Search results for " Mutation"

showing 10 items of 1212 documents

Calreticulin Mutations in Myeloproliferative Neoplasms: Comparison of Three Diagnostic Methods

2015

International audience; Calreticulin (CALR) mutations have recently been reported in 70-84% of JAK2V617F-negative myeloproliferative neoplasms (MPN), and this detection has become necessary to improve the diagnosis of MPN. In a large single-centre cohort of 298 patients suffering from Essential Thrombocythemia (ET), the JAK2V617F, CALR and MPL mutations were noted in 179 (60%), 56 (18.5%) and 13 (4.5%) respectively. For the detection of the CALR mutations, three methods were compared in parallel: high-resolution melting-curve analysis (HRM), product-sizing analysis and Sanger sequencing. The sensitivity for the HRM, product-sizing analysis and Sanger sequencing was 96.4%, 98.2% and 89.3% re…

AdultMaleSequence analysislcsh:MedicineBiologymedicine.disease_causeSensitivity and SpecificityDNA sequencingFrameshift mutationYoung Adult03 medical and health sciencessymbols.namesake0302 clinical medicineINDEL MutationmedicineHumanslcsh:ScienceFrameshift MutationAged030304 developmental biologyAged 80 and overSanger sequencingGenetics0303 health sciencesMutationMultidisciplinaryEssential thrombocythemialcsh:RMiddle Agedmedicine.disease3. Good health030220 oncology & carcinogenesisBone marrow neoplasmMutationbiology.proteinsymbolslcsh:QFemaleBone Marrow NeoplasmsCalreticulinSequence AnalysisCalreticulin[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyResearch ArticlePLOS ONE
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Variability of reverse transcriptase and overlapping S gene in hepatitis B virus isolates from untreated and lamivudine-resistant chronic hepatitis B…

2009

Background The high degree of diversity of the hepatitis B virus (HBV) quasispecies in chronically infected individuals raises the possibility that HBV genetic variants favouring resistance to nucleoside/nucleotide analogues (NAs) might pre-exist to treatment. The aim of this study was to investigate the genetic variability of the entire HBV reverse transcriptase (RT) domain and of the overlapping S gene in a large series of untreated hepatitis B surface antigen carriers and in lamivudine (3TC)-resistant patients. Methods Sequencing analysis of the entire HBV RT domain of isolates from 100 untreated (treatment- naive group) and 59 3TC-resistant (3TC-resistant group) consecutive patients wit…

AdultMaleSettore MED/07 - Microbiologia E Microbiologia ClinicaHepatitis B virusAdult; Aged; Drug Resistance; Viral; Female; Genetic Variation; Hepatitis B Surface Antigens; Hepatitis B virus; Hepatitis B; Chronic; Humans; Lamivudine; Male; Middle Aged; Mutation; RNA-Directed DNA Polymerase; Reverse Transcriptase Inhibitors; Sequence Analysis; DNA; Treatment OutcomeDrug ResistanceViral quasispeciesmedicine.disease_causeVirusHepatitis B ChronicOrthohepadnavirusDrug Resistance ViralmedicineHumansPharmacology (medical)ViralChronicAgedPharmacologyHepatitis B virusSettore MED/12 - GastroenterologiaHepatitis B Surface AntigensbiologyReverse-transcriptase inhibitorLamivudineGenetic VariationRNA-Directed DNA PolymeraseSequence Analysis DNADNAMiddle Agedbiology.organism_classificationHepatitis BVirologyReverse transcriptaseInfectious DiseasesTreatment OutcomeHepadnaviridaeLamivudineMutationReverse Transcriptase InhibitorsHBV reverse transcriptase gene S lamivudine resistantFemaleSequence Analysismedicine.drug
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Autosomal-recessive SASH1 variants associated with a new genodermatosis with pigmentation defects, palmoplantar keratoderma and skin carcinoma

2014

SASH1 (SAM and SH3 domain-containing protein 1) is a tumor suppressor gene involved in the tumorigenesis of a spectrum of solid cancers. Heterozygous SASH1 variants are known to cause autosomal-dominant dyschromatosis. Homozygosity mapping and whole-exome sequencing were performed in a consanguineous Moroccan family with two affected siblings presenting an unclassified phenotype associating an abnormal pigmentation pattern (hypo- and hyperpigmented macules of the trunk and face and areas of reticular hypo- and hyperpigmentation of the extremities), alopecia, palmoplantar keratoderma, ungueal dystrophy and recurrent spinocellular carcinoma. We identified a homozygous variant in SASH1 (c.1849…

AdultMaleSkin NeoplasmsDNA Mutational AnalysisMutation MissenseGenes RecessiveConsanguinityBiologyArticleConsanguinityKeratoderma PalmoplantarGeneticsmedicineHumansExomeGenetic Predisposition to DiseaseGenetics (clinical)Pigmentation disorderSkinFamily HealthGeneticsSiblingsTumor Suppressor ProteinsHomozygoteGenodermatosisSequence Analysis DNAFibroblastsmedicine.diseaseDisease gene identificationHyperpigmentationPedigreePalmoplantar keratodermaFemaleSkin cancermedicine.symptomSkin CarcinomaPigmentation DisordersEuropean Journal of Human Genetics
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Autosomal dominant hereditary spastic paraplegia: report of a large italian family with R581X spastin mutation

