Search results for "MUTATION"

showing 10 items of 2830 documents

Frequent reduction or absence of detection of the JAK2-mutated clone in JAK2V617F-positive patients within the first years of hydroxyurea therapy

2008

Abstract Objective: To analyse the effect of hydroxyurea (HU) on the JAK2-V617F allelic ratio (%JAK2-V617F) of patients with Polycythaemia Vera (PV) and Essential Thrombocythaemia (ET). Methods: Thirty-six patients were examined sequentially prior to and after on-set of (HU) therapy (8 PV, 17 ET), or while remaining untreated (2 PV, 9 ET). For all patients, the %JAK2-V617F was determined in purified blood granulocytes using sensitive allele-specific, quantitative PCRs. In a second study, two distinct groups of patients were examined at a single time point at the time of diagnosis (99 PV, 178 ET) or while receiving HU (36 PV, 98 ET). Results: HU therapy (median duration: 15 months) reduced t…

MalePediatricsmedicine.medical_specialtymedicine.drug_classImmunologyClone (cell biology)Allelic ratioBiochemistryAntimetaboliteGastroenterologyCohort StudiesHydroxycarbamidePolycythemia veraAntisickling Agentshemic and lymphatic diseasesInternal medicinemedicineHumansHydroxyureaProspective cohort studyPolycythemia VeraMyeloproliferative neoplasmAgedDNA PrimersRetrospective StudiesAged 80 and overJanus kinase 2HematologybiologyEssential thrombocythemiabusiness.industryCell BiologyHematologyJanus Kinase 2Middle Agedmedicine.diseaseSurgeryAmino Acid SubstitutionMutationbiology.proteinFemalebusinessGranulocytesThrombocythemia Essentialmedicine.drugHaematologica
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A methodological strategy for PAH genotyping in populations with a marked molecular heterogeneity of hyperphenylalaninemia.

2001

Abstract The elucidation of the molecular basis of hyperphenylalaninemia in various world populations (PKU Consortium Database: http://www.mcgill.ca/pahdb/) has revealed a remarkable molecular heterogeneity at the locus encoding for phenylalanine hydroxylase. As a consequence, genotyping of HPA patients has prompted the establishment of an impressive number of mutation detection protocols. In spite of the large variety of methods proposed so far, no comprehensive strategy has been yet developed for the detection of PAH gene mutations. Therefore, new approaches, combining the advantages of individual methods are required, especially in populations with a high number of PAH gene mutations. In…

MalePhenylalanine hydroxylaseGenotypeDNA Mutational AnalysisLocus (genetics)Gene mutationMolecular heterogeneityPolymerase Chain ReactionHyperphenylalaninemiaPhenylketonuriasmedicineHumansMutation detectionGenetic TestingMolecular BiologyGenotypingSicilyReverse dot blotGeneticsbiologyGenetic VariationNucleic Acid HybridizationPhenylalanine HydroxylaseCell BiologyExonsmedicine.diseasePedigreeHaplotypesMutationbiology.proteinFemaleOligonucleotide ProbesMolecular and cellular probes
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TP53 in gastric cancer: mutations in the l3 loop and LSH motif DNA-binding domains of TP53 predict poor outcome.

2004

The aim of this study was to clarify whether specific p53 mutations may have biological relevance in terms of disease relapse or death in gastric carcinomas (GC). Resected specimens from a consecutive series of 62 patients with GC undergoing potentially curative surgery were prospectively studied. The mutational status of exons 5-8 of the p53 gene was investigated in 62 cases using the PCR-SSCP and sequencing. Presence of microsatellite instability (MSI) was evaluated in 56 cases by analyzing loci highly sensitive of MSI. Twenty mutations of p53 were detected in 17 of the 62 cases analyzed (27%). Ten mutations (50%) occurred in highly conserved domains. According to the p53 specific functio…

