Search results for "Sequencing"

showing 10 items of 1087 documents

Circulating miR-323-3p is a biomarker for cardiomyopathy and an indicator of phenotypic variability in Friedreich’s ataxia patients

2017

AbstractMicroRNAs (miRNAs) are noncoding RNAs that contribute to gene expression modulation by regulating important cellular pathways. In this study, we used small RNA sequencing to identify a series of circulating miRNAs in blood samples taken from Friedreich’s ataxia patients. We were thus able to develop a miRNA biomarker signature to differentiate Friedreich’s ataxia (FRDA) patients from healthy people. Most research on FDRA has focused on understanding the role of frataxin in the mitochondria, and a whole molecular view of pathological pathways underlying FRDA therefore remains to be elucidated. We found seven differentially expressed miRNAs, and we propose that these miRNAs represent …

AdultMale0301 basic medicineSmall RNAAtaxiaSciencePopulationCardiomyopathyBioinformaticsArticleYoung Adult03 medical and health sciencesmicroRNAmedicineHumanseducationCells CulturedAgedCell ProliferationGeneticseducation.field_of_studyMultidisciplinarybiologyQRHigh-Throughput Nucleotide SequencingMiddle AgedPrognosismedicine.diseasePhenotypeMicroRNAs030104 developmental biologyBiological Variation PopulationFriedreich AtaxiaCase-Control StudiesFrataxinbiology.proteinBiomarker (medicine)MedicineFemalemedicine.symptomCardiomyopathiesBiomarkersFollow-Up StudiesScientific Reports
researchProduct

A constitutive BCL2 down-regulation aggravates the phenotype of PKD1-mutant-induced polycystic kidney disease

2017

IF 5.340; International audience; The main identified function of BCL2 protein is to prevent cell death by apoptosis. Mice knock-out for Bcl2 demonstrate growth retardation, severe polycystic kidney disease (PKD), gray hair and lymphopenia, and die prematurely after birth. Here, we report a 40-year-old male referred to for abdominal and thoracic aortic dissection with associated aortic root aneurysm, PKD, lymphocytopenia with a history of T cell lymphoblastic lymphoma, white hair since the age of 20, and learning difficulties. PKD, which was also detected in the father and sister, was related to an inherited PKD1 mutation. The combination of PKD with gray hair and lymphocytopenia was also r…

AdultMale0301 basic medicineTRPP Cation Channelsphenotypebcl2 geneBiologymicro rnaMice03 medical and health sciencesdown-regulationsymptom aggravating factorshemic and lymphatic diseasest-lymphocyteGene expressionGeneticsmedicinePolycystic kidney diseaseAnimalsHumansGenetic Predisposition to Disease[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsgenesMolecular BiologyGeneGenetics (clinical)Exome sequencingMice KnockoutPKD1apoptosisExonsGeneral MedicinePolycystic Kidney Autosomal Dominantmedicine.diseasePhenotypePedigreeUp-Regulation3. Good healthMicroRNAs030104 developmental biologyMRNA SequencingProto-Oncogene Proteins c-bcl-2[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsImmunologyCancer researchLymphocytopeniapolycystic kidney diseasesbcl-2 proteinHuman Molecular Genetics
researchProduct

Hepatitis C virus early kinetics and resistance-associated substitution dynamics during antiviral therapy with direct-acting antivirals

2018

The emergence of resistance-associated substitutions (RASs) can compromise the high efficacy of direct-acting antivirals (DAAs). Little is known about RASs selection at very early time points during DAA treatment. Therefore, we analyzed the potential emergence of RASs immediately after therapy initiation. Samples of 71 patients treated with different DAAs were collected at baseline, during therapy (hours 4 and 8; days 1-7; weeks 2-4) or until target not detected. HCV-RNA levels were determined by qPCR, and RASs were detected by deep sequencing. Sixty-three (89%) patients achieved a sustained virological response (SVR), 7 (10%) relapsed, and 1 (1%) experienced a breakthrough. Almost all non-…