2007

We describe a large kindred with a typical pure form of autosomal dominant hereditary spastic paraplegia (ADHSP). On the basis of maximum LOD score of 1.94 at theta (max)=0 with marker D2S367, we obtained suggestive evidence for linkage of ADHSP to SPG4 locus. Denaturing high-performance liquid chromatography (DHPLC) and direct sequence analysis allowed us to identify a nonsense mutation (1741* C > T) in exon 17 of the Spastin gene. This transition, carried by all the affected family members and two apparently healthy individuals, lead to truncation of the last 36 amino acids in the C-terminus of the protein. These results confirm the existence of mutation in the SPG4 gene with a reduced pe…

AdultMaleSpastinGenotypeSequence analysisHereditary spastic paraplegiaDNA Mutational AnalysisNonsense mutationLocus (genetics)DermatologyBiologyArginineSpastinExonHereditary spastic paraplegia Spastin Neurological diseasemedicineHumansGeneAgedAdenosine TriphosphatasesFamily HealthGeneticsSpastic Paraplegia HereditaryGeneral MedicineMiddle Agedmedicine.diseaseMolecular biologyPenetrancePsychiatry and Mental healthItalyMutationFemaleNeurology (clinical)Lod ScoreNeurological Sciences
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Phenotypic variability in patients with generalised resistance to thyroid hormone.

1995

Genetic linkage of generalised resistance to thyroid hormone (GRTH) to the human thyroid receptor beta 1 gene has been identified. To date 38 different mutations in several kindreds have been documented. We report on a family with GRTH displaying an adenine for guanine substitution at nucleotide 1234 resulting in a threonine for alanine substitution at codon 317 of exon 9. This mutation has been described for different phenotypes, suggesting that the heterogeneity in GRTH may be the result of multiple genetic factors.

AdultMaleThyroid Hormone Resistance SyndromeThyroid Hormonesmedicine.medical_specialtyGenetic LinkageMolecular Sequence DataThyroid Function TestsBiologymedicine.disease_causeThyroid function testsGenetic HeterogeneityExonGenetic linkageInternal medicineGeneticsmedicineHumansPoint MutationAmino Acid SequenceChildGeneGenetics (clinical)GeneticsMutationReceptors Thyroid HormoneBase Sequencemedicine.diagnostic_testGenetic heterogeneityPoint mutationThyroidPedigreePhenotypemedicine.anatomical_structureEndocrinologyChild PreschoolFemaleResearch ArticleJournal of Medical Genetics
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A novel constitutional mutation affecting splicing of retinoblastoma tumor suppressor gene intron 23 causes partial loss of pRB activity.

2005

Hereditary predisposition to retinoblastoma is caused by germ line mutations in the RB1 gene. Genetic counseling of affected individuals and accurate risk prediction for their families requires identification of the disease causing mutation. Furthermore, the nature of a mutation can determine genetic penetrance, disease presentation and prognosis. We describe, and functionally characterize here, a novel mutant allele of RB1 present in the germ line of a patient with sporadic bilateral retinoblastoma. The mutation generates an operational splice acceptor site resulting in a predicted protein product with loss of 81 amino acids from its carboxy terminus. We demonstrate that the aberrantly spl…

AdultMaleTumor suppressor geneRNA SplicingRetinal NeoplasmsDNA Mutational AnalysisRetinoblastoma ProteinGeneticsmedicineMissense mutationHumansDisease-causing MutationExpressivity (genetics)Genes RetinoblastomaGenetics (clinical)GeneticsbiologyRetinoblastomaRetinoblastoma proteinRetinoblastomamedicine.diseasePenetranceeye diseasesIntronsPedigreeMutation (genetic algorithm)Mutationbiology.proteinHuman mutation
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Clinical features and molecular genetic analysis in a Turkish family with oral white sponge nevus

2018

Background Oral white sponge nevus (WSN) is a rare autosomal dominant benign condition, characterized by asymptomatic spongy white plaques. Mutations in Keratin 4 (KRT4) and 13 (KRT13) have been shown to cause WSN. Familial cases are uncommon due to irregular penetrance. Thus, the aim of the study was: a) to demonstrate the clinical and histopathological features of a three-generation Turkish family with oral WSN b) to determine whether KRT4 or KRT13 gene mutation was the molecular basis of WSN. Material and Methods Out of twenty members of the family ten were available for assessment. Venous blood samples from six affected and five unaffected members and 48 healthy controls were obtained f…

