Search results for "gene mutation"

showing 10 items of 187 documents

Hereditary angioedema with a mutation in the plasminogen gene

2017

Background Hereditary angioedema (HAE) with normal C1-INH (HAEnCI) may be linked to specific mutations in the coagulation factor 12 (FXII) gene (HAE-FXII) or functional mutations in other genes that are still unknown. We sought to identify and characterize a hitherto unknown type of HAE with normal C1-INH and without mutation in the F12 gene. Methods The study comprised analysis of whole-exome sequencing, Sanger sequencing, and clinical data of patients. Results We detected a mutation in the plasminogen (PLG) gene in patients with HAEnCI. The mutation c.9886A>G was located in exon 9 leading to the missense mutation p.Lys330Glu (K330E) in the kringle 3 domain of the PLG protein. The mutation…

AdultMale0301 basic medicinePathologymedicine.medical_specialtyAdolescentImmunologyMutation MissenseGene mutationBiologyYoung Adult03 medical and health sciencesExonsymbols.namesake0302 clinical medicineGermanyExome SequencingmedicineHumansImmunology and AllergyMissense mutationChildExome sequencingAgedSanger sequencingAngioedemas HereditaryAutosomal dominant traitPlasminogenMiddle Agedmedicine.disease030104 developmental biology030228 respiratory systemChild PreschoolMutationMutation (genetic algorithm)Hereditary angioedemasymbolsFemaleAllergy
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Molecular characterization of congenital myasthenic syndromes in Spain.

2017

Congenital myasthenic syndromes (CMS) are a heterogeneous group of genetic disorders, all of which impair neuromuscular transmission. Epidemiological data and frequencies of gene mutations are scarce in the literature. Here we describe the molecular genetic and clinical findings of sixty-four genetically confirmed CMS patients from Spain. Thirty-six mutations in the CHRNE, RAPSN, COLQ, GFPT1, DOK7, CHRNG, GMPPB, CHAT, CHRNA1, and CHRNB1 genes were identified in our patients, with five of them not reported so far.. These data provide an overview on the relative frequencies of the different CMS subtypes in a large Spanish population. CHRNE mutations are the most common cause of CMS in Spain, …

AdultMale0301 basic medicineSlow-channel syndromeAdolescentNeuromuscular transmissionGMPPBGene mutationCOLQCongenital myasthenic syndromeYoung Adult03 medical and health sciences0302 clinical medicineDOK7COLQmedicineHumansCHRNECHRNEGeneGenetics (clinical)health care economics and organizationsMyasthenic Syndromes CongenitalGeneticsbiologyRAPSNMiddle AgedCongenital myasthenic syndromemedicine.diseasePhenotype3. Good healthGenetic mutationsRAPSN030104 developmental biologyGFPT1NeurologySpainPediatrics Perinatology and Child Healthbiology.proteinFemaleNeurology (clinical)030217 neurology & neurosurgery
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Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal-Dystrophy (APECED) in Sicily: confirmation that R203X is the peculiar AIRE gene mutation.

2011

Background: Autoimmune polyendocrinopathycandidiasis-ectodermal-dystrophy (APECED), also known as autoimmune polyendocrine syndrome type 1 (APS-1) (OMIM 240300), is a very rare disease. Accepted criteria for diagnosis require the presence of at least 2 of 3 major clinical features: chronic mucocutaneous candidiasis (CMC), chronic hypoparathyroidism (CH), and Addison's disease (AD). Aim: We analyzed AIRE gene mutations and genotype-phenotype correlation in APECED patients originating from Sicily and in their relatives. Subjects and methods: In 4 patients, clinical evaluations, genetic analysis of AIRE, and APECED-related autoantibodies were performed. Results: Two patients carried the mutati…

AdultMaleChronic mucocutaneous candidiasisMutationAutoimmune polyendocrine syndrome type 1HumansFemaleAddison's diseasePolyendocrinopathies AutoimmuneSicilyChronic hypoparathyroidismAIRE gene mutation Addison’s disease APECED autoimmune polyendocrine syndrome type 1 chronic mucocutaneous candidiasis chronic hypoparathyroidismAPECEDTranscription Factors
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A novel mutation in the coagulation factor 12 gene in subjects with hereditary angioedema and normal C1-inhibitor.

