Search results for " DNA Mutational Analysis"

showing 10 items of 13 documents

Spectrum of mutations in Italian patients with familial hypercholesterolemia: New results from the LIPIGEN study

2017

Abstract Background Familial hypercholesterolemia (FH) is an autosomal dominant disease characterized by elevated plasma levels of LDL-cholesterol that confers an increased risk of premature atherosclerotic cardiovascular disease. Early identification and treatment of FH patients can improve prognosis and reduce the burden of cardiovascular mortality. Aim of this study was to perform the mutational analysis of FH patients identified through a collaboration of 20 Lipid Clinics in Italy (LIPIGEN Study). Methods We recruited 1592 individuals with a clinical diagnosis of definite or probable FH according to the Dutch Lipid Clinic Network criteria. We performed a parallel sequencing of the major…

0301 basic medicineApolipoprotein ECandidate geneSettore MED/09 - Medicina InternaDatabases FactualApolipoprotein BDNA Mutational AnalysisFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosityPCSK90302 clinical medicineRisk FactorsReceptorsGeneticsHomozygoteAutosomal dominant traitPathogenic variantsGeneral MedicinePrognosisAPOB; Familial hypercholesterolemia; LDLR; PCSK9; Pathogenic variantsCholesterolPhenotypeItalyAutosomal Recessive HypercholesterolemiaApolipoprotein B-100lipids (amino acids peptides and proteins)Proprotein Convertase 9APOBCardiology and Cardiovascular MedicinePreliminary DataGenetic MarkersFamilial hypercholesterolemiaLDLRPCSK9APOBPathogenic variantsHeterozygoteFamilial hypercholesterolemiaBiologyPathogenic variantLDLHyperlipoproteinemia Type II03 medical and health sciencesDatabasesmedicineInternal MedicineHumansAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Internal Medicine; Cardiology and Cardiovascular MedicineGenetic Predisposition to DiseaseFactualPCSK9Settore MED/13 - ENDOCRINOLOGIAAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Cardiology and Cardiovascular Medicine; Internal Medicinemedicine.diseaseAtherosclerosis030104 developmental biologyLDLRReceptors LDLMutationbiology.proteinAPOB; Familial hypercholesterolemia; LDLR; Pathogenic variants; PCSK9; Apolipoprotein B-100; Atherosclerosis; Cholesterol; DNA Mutational Analysis; Databases Factual; Genetic Markers; Genetic Predisposition to Disease; Heterozygote; Homozygote; Humans; Hyperlipoproteinemia Type II; Italy; Phenotype; Preliminary Data; Prognosis; Proprotein Convertase 9; Receptors LDL; Risk Factors; Mutation; Internal Medicine; Cardiology and Cardiovascular Medicine
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Familial hypercholesterolemia: The Italian Atherosclerosis Society Network (LIPIGEN)

2017

Background and aims: Primary dyslipidemias are a heterogeneous group of disorders characterized by abnormal levels of circulating lipoproteins. Among them, familial hypercholesterolemia is the most common lipid disorder that predisposes for premature cardiovascular disease. We set up an Italian nationwide network aimed at facilitating the clinical and genetic diagnosis of genetic dyslipidemias named LIPIGEN (LIpid TransPort Disorders Italian GEnetic Network). Methods: Observational, multicenter, retrospective and prospective study involving about 40 Italian clinical centers. Genetic testing of the appropriate candidate genes at one of six molecular diagnostic laboratories serving as nationw…

0301 basic medicineCandidate geneGenetic testingSettore MED/09 - Medicina InternaDatabases FactualDNA Mutational AnalysisDiseaseFamilial hypercholesterolemia030204 cardiovascular system & hematology0302 clinical medicineDyslipidemias; Genetic testing; National network; Internal Medicine; Cardiology and Cardiovascular MedicineRisk FactorsProspective StudiesProgram DevelopmentProspective cohort studymedicine.diagnostic_testGeneral MedicinePrognosisCholesterolPhenotypeItalyCardiology and Cardiovascular MedicineGenetic Markersmedicine.medical_specialtyNational networkDyslipidemias; Genetic testing; National networkMEDLINEHyperlipoproteinemia Type II03 medical and health sciencesDatabasesInternal medicinemedicineInternal MedicineHumansGenetic Predisposition to DiseaseFactualGenetic testingRetrospective StudiesDyslipidemiasbusiness.industrySettore MED/13 - ENDOCRINOLOGIARetrospective cohort studymedicine.diseaseAtherosclerosisDyslipidemias; Genetic testing; National network; Atherosclerosis; Cholesterol; DNA Mutational Analysis; Databases Factual; Genetic Markers; Genetic Predisposition to Disease; Humans; Hyperlipoproteinemia Type II; Italy; Phenotype; Prognosis; Program Development; Prospective Studies; Retrospective Studies; Risk Factors; Mutation; Internal Medicine; Cardiology and Cardiovascular Medicine030104 developmental biologyEndocrinologyDyslipidemiaGenetic markerMutationbusiness
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Clinical and molecular characterization of 112 single-center patients with Neurofibromatosis type 1.

