Search results for " sequencing"

showing 10 items of 976 documents

Biological and clinical significance of dysplastic hematopoiesis in patients with newly diagnosed multiple myeloma

2020

On behalf of the PETHEMA/GEM Cooperative Group.

MaleOncologyPhysics::Instrumentation and Detectorsmedicine.medical_treatmentKaplan-Meier EstimateHematopoietic stem cell transplantationBiochemistryhemic and lymphatic diseasesAntineoplastic Combined Chemotherapy ProtocolsTumor MicroenvironmentProspective StudiesComputer Science::Operating SystemsIn Situ Hybridization FluorescenceMultiple myelomaRandomized Controlled Trials as TopicComputer Science::Cryptography and SecurityHazard ratioHematopoietic Stem Cell TransplantationHigh-Throughput Nucleotide SequencingHematologyMiddle AgedFlow CytometryPrognosisCombined Modality TherapyProgression-Free Survivalmedicine.anatomical_structureFemaleClonal HematopoiesisMultiple Myelomamedicine.medical_specialtyImmunologyTransplantation AutologousInternal medicinemedicineHumansClinical significanceProgression-free survivalComputer Science::Distributed Parallel and Cluster ComputingAgedAntineoplastic Combined Chemotherapy Protocolbusiness.industryCell Biologymedicine.diseaseTransplantationClinical Trials Phase III as TopicMyelodysplastic SyndromesMutationBone marrowbusinessMonoclonal gammopathy of undetermined significance
researchProduct

Rare variants in the genetic background modulate cognitive and developmental phenotypes in individuals carrying disease-associated variants

2019

Purpose: To assess the contribution of rare variants in the genetic background toward variability of neurodevelopmental phenotypes in individuals with rare copy-number variants (CNVs) and gene-disruptive variants. Methods: We analyzed quantitative clinical information, exome sequencing, and microarray data from 757 probands and 233 parents and siblings who carry disease-associated variants. Results: The number of rare likely deleterious variants in functionally intolerant genes (“other hits”) correlated with expression of neurodevelopmental phenotypes in probands with 16p12.1 deletion (n=23, p=0.004) and in autism probands carrying gene-disruptive variants (n=184, p=0.03) compared with thei…

MaleParents0301 basic medicineProbandNeuronalGenetic Carrier Screening16p11.2 deletion030105 genetics & heredityCognitionFamily historyNeural Cell Adhesion MoleculesGenetics (clinical)Exome sequencingSequence DeletionGeneticsGenetic Carrier ScreeningPhenotypePenetrancePedigreePhenotypeAutistic Disorder/genetics; Autistic Disorder/physiopathology; Cell Adhesion Molecules Neuronal/genetics; Chromosomes Human Pair 16/genetics; Cognition/physiology; DNA Copy Number Variations/genetics; Female; Gene Expression Regulation/genetics; Genetic Background; Genetic Carrier Screening; Humans; Male; Methyltransferases/genetics; Nerve Tissue Proteins/genetics; Parents; Pedigree; Phenotype; Proteins/genetics; Sequence Deletion/genetics; Siblings; 16p11.2 deletion; CNV; autism; modifier; phenotypic variabilityFemaleGenetic BackgroundHumanDNA Copy Number VariationsCell Adhesion Molecules NeuronalCNVautismNerve Tissue ProteinsBiologyChromosomesArticle03 medical and health sciencesmental disordersmedicineHumansAutistic DisorderBiologyGenemodifierPair 16SiblingsCalcium-Binding ProteinsProteinsMethyltransferasesmedicine.disease16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Genetics (clinical)Cytoskeletal Proteins030104 developmental biologyGene Expression Regulation[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutismphenotypic variabilityHuman medicine16p11.2 deletion; autism; CNV; modifier; phenotypic variability; Autistic Disorder; Cell Adhesion Molecules Neuronal; Chromosomes Human Pair 16; Cognition; DNA Copy Number Variations; Female; Gene Expression Regulation; Genetic Background; Humans; Male; Methyltransferases; Nerve Tissue Proteins; Parents; Pedigree; Phenotype; Proteins; Sequence Deletion; Siblings; Genetic Carrier ScreeningCell Adhesion MoleculesChromosomes Human Pair 16Transcription FactorsGenetics in Medicine
researchProduct

Delineation of the 3p14.1p13 microdeletion associated with syndromic distal limb contractures