AdultMale0301 basic medicinemedicine.medical_specialtySustained Virologic ResponseHepatitis C virusHepacivirusViral quasispeciesReal-Time Polymerase Chain ReactionDIRECT ACTING ANTIVIRALSmedicine.disease_causeAntiviral AgentsGastroenterologyDeep sequencingVirological response03 medical and health sciences0302 clinical medicineRecurrenceGenetic EvolutionVirologyInternal medicineDrug Resistance ViralHumansMedicineProspective StudiesSelection GeneticAgedAged 80 and overHepatologybusiness.industryAntiviral therapyvirus diseasesHepatitis C ChronicMiddle AgedViral Loaddigestive system diseases030104 developmental biologyInfectious DiseasesAmino Acid SubstitutionRNA ViralFemale030211 gastroenterology & hepatologySensitivity limitbusinessJournal of Viral Hepatitis
researchProduct

Phenotype associated with TAF2 biallelic mutations: a clinical description of four individuals and review of the literature

2021

International audience; Transcription factor IID is a multimeric protein complex that is essential for the initiation of transcription by RNA polymerase II. One of its critical components, the TATA-binding protein-associated factor 2, is encoded by the gene TAF2. Pathogenic variants of this gene have been shown to be responsible for the Mental retardation, autosomal recessive 40 syndrome. This syndrome is characterized by severe intellectual disability, postnatal microcephaly, pyramidal signs and thin corpus callosum. Until now, only three families have been reported separately. Here we report four individuals, from two unrelated families, who present with severe intellectual disability and…

AdultMaleAdolescentFoot Deformities CongenitalDevelopmental DisabilitiesAutosomal recessiveIntellectual disabilityPostnatal microcephaly[SDV.GEN] Life Sciences [q-bio]/GeneticsBiologyCorpus Callosum03 medical and health sciencesNeurodevelopmental disorderNeurodevelopmental disorderIntellectual disabilityGeneticsmedicineHumansMissense mutationGlobal developmental delayTAF2ChildGeneAllelesGenetics (clinical)Exome sequencing030304 developmental biologyGeneticsTATA-Binding Protein Associated Factors0303 health sciences[SDV.GEN]Life Sciences [q-bio]/Genetics030305 genetics & heredityGeneral Medicinemedicine.diseasePhenotypeChild PreschoolTAF2MicrocephalyFemaleTranscription Factor TFIID
researchProduct

Expanding the clinical phenotype of patients with a ZDHHC9 mutation.

2013

In 2007, 250 families with X-linked intellectual disability (XLID) were screened for mutations in genes on the X-chromosome, and in 4 of these families, mutations in the ZDHHC9 gene were identified. The ID was either isolated or associated with a marfanoid habitus. ZDHHC9 encodes a palmitoyl transferase that catalyzes the posttranslational modification of NRAS and HRAS. Since this first description, no additional patient with a ZDHHC9 mutation has been reported in the literature. Here, we describe a large family in which we identified a novel pathogenic ZDHHC9 nonsense mutation (p.Arg298*) by parallel sequencing of all X-chromosome exons. The mutation cosegregated with the clinical phenotyp…

AdultMaleAdolescentX-linked intellectual disabilityGenetic counselingNonsense mutationNeuropsychological TestsBioinformaticsYoung AdultFatal OutcomeGenes X-LinkedIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansHRASChildGenetics (clinical)GeneticsMassive parallel sequencingAcrocyanosisbusiness.industryBrainFaciesmedicine.diseaseMagnetic Resonance ImagingPedigreePhenotypeMutation (genetic algorithm)MutationbusinessAcyltransferasesAmerican journal of medical genetics. Part A
researchProduct

Both rare and de novo copy number variants are prevalent in agenesis of the corpus callosum but not in cerebellar hypoplasia or polymicrogyria.