2018

Abstract Background The aim of this retrospective study was to define clinical and molecular characteristics of a large sample of neurofibromatosis type 1 (NF1) patients, as well as to evaluate mutational spectrum and genotype-phenotype correlation. NF1 is a relatively common neurogenetic disorder (1:2500–1:3000 individuals). It is caused by mutations of the NF1 gene on chromosome 17ql1.2, with autosomal dominant pattern of inheritance and wide phenotypical variability. Café-au-lait spots (CALs), cutaneous and/or subcutaneous neurofibromas (CNFs/SCNFs), skinfold freckling, skeletal abnormalities, Lisch nodules of the iris and increased risk of learning and intellectual disabilities, as well…

0301 basic medicineGenotype-phenotype correlation; New mutation; NF1 gene; NF1 microdeletion syndrome; Adolescent; Adult; Age Factors; Child; Child Preschool; Cohort Studies; DNA Mutational Analysis; Female; Genes Neurofibromatosis 1; Genetic Association Studies; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Neurofibromatosis 1; Prevalence; Prognosis; Retrospective Studies; Risk Assessment; Sex Factors; Young Adult; Mutation MissenseMaleGenotype-phenotype correlationDNA Mutational AnalysisDiseaseCohort Studies0302 clinical medicineDNA Mutational AnalysisGenotypePrevalenceMedicineYoung adultChildNew mutationlcsh:RJ1-570Age FactorsMiddle AgedPrognosisItalyNF1 geneChild PreschoolCohortFemaleNF1 microdeletion syndromeCohort studyAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosis 1AdolescentMutation MissenseRisk Assessment03 medical and health sciencesYoung AdultSex FactorsGenes Neurofibromatosis 1HumansGenetic Predisposition to DiseaseNeurofibromatosisPreschoolGenetic Association StudiesRetrospective Studiesbusiness.industryResearchRetrospective cohort studylcsh:Pediatricsmedicine.diseaseDermatology030104 developmental biologyGenesPediatrics Perinatology and Child HealthMutationMissensebusiness030217 neurology & neurosurgeryItalian journal of pediatrics
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The neuropsychology of variant CJD: a comparative study with inherited and sporadic forms of prion disease.

2005

Objective: To assess cognitive function in variant Creutzfeldt-Jakob disease (vCJD). We describe the neuropsychological profiles of 10 cases and compare these data with cross sectional data obtained from patients with histologically confirmed sporadic CJD and cases with inherited prion disease with confirmed mutations in the prion protein gene. Methods: Patients referred to the Specialist Cognitive Disorders Clinic at the National Hospital for Neurology and Neurosurgery and the National Prion Clinic at St Mary's Hospital, London for further investigation of suspected CJD were recruited into the study. The neuropsychological test battery evaluated general intelligence, visual and verbal memo…

AdultMalePaperPediatricsmedicine.medical_specialtyPrionsanimal diseasesDNA Mutational AnalysisNeuropsychological TestsCreutzfeldt-Jakob SyndromePrion DiseasesNational Prion Clinicmental disordersmedicineDementiaHumansCognitive declinePsychiatrymedicine.diagnostic_testSettore M-PSI/02 - Psicobiologia E Psicologia Fisiologicabusiness.industryNeuropsychologyNeuropsychological testCreutzfeldt-Jakob SyndromeMiddle Agedmedicine.diseasenervous system diseasesPsychiatry and Mental healthCross-Sectional StudiesAdult Cognition Disorders/etiology Creutzfeldt-Jakob Syndrome/complications Creutzfeldt-Jakob Syndrome/genetics Creutzfeldt-Jakob Syndrome/psychology Cross-Sectional Studies DNA Mutational Analysis Disease Progression Female Humans Male Middle Aged Neuropsychological Tests Prion Diseases/genetics Prion Diseases/psychology Prions/genetics Visual PerceptionDisease ProgressionVisual PerceptionSurgeryFemaleNeurology (clinical)Verbal memorybusinessCognition DisordersExecutive dysfunctionJournal of neurology, neurosurgery, and psychiatry
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Diagnostic algorithm for familial chylomicronemia syndrome