MalePhysiologyClinical BiochemistryBiologyBioinformaticsExonchemistry.chemical_compoundAge DistributionStomach NeoplasmsmedicineHumansCancer mutationsTP53Prospective StudiesProspective cohort studyGeneSurvival analysisPolymorphism Single-Stranded ConformationalAgedNeoplasm StagingCarcinomaMicrosatellite instabilityCell BiologyDNA-binding domainDNA NeoplasmExonsMiddle Agedmedicine.diseaseGenes p53PrognosisSurvival AnalysisProtein Structure TertiarychemistryItalyMutationCancer researchFemaleDNAFollow-Up StudiesMicrosatellite RepeatsJournal of cellular physiology
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Intranuclear nemaline rod myopathy

2006

The clinical, pathologic, and genetic findings of a boy with intranuclear nemaline rod myopathy are described. Serial muscle biopsies revealed myocyte nuclei containing inclusions that were immunoreactive for α-actinin and increased with age. Genetic analysis revealed a Val163Leu ACTA1 mutation previously associated with nemaline rod myopathy. Although initially delayed, he has reached all milestones and remains stable. These findings suggest intranuclear rods may increase with time and do not necessarily imply a poor prognosis. Muscle Nerve, 2006

MalePoor prognosisPathologymedicine.medical_specialtyPhysiologyBiopsyIntranuclear Inclusion BodiesMyopathies Nemalinemedicine.disease_causeCellular and Molecular NeuroscienceNemaline myopathyPhysiology (medical)BiopsymedicineHumansMyocyteIntranuclear Nemaline Rod MyopathyChildMuscle SkeletalMyopathyActinCell NucleusMutationmedicine.diagnostic_testbusiness.industrymedicine.diseaseNeurology (clinical)medicine.symptombusinessMuscle & Nerve
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A novel two base pair deletion in the factor V gene associated with severe factor V deficiency

2001

We studied a family in which the proband, a 13-year-old boy, had unmeasurable plasma levels of coagulation factor V antigen and activity. Clinical symptoms were severe, with several episodes of haemorrhages in the mucosal tracts (gastrointestinal, nose and urinary) and recurrent haemarthroses that caused permanent arthropathy. Sequence analysis of the factor V gene demonstrated the presence of a novel 2 base pair (bp) homozygous deletion in exon 13 at positions 2833-2834. This mutation, present in the heterozygous state in the asymptomatic mother and absent in the healthy brother, introduced a frameshift and a premature stop at codon 900. This would predict the synthesis of a truncated fact…

MaleProbandFactor V DeficiencyAdolescentMutantBiologymedicine.disease_causeFrameshift mutationExonmedicineHumansRNA MessengerBase PairingGeneGeneticsMutationReverse Transcriptase Polymerase Chain ReactionHomozygoteFactor VFactor VSequence Analysis DNAHematologyMolecular biologybiology.proteinBlood Coagulation TestsFactor V DeficiencyGene DeletionBritish Journal of Haematology
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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
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Two distinct phenotypes, hemiplegic migraine and episodic Ataxia type 2, caused by a novel common CACNA1A variant

2020

Abstract Background To investigate the genetic and environmental factors responsible for phenotype variability in a family carrying a novel CACNA1A missense mutation. Mutations in the CACNA1A gene were identified as responsible for at least three autosomal dominant disorders: FHM1 (Familial Hemiplegic Migraine), EA2 (Episodic Ataxia type 2), and SCA6 (Spinocerebellar Ataxia type 6). Overlapping clinical features within individuals of some families sharing the same CACNA1A mutation are not infrequent. Conversely, reports with distinct phenotypes within the same family associated with a common CACNA1A mutation are very rare. Case presentation A clinical, molecular, neuroradiological, neuropsy…

MaleProbandmedicine.medical_specialtyNeurologyMigraine with AuraFamilial hemiplegic migraine type 1Mutation MissenseneuropsychologyCase Reportmedicine.disease_causeNystagmus Pathologiclcsh:RC346-42903 medical and health sciences0302 clinical medicinemedicineHumansSpinocerebellar ataxia type 6Missense mutationFamilyChildFamilial hemiplegic migrainelcsh:Neurology. Diseases of the nervous system030304 developmental biologyEpisodic ataxiaGenetics0303 health sciencesMutationbusiness.industryCACNA1A geneEpisodic ataxia type2Cognitive affective syndromeGeneral Medicinemedicine.diseasePhenotypePhenotypeAtaxiaCalcium ChannelsNeurology (clinical)businessCognitive affective syndrome neuropsychology.030217 neurology & neurosurgeryBMC Neurology
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Natural and engineered carboxy-terminal variants: decreased secretion and gain-of-function result in asymptomatic coagulation factor VII deficiency.