2011

In hereditary angioedema with normal C1-inhibitor two different missense mutations of codon p.Thr328* in the coagulation factor 12 gene have been reported in some families. In this study a novel factor 12 gene mutation, the deletion of 72 base pairs (bp) (c.971_1018+24del72*), was identified in a family of Turkish origin, in two sisters with recurrent skin swellings and abdominal pain attacks and in their symptom-free father. This deletion caused a loss of 48 bp of exon 9 (coding amino acids 324* to 340*) in addition to 24 bp of intron 9, including the authentic donor splice site of exon 9. The large deletion of 72 bp was located in the same F12 gene region as the missense mutations p.Thr32…

AdultMaleFactor XII DeficiencyTurkeyImmunologyDNA Mutational AnalysisMutation MissenseGene mutationmedicine.disease_causeC1-inhibitorExonImmunology and AllergyMedicineMissense mutationHumansHereditary Angioedema Type IIISequence DeletionGeneticsMutationAngioedemabiologybusiness.industryAngioedemas HereditaryExonsmedicine.diseaseMolecular biologyIntronsPedigreeHereditary angioedemaFactor XIIMutationbiology.proteinFemalemedicine.symptombusinessComplement C1 Inhibitor ProteinClinical immunology (Orlando, Fla.)
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Characterization of non-expressed C4 genes in a case of complete C4 deficiency: identification of a novel point mutation leading to a premature stop …

1998

The genetic basis of complete C4 deficiency in a patient with SLE was investigated. Previous studies have demonstrated that this patient has two different major histocompatibility complex (MHC) haplotypes that each contain a major deletion and a non-expressed C4 gene. In the present study, non-expression of the C4 genes was explained by the finding of two distinct C4 gene mutations. A previously described two base pair insertion in exon 29 of the C4 gene was detected in the paternal MHC haplotype [HLA-A2, B40, SC00, DR6]. The maternal haplotype [HLA-A30, B18, F1C00, DR3] carried a C4 gene with a one base pair deletion in exon 20 generating a premature stop codon. This mutation was neither f…

AdultMaleHeterozygoteImmunologyGene mutationBiologymedicine.disease_causePolymerase Chain ReactionCell LineMajor Histocompatibility ComplexExonmedicineImmunology and AllergyHumansLupus Erythematosus SystemicPoint MutationGenePolymorphism Single-Stranded ConformationalGeneticsMutationPoint mutationHaplotypeC4AComplement C4General MedicineExonsSequence Analysis DNAMolecular biologyIsotypePedigreeHaplotypesCodon TerminatorFemalePolymorphism Restriction Fragment LengthHuman immunology
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Evaluation of clinical diagnosis criteria of familial ligand defective apoB 100 and lipoprotein phenotype comparison between LDL receptor gene mutati…

2007

Familial hypercholesterolemia (FH) and familial defective apoB 100 (FDB) are characterized by increased plasma low-density lipoprotein cholesterol (LDLc) levels and risk of coronary heart disease (CHD). FDB is clinically indistinguishable from FH. The aims of this study were to evaluate clinical diagnosis criteria for FDB and to compare the lipoprotein phenotype between carriers of LDL receptor (LDLR) gene mutations that affect the ligand-binding domain and subjects with the R3500Q mutation in apoB gene. We studied 213 subjects (113 probands) with FH and 19 heterozygous FDB subjects. Genetic diagnosis was determined by following a protocol based on Southern blot and polymerase chain reactio…

AdultMaleHeterozygotemedicine.medical_specialtyGenotypeApolipoprotein BPopulationMutation MissenseCoronary DiseaseFamilial hypercholesterolemiaGene mutationBiologyWhite PeopleHyperlipoproteinemia Type IIchemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansMissense mutationeducationPolymorphism Single-Stranded Conformationaleducation.field_of_studyBinding SitesCholesterolGenetic Carrier ScreeningBiochemistry (medical)Public Health Environmental and Occupational HealthCholesterol LDLGeneral MedicineMiddle Agedmedicine.diseaseFounder EffectProtein Structure TertiaryEuropePhenotypeEndocrinologyReceptors LDLchemistryApolipoprotein B-100LDL receptorbiology.proteinFemalelipids (amino acids peptides and proteins)LipoproteinTranslational Research
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Thrombosis in inherited factor VII deficiency

2003

Thrombosis in congenital factor (F) VII deficiency was investigated through extensive phenotypic and molecular-genetic studies. Patients with a history of thrombosis among 514 entries in the FVII Deficiency Study Group database were evaluated. Thrombotic events were arterial in one case, disseminated intravascular coagulation in another and venous in seven. Gene mutations were characterized in eight patients: three were homozygous, three compound heterozygous and two heterozygous. FXa and IIa generation assays were consistent with the genetic lesions. One patient was heterozygous for the FV Leiden and one for the FIIG20210A mutation. In seven patients, surgical interventions and/or replacem…

AdultMaleHeterozygotemedicine.medical_specialtyPathologyTime FactorsAdolescentFactor VII DeficiencyGene mutationCompound heterozygosityThrombophiliaGastroenterologyInternal medicinemedicineHumansThrombophiliaAgedVenous ThrombosisDisseminated intravascular coagulationbiologybusiness.industryHomozygoteFactor VFactor VThrombosisHematologyCongenital FVII deficiency; Replacement therapy; Surgery; Thrombophilia; Thrombosis;Disseminated Intravascular CoagulationMiddle Agedmedicine.diseaseThrombosisZygosityVenous thrombosisPhenotypeDatabases as TopicFactor XaMutationbiology.proteinFemaleProthrombinbusinessJournal of Thrombosis and Haemostasis
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Evaluation of the autoimmune regulator (AIRE) gene mutations in a cohort of Italian patients with autoimmune-polyendocrinopathy-candidiasis-ectoderma…