2016

International audience; Background: Familial chylomicronemia syndrome (FCS) is a rare genetic disease that leads to severe hypertriglyceridemia often associated with recurrent episodes of pancreatitis. The recognition and correct diagnosis of the disease is challenging due to its rarity, and to the lack of specificity of signs and symptoms. Lipid experts, endocrinologists, gastroenterologists, pancreatologists, and general practitioners may encounter patients who potentially have FCS. Therefore, cooperation between experts and improved knowledge of FCS is essential in improving the diagnosis. Currently, a consensus on best practice for the diagnosis of FCS is lacking. Methods: Aiming to def…

Chylomicrons; Familial chylomicronemia syndrome; Hyperlipoproteinemia; Lipoprotein lipase deficiency; Pancreatitis; Biomarkers; Genetic Markers; Genetic Predisposition to Disease; Humans; Hyperlipoproteinemia Type I; Lipids; Lipoprotein Lipase; Phenotype; Practice Guidelines as Topic; Predictive Value of Tests; Prognosis; Algorithms; Critical Pathways; DNA Mutational Analysis; Decision Support Techniques; Mutation; Internal Medicine; Cardiology and Cardiovascular MedicineSettore MED/09 - Medicina InternaACUTE-PANCREATITIS[SDV]Life Sciences [q-bio]DNA Mutational AnalysisPredictive Value of TestDisease030204 cardiovascular system & hematologyVARIANTSDecision Support Technique0302 clinical medicineDOMAINGenetic MarkerBINDINGChylomicronsHYPERTRIGLYCERIDEMICMedicine030212 general & internal medicinePANCREATITISLipoprotein lipase deficiencyGeneral MedicineFamilial ChylomicronemiaLipidPrognosisLipids3. Good healthAlgorithmDEFICIENCYPhenotypeCritical PathwayPractice Guidelines as TopicCritical PathwaysHyperlipoproteinemia Type Ilipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAlgorithmAlgorithmsHumanGenetic MarkersSevere hypertriglyceridemiaFamilial chylomicronemia syndromePrognosiSigns and symptomsLIPOPROTEIN-LIPASEHyperlipoproteinemiaCLASSIFICATIONDecision Support TechniquesSecondary careChylomicronDNA Mutational Analysi03 medical and health sciencesPredictive Value of TestsInternal MedicineMANAGEMENTHumansGenetic Predisposition to DiseasePancreatitibusiness.industryBiomarkerLipoprotein LipaseMutationbusinessBiomarkers
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The FBN2 gene: new mutations, locus-specific database (Universal Mutation Database FBN2), and genotype-phenotype correlations.

2009

International audience; Congenital contractural arachnodactyly (CCA) is an extremely rare disease, due to mutations in the FBN2 gene encoding fibrillin-2. Another member of the fibrillin family, the FBN1 gene, is involved in a broad phenotypic continuum of connective-tissue disorders including Marfan syndrome. Identifying not only what is in common but also what differentiates these two proteins should enable us to better comprehend their respective functions and better understand the multitude of diseases in which these two genes are involved. In 1995 we created a locus-specific database (LSDB) for FBN1 mutations with the Universal Mutation Database (UMD) tool. To facilitate comparison of …

Fibrillin-2MESH : Polymorphism GeneticFibrillin-1DNA Mutational AnalysisMESH : Genotype[SDV.GEN] Life Sciences [q-bio]/Geneticscomputer.software_genreMESH: Genotype0302 clinical medicineGenotypeDatabases GeneticMissense mutationCongenital contractural arachnodactylyMESH: DNA Mutational AnalysisGenetics (clinical)MESH: Databases GeneticRegulation of gene expressionGenetics0303 health sciencesDatabaseMESH : Gene Expression RegulationMicrofilament ProteinsPhenotypeMESH: Gene Expression RegulationBeals-Hecht syndrome3. Good healthINCMESH : PhenotypePhenotypeMESH : MutationFibrillinmusculoskeletal diseasesMESH: MutationGenotypeMESH : Microfilament Proteinsdatabase OFFICIAL JOURNAL wwwhgvsorg & 2008 WILEY-LISSLocus (genetics)fibrillinMESH : DNA Mutational AnalysisBiologyFibrillinsMESH: PhenotypeMESH: Sequence Homology Nucleic Acidcongenital contractural arachnodactyly03 medical and health sciencesMESH: Microfilament ProteinsSequence Homology Nucleic AcidMESH: Polymorphism GeneticGeneticsmedicineHumansMESH : Sequence Homology Nucleic AcidFBN2CCAMESH : Databases GeneticGene030304 developmental biology[SDV.GEN]Life Sciences [q-bio]/GeneticsPolymorphism GeneticMESH: HumansMESH : Humansmedicine.diseaseGene Expression RegulationMutation[ SDV.GEN ] Life Sciences [q-bio]/Geneticscomputer030217 neurology & neurosurgery
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Lack of SCN1A Mutations in Familial Febrile Seizures