2012

We report 2 asymptomatic homozygotes for the nonsense p.R462X mutation affecting the carboxy-terminus of coagulation factor VII (FVII, 466 aminoacids). FVII levels of 3-5% and 2.7 ± 0.4% were found in prothrombin time-based and activated factor X (FXa) generation assays with human thromboplastins. Noticeably, FVII antigen levels were barely detectable (0.7 ± 0.2%) which suggested a gain-of-function effect. This effect was more pronounced with bovine thromboplastin (4.8 ± 0.9%) and disappeared with rabbit thromboplastin (0.7 ± 0.2%). This suggests that the mutation influences tissue factor/FVII interactions. Whereas the recombinant rFVII-462X variant confirmed an increase in specific activit…

MaleProteasesHeterozygoteFactor VII DeficiencyEnzyme-Linked Immunosorbent AssayFVIIBiologymedicine.disease_causeThromboplastinTissue factorchemistry.chemical_compoundCarboxy-terminalhemic and lymphatic diseasesmedicineFACTOR VII DEFICIENCY MOLECULAR VARIANTSThromboplastinMissense mutationAnimalsHumanscardiovascular diseasesChildBlood CoagulationProthrombin timeMutationmedicine.diagnostic_testFactor VIIHomozygoteHematologyFactor VIIMiddle AgedMolecular biologyAsymptomatic; Carboxy-terminal; FVII; Mutation;AsymptomaticchemistryCoagulationCodon NonsenseMutationMutagenesis Site-DirectedProthrombin TimeCattleFemaleRabbitsOriginal Articles and Brief Reports
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New Hyperekplexia Mutations Provide Insight into Glycine Receptor Assembly, Trafficking, and Activation Mechanisms*

2013

Hyperekplexia is a syndrome of readily provoked startle responses, alongside episodic and generalized hypertonia, that presents within the first month of life. Inhibitory glycine receptors are pentameric ligand-gated ion channels with a definitive and clinically well stratified linkage to hyperekplexia. Most hyperekplexia cases are caused by mutations in the α1 subunit of the human glycine receptor (hGlyR) gene (GLRA1). Here we analyzed 68 new unrelated hyperekplexia probands for GLRA1 mutations and identified 19 mutations, of which 9 were novel. Electrophysiological analysis demonstrated that the dominant mutations p.Q226E, p.V280M, and p.R414H induced spontaneous channel activity, indicat…

MaleProtein subunitMutation MissenseBiologyBiochemistryProtein Structure SecondaryReceptors GlycinemedicineHumansHyperekplexiaReceptorMolecular BiologyGlycine receptorIon channelGeneticsWild typeMolecular Bases of DiseaseCell BiologyMuscle RigidityProtein Structure TertiaryAmino Acid SubstitutionGene Expression RegulationFemalemedicine.symptomIon channel linked receptorsCys-loop receptors
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BRAF V600E Mutation in Two Distinct Meningeal Melanocytomas Associated With a Nevus of Ota

2014

MaleProto-Oncogene Proteins B-rafCancer ResearchSkin NeoplasmsAdolescentGlutamic AcidNevus of OtaValineMeningeal NeoplasmsmedicineHumansMelanomabusiness.industryValinemedicine.diseaseNevus of OtaBRAF V600ECell Transformation NeoplasticOncologyMutationMutation (genetic algorithm)Cancer researchMelanocytesSignal transductionbusinessSignal TransductionJournal of Clinical Oncology
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