2013

Agenesis of the corpus callosum (ACC), cerebellar hypoplasia (CBLH), and polymicrogyria (PMG) are severe congenital brain malformations with largely undiscovered causes. We conducted a large-scale chromosomal copy number variation (CNV) discovery effort in 255 ACC, 220 CBLH, and 147 PMG patients, and 2,349 controls. Compared to controls, significantly more ACC, but unexpectedly not CBLH or PMG patients, had rare genic CNVs over one megabase (p = 1.48×10−3; odds ratio [OR] = 3.19; 95% confidence interval [CI] = 1.89–5.39). Rare genic CNVs were those that impacted at least one gene in less than 1% of the combined population of patients and controls. Compared to controls, significantly more AC…

AdultMaleCancer ResearchMicrocephalycongenital hereditary and neonatal diseases and abnormalitiesAdolescentDNA Copy Number Variationslcsh:QH426-470Developmental DisabilitiesPopulationGenome-wide association studyBiologyNervous System MalformationsCorpus callosumPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineCerebellummental disordersGeneticsPolymicrogyriamedicineHumansCopy-number variationChildAgenesis of the corpus callosumeducationMolecular BiologyGenetics (clinical)Ecology Evolution Behavior and SystematicsExome sequencing030304 developmental biologyGenetics0303 health scienceseducation.field_of_studyGenome HumanInfant NewbornInfantMiddle Agedmedicine.disease3. Good healthMalformations of Cortical Developmentlcsh:GeneticsChild PreschoolFemaleAgenesis of Corpus Callosum030217 neurology & neurosurgeryResearch ArticleGenome-Wide Association StudyPLoS Genetics
researchProduct

Demethylation treatment restores hic1 expression and impairs aggressiveness of head and neck squamous cell carcinoma.

2010

Promoter hypermethylation of tumor suppressor genes is a common feature of primary cancer cells. However, at date the somatic epigenetic events that occur in head and neck squamous cell carcinoma (HNSCC) tumorigenesis are not yet been well defined. In the present study we analysed the methylation status of the gene hypermethylated in cancer-1 (hic1), a gene located on chromosome 17p13.3, a region frequently lost in HNSCC. We analysed 22 HNSCC samples and three cell lines using methylation specific PCR (MSP). We found hic1 methylated in 21 out of 22 samples and in all three cell lines. Treatment of the cell lines with the demethylating agent 5-Azacytidin (5-Aza) resulted in the demethylation…

AdultMaleCancer ResearchPathologymedicine.medical_specialtyAntimetabolites AntineoplasticTumor suppressor geneBisulfite sequencingKruppel-Like Transcription FactorsBiologymedicine.disease_causechemistry.chemical_compoundCell Line TumormedicineHumansGenes Tumor SuppressorNeoplasm InvasivenessPromoter Regions GeneticneoplasmsAgedMethylationDNA MethylationMiddle Agedmedicine.diseaseHead and neck squamous-cell carcinomaDemethylating agentGene Expression Regulation Neoplasticstomatognathic diseasesOncologychemistryEpidermoid carcinomaHead and Neck NeoplasmsCancer cellCancer researchAzacitidineCarcinoma Squamous CellFemaleOral SurgeryCarcinogenesisOral oncology
researchProduct

Clinical relevance of postzygotic mosaicism in Cornelia de Lange syndrome and purifying selection of NIPBL variants in blood.