2014

International audience; Distal limb contractures (DLC) represent a heterogeneous clinical and genetic condition. Overall, 20–25% of the DLC are caused by mutations in genes encoding the muscle contractile apparatus. Large interstitial deletions of the 3p have already been diagnosed by standard chromosomal analysis, but not associated with a specific phenotype. We report on four patients with syndromic DLC presenting with a de novo 3p14.1p13 micro-deletion. The clinical features associated multiple contractures, feeding problems, developmental delay, and intellectual disability. Facial dysmorphism was constant with low-set posteriorly rotated ears and blepharophimosis. Review of previously r…

MalePathologymedicine.medical_specialtyContracture[SDV]Life Sciences [q-bio]Locus (genetics)FOXP1BiologyMicedistal limb contracturessymbols.namesakeExonEIF4E3Intellectual disabilityGeneticsmedicineAnimalsHumans[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]3p141p13 microdeletionGenetics (clinical)ArthrogryposisChromosome AberrationsMice KnockoutSanger sequencingGeneticsComparative Genomic Hybridization[ SDV ] Life Sciences [q-bio]ExtremitiesForkhead Transcription FactorsSyndromeFOXP1Microdeletion syndromemedicine.diseaseBlepharophimosisPhenotypeRepressor Proteins[SDV] Life Sciences [q-bio]array-CGH[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]symbolsFemale[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Chromosomes Human Pair 3FranceCarrier Proteinsintronic regulatory sequenceAmerican Journal of Medical Genetics Part A
researchProduct

Targeted next-generation sequencing of deafness genes in hearing-impaired individuals uncovers informative mutations

2014

Purpose: Targeted next-generation sequencing provides a remarkable opportunity to identify variants in known disease genes, particularly in extremely heterogeneous disorders such as nonsyndromic hearing loss. The present study attempts to shed light on the complexity of hearing impairment. Methods: Using one of two next-generation sequencing panels containing either 80 or 129 deafness genes, we screened 30 individuals with nonsyndromic hearing loss (from 23 unrelated families) and analyzed 9 normal-hearing controls. Results: Overall, we found an average of 3.7 variants (in 80 genes) with deleterious prediction outcome, including a number of novel variants, in individuals with nonsyndromic h…

MaleProbandUsher syndromeGene DosageDeafnessBioinformaticsmedicine.disease_causesensorineural hearing lossConnexinsCohort Studiestargeted next-generation sequencingOriginal Research Articlemutational loadChildGenetics (clinical)Oligonucleotide Array Sequence AnalysisGeneticsMutationmedicine.diagnostic_testHomozygoteHigh-Throughput Nucleotide SequencingPedigreeConnexin 26Treatment OutcomeChild PreschoolFemalemedicine.symptomAdultAdolescentSequence analysisHearing lossdeafness gene panelMolecular Sequence DataBiologynonsyndromic hearing lossDNA sequencingYoung AdultAudiometryGenetic variationotorhinolaryngologic diseasesmedicineHumansGenetic Predisposition to DiseaseFamily HealthBase SequenceGenetic VariationInfantDNASequence Analysis DNAmedicine.diseaseMutationAudiometryGene DeletionGenetics in Medicine
researchProduct

Identification of novel, clonally stable, somatic mutations targeting transcription factors PAX5 and NKX2-3, the epigenetic regulator LRIF1, and BRAF…

2021

Diagnosis of B-cell chronic lymphocytic leukemia (B-CLL) is usually straightforward, involving clinical, immunophenotypic (Matutes score), and (immuno)genetic analyses (to refine patient prognosis for treatment). CLL cases with atypical presentation (e.g., Matutes ≤ 3) are also encountered, and for these diseases, biology and prognostic impact are less clear. Here we report the genomic characterization of a case of atypical B-CLL in a 70-yr-old male patient; B-CLL cells showed a Matutes score of 3, chromosomal translocation t(14;18)(q32;q21) (BCL2/IGH), mutated IGHV, deletion 17p, and mutations in BCL2, NOTCH1 (subclonal), and TP53 (subclonal). Quite strikingly, a novel PAX5 mutation that w…

MaleProto-Oncogene Proteins B-rafChronic lymphocytic leukemiaCell Cycle ProteinsBiologymedicine.disease_causeSomatic evolution in cancerTranslocation GeneticEpigenesis Genetichematological neoplasmClonal Evolutionimmune system diseaseshemic and lymphatic diseasesExome SequencingmedicineHumansEpigeneticsReceptor Notch1neoplasmsLoss functionExome sequencingAgedHomeodomain ProteinsMutationPAX5 Transcription FactorGeneral Medicinemedicine.diseasePrognosisLeukemia Lymphocytic Chronic B-CellProto-Oncogene Proteins c-bcl-2MutationCancer researchPAX5Tumor Suppressor Protein p53IGHV@Rapid Cancer CommunicationTranscription FactorsCold Spring Harbor Molecular Case Studies
researchProduct