2009

Summary Objective   Autoimmune-polyendocrinopathy-candidiasis-ectodermal-dystrophy (APECED) is a rare syndrome characterized by chronic candidiasis, chronic hypoparathyroidism and Addison's disease. APECED has been associated with mutations in autoimmune regulator (AIRE) gene. Our aim is to perform a genetic analysis of the AIRE gene in Italian APECED patients and in their relatives. Design  AIRE mutations were determined by DNA sequencing in all subjects. Patients were tested for clinical autoimmune or non-autoimmune diseases, or for organ and non-organ specific autoantibodies. Patients   A total of 24 Italian patients with APECED (15 from the Venetian region, 2 from Southern-Tyrol, 4 from…

AdultMaleHeterozygotemedicine.medical_specialtyanimal structuresAdolescentHypoparathyroidismEndocrinology Diabetes and MetabolismGene mutationmedicine.disease_causeCompound heterozygositySettore MED/13 - EndocrinologiaCohort StudiesLoss of heterozygosityYoung AdultEndocrinologyAddison DiseaseInternal medicinemedicineHumansChildPolyendocrinopathies AutoimmuneAgedGeneticsMutationGenetic heterogeneitybusiness.industryHomozygoteCandidiasisAutoantibodyAutoimmune polyendocrinopathyMiddle AgedAutoimmune regulatorEndocrinologyItalyCase-Control StudiesMutationAPS1 AIRE APECEDFemalebusinessTranscription Factors
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Clonal evolution in relapsed NPM1-mutated acute myeloid leukemia.

2013

Mutations in the nucleophosmin 1 (NPM1) gene are considered a founder event in the pathogenesis of acute myeloid leukemia (AML). To address the role of clonal evolution in relapsed NPM1-mutated (NPM1mut) AML, we applied high-resolution, genome-wide, single-nucleotide polymorphism array profiling to detect copy number alterations (CNAs) and uniparental disomies (UPDs) and performed comprehensive gene mutation screening in 53 paired bone marrow/peripheral blood samples obtained at diagnosis and relapse. At diagnosis, 15 aberrations (CNAs, n = 10; UPDs, n = 5) were identified in 13 patients (25%), whereas at relapse, 56 genomic alterations (CNAs, n = 46; UPDs, n = 10) were detected in 29 patie…

AdultMaleNPM1MyeloidImmunologyBiologyGene mutationBiochemistrySomatic evolution in cancerPolymorphism Single NucleotideDNA Methyltransferase 3AClonal EvolutionYoung AdultRecurrenceRisk FactorsmedicineHumansDNA (Cytosine-5-)-MethyltransferasesAgedChromosomes Human Pair 13Myeloid leukemiaNuclear ProteinsCell BiologyHematologyMiddle Agedmedicine.diseasePrognosisMinimal residual diseaseDNA FingerprintingLeukemiaETV6Leukemia Myeloid Acutemedicine.anatomical_structureCancer researchFemaleChromosomes Human Pair 9NucleophosminGene DeletionBlood
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Bcl-6 mutation status provides clinically valuable information in early-stage B-cell chronic lymphocytic leukemia

2004

In B-cell chronic lymphocytic leukemia (B-CLL), somatic mutation of IgVH genes defines a subgroup with favorable prognosis, whereas the absence of IgVH mutations is correlated with a worse outcome. Mutations of the BCL-6 gene are also observed in a subset of B-CLL, but the clinical significance of this molecular alteration remains uncertain. We examined the distribution of IgVH and BCL-6 gene mutations in 95 well-characterized patients with Binet stage A B-CLL, and correlated them with clinical, laboratory, cytogenetic findings and disease progression. Mutations of the BCL-6 gene were observed only in cases harboring mutated IgVH. Unexpectedly, coexistence of IgVH and BCL-6 mutations was co…

AdultMaleOncologyCancer Researchmedicine.medical_specialtyChronic lymphocytic leukemiaImmunoglobulin Variable RegionLocus (genetics)BiologyGene mutationDisease-Free SurvivalGermline mutationProto-Oncogene ProteinsInternal medicinemedicineHumansB-cell chronic lymphocytic leukemiaClinical significanceProspective StudiesGeneAgedAged 80 and overHematologyChromosomes Human Pair 11HematologyMiddle AgedPrognosismedicine.diseaseLeukemia Lymphocytic Chronic B-CellDNA-Binding ProteinsOncologyMutationImmunologyProto-Oncogene Proteins c-bcl-6FemaleChromosome DeletionChromosomes Human Pair 17Follow-Up StudiesTranscription FactorsLeukemia
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