2002

Summary:  Purpose: Mutations in the voltage-gated sodium channel subunit gene SCN1A have been associated with febrile seizures (FSs) in autosomal dominant generalized epilepsy with febrile seizures plus (GEFS+) families and severe myoclonic epilepsy of infancy. The present study assessed the role of SCN1A in familial typical FSs. Methods: FS families were selected throughout a collaborative study of the Italian League Against Epilepsy. For each index case, the entire coding region of SCN1A was screened by denaturant high-performance liquid chromatography. DNA fragments showing variant chromatograms were subsequently sequenced. Results: Thirty-two FS families accounting for 91 affected indiv…

GAMMA-2-SUBUNITMaleFebrile convulsionsDNA Mutational Analysismedicine.disease_causePolymerase Chain ReactionSodium ChannelsFebrileEpilepsyExonPLUSDNA Mutational AnalysisGene duplicationChildIndex caseChromatography High Pressure LiquidGeneticsChromatographyMutationIdiopathic epilepsyExonsNeurologyIon channelsHigh Pressure LiquidFemaleGeneralized epilepsy with febrile seizures plusMutationsAdultAdolescentGENERALIZED EPILEPSYNerve Tissue ProteinsSeizures FebrileSeizuresGeneticsmedicineHumansFamilybusiness.industryCONVULSIONSGene AmplificationSODIUM-CHANNELmedicine.diseaseGENEDYSFUNCTIONNAV1.1 Voltage-Gated Sodium ChannelFebrile convulsions; Genetics; Idiopathic epilepsy; Ion channels; Mutations; Adolescent; Adult; Child; Chromatography High Pressure Liquid; DNA Mutational Analysis; Exons; Female; Gene Amplification; Humans; Male; Mutation; NAV1.1 Voltage-Gated Sodium Channel; Nerve Tissue Proteins; Polymerase Chain Reaction; Seizures Febrile; Sodium Channels; FamilyMutationMyoclonic epilepsyNeurology (clinical)businessEpilepsia
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Mutations in the Matrin 3 gene cause familial amyotrophic lateral sclerosis.

2013

MATR3 is an RNA- and DNA-binding protein that interacts with TDP-43, a disease protein linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Using exome sequencing, we identified mutations in MATR3 in ALS kindreds. We also observed MATR3 pathology in ALS-affected spinal cords with and without MATR3 mutations. Our data provide more evidence supporting the role of aberrant RNA processing in motor neuron degeneration. © 2014 Nature America, Inc. All rights reserved.

MaleAged Aged; 80 and over Amyotrophic Lateral Sclerosis; genetics/pathology Computational Biology DNA Mutational Analysis DNA-Binding Proteins; metabolism Family Health Female Genetic Predisposition to Disease; genetics Genotype Humans Male Middle Aged Muscle; Skeletal; metabolism/pathology Mutation; genetics Neurologic Examination Nuclear Matrix-Associated Proteins; genetics/metabolism RNA-Binding Proteins; genetics/metabolism Spinal Cord; metabolism/pathologyDNA Mutational Analysisgenetics/metabolismRNA-binding proteinSettore MED/03 - GENETICA MEDICAmedicine.disease_cause0302 clinical medicineNuclear Matrix-Associated ProteinsGenotype80 and overgeneticsAmyotrophic lateral sclerosisExome sequencingGeneticsAged 80 and overNeurologic Examination0303 health sciencesMutationGeneral NeuroscienceRNA-Binding ProteinsSkeletalMiddle AgedDNA-Binding ProteinsMATR3medicine.anatomical_structureSpinal Cordfamilial amyotrophic lateral sclerosisMuscleSettore MED/26 - NeurologiaFemaleFrontotemporal dementiametabolism/pathologyGenotypeArticle03 medical and health sciencesgenetics; familial amyotrophic lateral sclerosismental disordersmedicineHumansGenetic Predisposition to DiseaseMuscle Skeletal030304 developmental biologyAgedFamily Healthbusiness.industryAmyotrophic Lateral Sclerosisgenetics/pathologyRNAComputational BiologySpinal cordmedicine.diseaseMutationgeneticbusinessNeurosciencemetabolism030217 neurology & neurosurgery
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Whole-exome sequencing and targeted gene sequencing provide insights into the role of PALB2 as a male breast cancer susceptibility gene