Epigenetic Control of the foxp3 Locus in Regulatory T Cells

2007

Compelling evidence suggests that the transcription factor Foxp3 acts as a master switch governing the development and function of CD4+ regulatory T cells (Tregs). However, whether transcriptional control of Foxp3 expression itself contributes to the development of a stable Treg lineage has thus far not been investigated. We here identified an evolutionarily conserved region within the foxp3 locus upstream of exon-1 possessing transcriptional activity. Bisulphite sequencing and chromatin immunoprecipitation revealed complete demethylation of CpG motifs as well as histone modifications within the conserved region in ex vivo isolated Foxp3+CD25+CD4+ Tregs, but not in naïve CD25−CD4+ T cells. …

MaleQH301-705.5Bisulfite sequencingImmunologyMolecular Sequence Datachemical and pharmacologic phenomenaCell SeparationThymus GlandBiologyT-Lymphocytes RegulatoryGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticMiceTranscriptional regulationAnimalsEpigeneticsBiology (General)Regulation of gene expressionMice Inbred BALB CGeneral Immunology and MicrobiologyBase SequenceGeneral NeuroscienceInterleukin-2 Receptor alpha SubunitFOXP3Homo (human)hemic and immune systemsForkhead Transcription FactorsDNA MethylationFlow CytometryMolecular biologyMus (mouse)Cell biologyIn VitroDNA demethylationGene Expression RegulationDNA methylationCpG IslandsGeneral Agricultural and Biological SciencesChromatin immunoprecipitationResearch ArticlePLoS Biology
researchProduct

Intestinal malrotation in a female newborn affected by Osteopathia Striata with Cranial Sclerosis due to a de novo heterozygous nonsense mutation of …

2022

Abstract Background Osteopathia Striata with Cranial Sclerosis (OS-CS), also known as Horan-Beighton Syndrome, is a rare genetic disease; about 90 cases have been reported to date. It is associated with mutations (heterozygous for female subjects and hemizygous for males) of the AMER1 gene, located at Xq11.2, and shows an X-linked pattern of transmission. Typical clinical manifestations include macrocephaly, characteristic facial features (frontal bossing, epicanthal folds, hypertelorism, depressed nasal bridge, orofacial cleft, prominent jaw), hearing loss and developmental delay. Males usually present a more severe phenotype than females and rarely survive. Diagnostic suspicion is based o…

MaleSclerosisCase report Next generation sequencing OS-CS Skeletal dysplasia X-inactivationCleft LipTumor Suppressor ProteinsInfant NewbornGeneral MedicineMegalencephalyCleft PalateCodon NonsenseHumansFemaleBone DiseasesAdaptor Proteins Signal Transducing
researchProduct

Exome sequencing in suspected monogenic dyslipidemias.

2015

Background— Exome sequencing is a promising tool for gene mapping in Mendelian disorders. We used this technique in an attempt to identify novel genes underlying monogenic dyslipidemias. Methods and Results— We performed exome sequencing on 213 selected family members from 41 kindreds with suspected Mendelian inheritance of extreme levels of low-density lipoprotein cholesterol (after candidate gene sequencing excluded known genetic causes for high low-density lipoprotein cholesterol families) or high-density lipoprotein cholesterol. We used standard analytic approaches to identify candidate variants and also assigned a polygenic score to each individual to account for their burden of commo…

MaleSettore MED/09 - Medicina InternaMedical BiotechnologyDNA sequencing; exome; exome sequencing; genetics human; lipids; mendelian geneticsBiologyCardiorespiratory Medicine and HaematologyNovel genelipidsmendelian geneticsGene mappingClinical ResearchGenetics2.1 Biological and endogenous factorsHumansgeneticsExomeDNA sequencinghumanAetiologyMendelian disordersExomeGenetics (clinical)Exome sequencingDyslipidemiasGeneticsInborn ErrorsHuman GenomeHigh-Throughput Nucleotide SequencingAtherosclerosisMetabolismCardiovascular System & Hematologylipids (amino acids peptides and proteins)DNA sequencing; exome; genetics; human; lipidsFemalegeneticCardiology and Cardiovascular Medicineexome sequencingexomeMetabolism Inborn ErrorsCirculation. Cardiovascular genetics
researchProduct

AMPA receptor GluA2 subunit defects are a cause of neurodevelopmental disorders.

