMiddle AgedInflammatory Bowel DiseasesCROHNS-DISEASEMultidisciplinary SciencesQUANTITATIVE TRAITRARE VARIANTSScience & Technology - Other TopicsFemaleLOW-FREQUENCYSequence AnalysisINFLAMMATORY-BOWEL-DISEASE
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Mutations in FAM111B Cause Hereditary Fibrosing Poikiloderma with Tendon Contracture, Myopathy, and Pulmonary Fibrosis

2013

Congenital poikiloderma is characterized by a combination of mottled pigmentation, telangiectasia, and epidermal atrophy in the first few months of life. We have previously described a South African European-descent family affected by a rare autosomal-dominant form of hereditary fibrosing poikiloderma accompanied by tendon contracture, myopathy, and pulmonary fibrosis. Here, we report the identification of causative mutations in FAM111B by whole-exome sequencing. In total, three FAM111B missense mutations were identified in five kindreds of different ethnic backgrounds. The mutation segregated with the disease in one large pedigree, and mutations were de novo in two other pedigrees. All thr…

AdultMalePathologymedicine.medical_specialtyContractureAdolescentPulmonary FibrosisPoikilodermaCell Cycle Proteinsmedicine.disease_causeTendonssymbols.namesakeYoung AdultMuscular DiseasesReportPulmonary fibrosismedicineGeneticsMissense mutationHumansGenetics(clinical)MyopathyChildRothmund–Thomson syndromeGenetics (clinical)Sanger sequencingMutationbusiness.industryInfant NewbornRothmund-Thomson SyndromeInfantmedicine.diseasePedigreePhenotypeChild PreschoolMutationsymbolsFemalemedicine.symptomContracturebusiness
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Cutaneous Lymphadenoma Is a Distinct Trichoblastoma-like Lymphoepithelial Tumor With Diffuse Androgen Receptor Immunoreactivity, Notch1 Ligand in Ree…

2021

The term "cutaneous lymphadenoma" was coined in this journal for an unusual lymphoepithelial cutaneous adnexal neoplasm, possibly with immature pilosebaceous differentiation. Some authors further proposed that cutaneous lymphadenoma was an adamantinoid trichoblastoma. However, although a hair follicle differentiation is widely accepted, the fact that this is a lymphoepithelial tumor is not appropriately explained by the trichoblastoma hypothesis. Our goal was to further clarify the phenotypic and genotypic features of cutaneous lymphadenoma in a series of 11 cases. Histologically, a lobular architecture surrounded by a dense fibrous stroma was present in all cases. The lobules were composed…

AdultMalePathologymedicine.medical_specialtySkin NeoplasmsCD30EGFRDNA Mutational Analysisadamantinoid trichoblastomaGene mutationBiologyStem cell markerT-Lymphocytes RegulatoryPathology and Forensic MedicineLymphocytes Tumor-Infiltratingandrogen receptormedicineBiomarkers TumorHumansReceptor Notch1Reed-Sternberg CellsAgedNotch1Jagged-1cutaneous lymphadenomaHigh-Throughput Nucleotide SequencingEpithelial CellsOriginal ArticlesMiddle Agedmedicine.diseaseHair follicleAdenolymphomaImmunohistochemistryAndrogen receptorErbB ReceptorsTrichoblastomamedicine.anatomical_structureReceptors AndrogenMutationIntraepithelial lymphocyteSurgeryFemaleAnatomyHair FollicleImmunostainingThe American journal of surgical pathology
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Hearing impairment as an early sign of alpha-mannosidosis in children with a mild phenotype: Report of seven new cases.

2019

Alpha-mannosidosis (AM) is a very rare (prevalence: 1/500000 births) autosomal recessive lysosomal storage disorder. It is characterized by multi-systemic involvement associated with progressive intellectual disability, hearing loss, skeletal anomalies, and coarse facial features. The spectrum is wide, from very severe and lethal to a milder phenotype that usually progresses slowly. AM is caused by a deficiency of lysosomal alpha-mannosidase. A diagnosis can be established by measuring the activity of lysosomal alpha-mannosidase in leucocytes and screening for abnormal urinary excretion of mannose-rich oligosaccharides. Genetic confirmation is obtained with the identification of MAN2B1 muta…

AdultMalePediatricsmedicine.medical_specialtyAdolescentHearing lossAlpha-mannosidosisUrinary systemYoung Adultalpha-MannosidaseIntellectual DisabilityIntellectual disabilityExome SequencingGeneticsmedicineHumansChildHearing LossGenetics (clinical)Exome sequencingCoarse facial featuresbusiness.industrySiblingsEnzyme replacement therapymedicine.diseaseHypotoniaPhenotypeChild Preschoolalpha-MannosidosisFemalemedicine.symptombusinessLysosomesAmerican journal of medical genetics. Part A
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Whole-exome sequencing identifies the first French MODY 6 family with a new mutation in the NEUROD1 gene

2020

Abstract Aim The aim of the present study was to identify the affected gene in a French family with maturity-onset diabetes of the young (MODY) using whole-exome sequencing (WES). Methods WES was performed in one patient with MODY, and candidate variants were confirmed in members of the immediate family by Sanger sequencing. Results In the proband, a new heterozygous missense mutation (c.340A>C) was identified in the NEUROD1 gene by WES analysis and confirmed by Sanger sequencing. Additional Sanger sequencing of the proband's sister and mother revealed the same heterozygous mutation. The proband and his sister displayed typical clinical characteristics of MODY, while their mother had the sa…

AdultMaleProbandHeterozygoteEndocrinology Diabetes and Metabolism[SDV]Life Sciences [q-bio]Mutation MissenseMothers030209 endocrinology & metabolism030204 cardiovascular system & hematologyBiology03 medical and health sciencessymbols.namesake0302 clinical medicineEndocrinologyDiabetic NeuropathiesExome SequencingBasic Helix-Loop-Helix Transcription FactorsInternal MedicinemedicineHumansHypoglycemic AgentsInsulinMissense mutationDiabetic NephropathiesAge of OnsetGeneExome sequencingAgedSanger sequencingGeneticsDiabetic RetinopathySiblingsGeneral Medicinemedicine.disease[SDV] Life Sciences [q-bio]Diabetes Mellitus Type 2Mutation (genetic algorithm)symbolsFemaleFranceMODY 6NEUROD1 Gene
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