2016

Male breast cancer (MBC) is a rare disease whose etiology appears to be largely associated with genetic factors. BRCA1 and BRCA2 mutations account for about 10% of all MBC cases. Thus, a fraction of MBC cases are expected to be due to genetic factors not yet identified. To further explain the genetic susceptibility for MBC, whole-exome sequencing (WES) and targeted gene sequencing were applied to high-risk, BRCA1/2 mutation-negative MBC cases.Germ-line DNA of 1 male and 2 female BRCA1/2 mutation-negative breast cancer (BC) cases from a pedigree showing a first-degree family history of MBC was analyzed with WES. Targeted gene sequencing for the validation of WES results was performed for 48 …

MaleCancer ResearchDNA Mutational AnalysisBreast NeoplasmsBreast Neoplasms MaleDNA Mutational AnalysiGenetic susceptibility; Male breast cancer; N-acetyltransferase 1 (NAT1); Partner and localizer of BRCA2 (PALB2); Whole-exome sequencing; Oncology; Cancer ResearchGenetic susceptibilityHumansExomeGenetic Predisposition to DiseaseN-acetyltransferase 1 (NAT1)genetic susceptibility; male breast cancer; N-acetyltransferase 1 (NAT1); partner and localizer of BRCA2 (PALB2); whole-exome sequencing; BRCA1 Protein; BRCA2 Protein; Breast Neoplasms; Breast Neoplasms Male; Case-Control Studies; DNA Mutational Analysis; Exome; Fanconi Anemia Complementation Group N Protein; Female; Genetic Predisposition to Disease; Humans; Italy; Male; Mutation; Nuclear Proteins; Pedigree; Tumor Suppressor Proteins; Oncology; Cancer ResearchNuclear ProteinBRCA2 ProteinTumor Suppressor ProteinBRCA1 ProteinTumor Suppressor ProteinsPartner and localizer of BRCA2 (PALB2)Nuclear ProteinsPedigreeMale breast cancerItalyOncologyCase-Control StudiesWhole-exome sequencingMutationFemaleCase-Control StudieFanconi Anemia Complementation Group N ProteinBreast NeoplasmHuman
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Association of a functional deficit of the BKCa channel, a synaptic regulator of neuronal excitability, with autism and mental retardation

2006

International audience; Objective: Autism is a complex, largely genetic psychiatric disorder. In the majority of cases, the cause of autism is not known, but there is strong evidence for a genetic etiology. To identify candidate genes, the physical mapping of balanced chromosomal aberrations is a powerful strategy, since several genes have been characterized in numerous disorders. In this study, the authors analyzed a balanced reciprocal translocation arising de novo in a subject with autism and mental retardation. Method: The authors performed the physical mapping of the balanced 9q23/ 10q22 translocation by fluorescent in situ hybridization experiments using bacterial artificial chromosom…

MaleCandidate geneChromosomes Artificial BacterialIndolesDNA Mutational AnalysisRegulatorChromosomal translocationautism mental retardation KCNMA1 genelarge conductance Ca(2+)-activated K(+) (BK(Ca)) channel synaptic transmission chromosomal translocationSynaptic TransmissionTranslocation GeneticPair 10CA2+-ACTIVATED K+ CHANNELSCloning MolecularChildLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMUTATIONIn Situ HybridizationIn Situ Hybridization FluorescenceReverse Transcriptase Polymerase Chain ReactionBacterialChromosome MappingETIOLOGYPsychiatry and Mental healthArtificialKCNMA1 Gene[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]HaploinsufficiencyPsychologyChromosomes Human Pair 9POTASSIUM CHANNELSHumanPair 9Autistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes; Artificial; Bacterial; Chromosomes; Human; Pair 10; Chromosomes; Human; Pair 9; Cloning; Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization; Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation; GeneticTranslocationNeurotransmissionChromosomesFluorescenceGeneticIntellectual DisabilitymedicineHumansAutistic DisorderRELEASEChromosome AberrationsCOMPLEXChromosomes Human Pair 10MolecularAutistic Disorder; Child; Chromosome Aberrations; Chromosome Mapping; Chromosomes Artificial Bacterial; Chromosomes Human Pair 10; Chromosomes Human Pair 9; Cloning Molecular; DNA Mutational Analysis; Humans; In Situ Hybridization Fluorescence; Indoles; Intellectual Disability; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits; Male; Reverse Transcriptase Polymerase Chain Reaction; Synaptic Transmission; Translocation GeneticPERVASIVE DEVELOPMENTAL DISORDERSmedicine.diseaseDevelopmental disorderINDIVIDUALSLARGE-CONDUCTANCEAutismSCREENNeuroscience[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyCloning
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