2019

AMPA receptors (AMPARs) are tetrameric ligand-gated channels made up of combinations of GluA1-4 subunits encoded by GRIA1-4 genes. GluA2 has an especially important role because, following post-transcriptional editing at the Q607 site, it renders heteromultimeric AMPARs Ca2+-impermeable, with a linear relationship between current and trans-membrane voltage. Here, we report heterozygous de novo GRIA2 mutations in 28 unrelated patients with intellectual disability (ID) and neurodevelopmental abnormalities including autism spectrum disorder (ASD), Rett syndrome-like features, and seizures or developmental epileptic encephalopathy (DEE). In functional expression studies, mutations lead to a dec…

Male[SDV.GEN] Life Sciences [q-bio]/GeneticsIon channels in the nervous systemCohort Studiesfluids and secretionsLoss of Function MutationReceptorsAMPAAMPA receptorlcsh:ScienceChildreproductive and urinary physiologyAMPA receptor GluA2 neurodevelopmental disorders autism spectrum disorder glutamatergic synaptic transmission GRIA2neurodevelopmental disordersDevelopmental disordersQNeurodevelopmental disordersBrainMagnetic Resonance ImagingSettore MED/26 - NEUROLOGIAGluA2Child PreschoolFemaleAdultHeterozygoteAdolescentScienceautism spectrum disorderArticleYoung Adult[SDV.MHEP.PED] Life Sciences [q-bio]/Human health and pathology/PediatricsMESH: Intellectual Disability/genetics; Neurodevelopmental Disorders/genetics; Receptors AMPA/genetics; HeterozygoteIntellectual Disabilitymental disordersAdolescent; Adult; Brain; Child; Child Preschool; Cohort Studies; Female; Heterozygote; Humans; Infant; Intellectual Disability; Loss of Function Mutation; Magnetic Resonance Imaging; Male; Neurodevelopmental Disorders; Receptors AMPA; Young AdultHumansReceptors AMPAGRIA2PreschoolIon channel in the nervous system Developmental disorders Synaptic development NG sequencing[SDV.GEN]Life Sciences [q-bio]/Genetics[SDV.MHEP.PED]Life Sciences [q-bio]/Human health and pathology/Pediatricsglutamatergic synaptic transmission[SCCO.NEUR]Cognitive science/Neuroscience[SCCO.NEUR] Cognitive science/NeuroscienceInfantNG sequencingSynaptic developmentIon channel in the nervous systemNext-generation sequencinglcsh:Q
researchProduct

Mutations in SLC13A5 Cause Autosomal-Recessive Epileptic Encephalopathy with Seizure Onset in the First Days of Life

2014

International audience; Epileptic encephalopathy (EE) refers to a clinically and genetically heterogeneous group of severe disorders characterized by seizures, abnormal interictal electro-encephalogram, psychomotor delay, and/or cognitive deterioration. We ascertained two multiplex families (including one consanguineous family) consistent with an autosomal-recessive inheritance pattern of EE. All seven affected individuals developed subclinical seizures as early as the first day of life, severe epileptic disease, and profound developmental delay with no facial dysmorphism. Given the similarity in clinical presentation in the two families, we hypothesized that the observed phenotype was due …

Male[SDV]Life Sciences [q-bio]Genes Recessive[SDV.GEN] Life Sciences [q-bio]/GeneticsBiologymedicine.disease_causeCompound heterozygosity03 medical and health sciencesEpilepsy0302 clinical medicineSeizures[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyReportmedicineGeneticsRecessiveHumansIctalGenetics(clinical)[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Genetics (clinical)Exome sequencing030304 developmental biologySubclinical infectionGenetics0303 health sciencesMutation[SDV.GEN]Life Sciences [q-bio]/GeneticsBrain Diseases[SDV.MHEP] Life Sciences [q-bio]/Human health and pathology[ SDV ] Life Sciences [q-bio]SymportersGenetic heterogeneityCitrate transportmedicine.disease3. Good healthPedigree[SDV] Life Sciences [q-bio]Genes[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Mutation[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Female[ SDV.GEN ] Life Sciences [q-bio]/Genetics030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyThe American Journal of Human Genetics
researchProduct