2021

Postzygotic mosaicism (PZM) in NIPBL is a strong source of causality for Cornelia de Lange syndrome (CdLS) that can have major clinical implications. Here, we further delineate the role of somatic mosaicism in CdLS by describing a series of 11 unreported patients with mosaic disease-causing variants in NIPBL and performing a retrospective cohort study from a Spanish CdLS diagnostic center. By reviewing the literature and combining our findings with previously published data, we demonstrate a negative selection against somatic deleterious NIPBL variants in blood. Furthermore, the analysis of all reported cases indicates an unusual high prevalence of mosaicism in CdLS, occurring in 13.1% of p…

AdultMaleCornelia de Lange SyndromeAdolescent Adult Cell Cycle Proteins Child Child Preschool Comparative Genomic Hybridization De Lange Syndrome Female Gene Deletion High-Throughput Nucleotide Sequencing Humans Male Middle Aged Mosaicism Mutation Missense Phenotype Retrospective Studies Spain Young AdultAdolescentSomatic cellScienceGenetic counselingMedizinMutation MissenseDiseasesCell Cycle ProteinsBiologyPaediatric researchGermlineArticle03 medical and health sciencesNegative selectionYoung AdultMedical researchDe Lange SyndromeGenetics researchmedicineMissense mutationHumansClinical significanceChild030304 developmental biologyRetrospective StudiesGenetics0303 health sciencesComparative Genomic HybridizationMultidisciplinaryMosaicismQ030305 genetics & heredityRHigh-Throughput Nucleotide SequencingNIPBLMiddle Agedmedicine.diseasePhenotypeSettore MED/03 - Genetica MedicaSpainChild PreschoolMedicineFemaleGene Deletion
researchProduct

The EGR2 gene is involved in axonal Charcot-Marie-Tooth disease

2015

Background and purpose A three-generation family affected by axonal Charcot−Marie−Tooth disease (CMT) was investigated with the aim of discovering genetic defects and to further characterize the phenotype. Methods The clinical, nerve conduction studies and muscle magnetic resonance images of the patients were reviewed. A whole exome sequencing was performed and the changes were investigated by genetic studies, in silico analysis and luciferase reporter assays. Results A novel c.1226G>A change (p.R409Q) in the EGR2 gene was identified. Patients presented with a typical, late-onset axonal CMT phenotype with variable severity that was confirmed in the ancillary tests. The in silico studies sho…

AdultMaleEarly Growth Response Protein 2In silicomedicine.disease_causeCharcot-Marie-Tooth diseaseSeverity of Illness Indexhereditary motor sensory neuropathywhole exome sequencingYoung AdultCharcot-Marie-Tooth DiseasemedicineEGR2 geneHumansExomeeducationGeneExomeExome sequencingEarly Growth Response Protein 2Genetic testingAgedGeneticsAged 80 and overeducation.field_of_studyMutationmedicine.diagnostic_testbusiness.industryMiddle AgedPhenotypeAxonsPedigreePhenotypeNeurologyMutationFemaleNeurology (clinical)business
researchProduct

Two Novel Deletions (Array CGH Findings) in Pigment Dispersion Syndrome

2007

Purpose: We report the first male with pigment dispersion syndrome and a balanced translocation t(10;15)(p11.1;q11.1). Methods: Cytogenetic analyses using Giemsa banding and FISH methods, and array CGH were performed. Results: Array CGH analyses did not show altered DNA sequences in the breakpoints of the translocation, but revealed two novel deletions in 2q22.1 and 18q22.1. Conclusion: We suppose that the coexistence of t(10;15) and pigment dispersion syndrome in our patient is a coincidence. The deletion in 2q22.1, where the gene LRP1B has been located, may play a major role in the dysembryogenesis of the eye and cause the disorder.

AdultMaleEye DiseasesLRP1BG bandingChromosomal translocationBiologyTranslocation GeneticDNA sequencingmedicineHumansPigment Epithelium of EyeGeneIn Situ Hybridization FluorescenceGenetics (clinical)Sequence DeletionGeneticsChromosomes Human Pair 15Chromosomes Human Pair 10BreakpointNucleic Acid Hybridizationmedicine.diseaseMolecular biologyOphthalmologyPediatrics Perinatology and Child HealthPigment dispersion syndromeFish <Actinopterygii>Retinal PigmentsOphthalmic Genetics
researchProduct