AdultMaleTurkish populationAdolescentTurkeyLeukokeratosis Hereditary MucosalGene mutationBiology030207 dermatology & venereal diseases03 medical and health sciencesExonYoung Adult0302 clinical medicineWhite sponge nevusmedicineHumansChildGeneral DentistryGeneAllele frequencyGeneticsOral Medicine and PathologyResearchKeratin-13030206 dentistryMiddle Aged:CIENCIAS MÉDICAS [UNESCO]medicine.diseasePenetrancePedigreeOtorhinolaryngologyKeratin 4Case-Control StudiesUNESCO::CIENCIAS MÉDICASCytogenetic AnalysisMutationbiology.proteinSurgeryKeratin-4Medicina Oral, Patología Oral y Cirugía Bucal
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Factor V Leiden and prothrombin gene G20210A mutations in Italian patients with Behcet's disease and deep vein thrombosis

2004

OBJECTIVE: To evaluate the frequency and type of vascular lesions and to study the association of factor V gene G1691A (Leiden) and prothrombin gene G20210A polymorphisms with venous thrombosis in Italian patients with Behçet's disease (BD). METHODS: Included were 118 consecutive Italian BD patients followed over a 3-year period (1997-1999) who satisfied the International Study Group criteria for BD. The control group consisted of 132 healthy Italian blood donors. All BD patients and controls were genotyped by polymerase chain reaction and allele-specific restriction enzyme techniques for factor V Leiden and prothrombin gene G20210A polymorphisms. RESULTS: Vascular lesions were observed in …

AdultMaleVenous ThrombosisFactor V Leiden mutation Prothrombin G20210A mutationAdolescentGenotypeBehcet SyndromeFactor VMiddle AgedBehc ̧et’s disease; Deep vein thrombosis; Factor V Leiden mutation Prothrombin G20210A mutationAdolescent; Adult; Behcet Syndrome; Factor V; Female; Gene Frequency; Genotype; Humans; Italy; Male; Middle Aged; Prothrombin; Risk Factors; Venous Thrombosis; Point MutationGene FrequencyItalyDeep vein thrombosiRisk FactorsFactor V Leiden mutationHumansPoint MutationFemaleProthrombinProthrombin G20210A mutationBehcet’s disease
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Genotypic and phenotypic spectrum in tricho-rhino-phalangeal syndrome types I and III

2000

Tricho-rhino-phalangeal syndrome (TRPS) is characterized by craniofacial and skeletal abnormalities. Three subtypes have been described: TRPS I, caused by mutations in the TRPS1 gene on chromosome 8; TRPS II, a microdeletion syndrome affecting the TRPS1 and EXT1 genes; and TRPS III, a form with severe brachydactyly, due to short metacarpals, and severe short stature, but without exostoses. To investigate whether TRPS III is caused by TRPS1 mutations and to establish a genotype-phenotype correlation in TRPS, we performed extensive mutation analysis and evaluated the height and degree of brachydactyly in patients with TRPS I or TRPS III. We found 35 different mutations in 44 of 51 unrelated p…

AdultMaleanimal structuresAdolescentGenotypeDNA Mutational AnalysisMolecular Sequence DataLimb Deformities CongenitalBiologyOsteochondrodysplasiasPolymorphism Single NucleotideShort statureLanger–Giedion syndromeGeneticsmedicineHumansMissense mutationTricho–rhino–phalangeal syndromeGenetics(clinical)Amino Acid SequenceChildGenetics (clinical)GeneticsAnthropometryBase SequenceBrachydactylyInfantZinc FingersExonsSyndromeArticlesMiddle AgedMicrodeletion syndromemedicine.diseasePenetranceBody HeightPedigreeDNA-Binding ProteinsRadiographyPhenotypeChild PreschoolMutationTrichorhinophalangeal Syndrome Type IErythroid-Specific DNA-Binding FactorsFemalemedicine.symptomChromosomes Human Pair 8Transcription Factors
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MFAP5 Loss-of-Function Mutations Underscore the Involvement of Matrix Alteration in the Pathogenesis of Familial Thoracic Aortic Aneurysms and Dissec…

2014

Thoracic aortic aneurysm and dissection (TAAD) is an autosomal-dominant disorder with major life-threatening complications. The disease displays great genetic heterogeneity with some forms allelic to Marfan and Loeys-Dietz syndrome, and an important number of cases still remain unexplained at the molecular level. Through whole-exome sequencing of affected members in a large TAAD-affected family, we identified the c.472CT (p.Arg158(∗)) nonsense mutation in MFAP5 encoding the extracellular matrix component MAGP-2. This protein interacts with elastin fibers and the microfibrillar network. Mutation screening of 403 additional probands identified an additional missense mutation of MFAP5 (c.62GT …

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesAdolescentExtracellular matrix componentNonsense mutationHaploinsufficiencyThoracic aortic aneurysmPathogenesisContractile ProteinsReportGeneticsmedicineHumansMissense mutationGenetics(clinical)ExomeChildGenetics (clinical)AgedGlycoproteinsAged 80 and overGeneticsAortic Aneurysm ThoracicbiologyGenetic heterogeneitySequence Analysis DNAFibroblastsMiddle Agedmedicine.diseasePedigree3. Good healthAortic DissectionAmino Acid SubstitutionCodon Nonsensebiology.proteinIntercellular Signaling Peptides and ProteinsFemaleHaploinsufficiencyElastinThe American Journal of Human Genetics
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