Search results for " Missense"

showing 10 items of 168 documents

Clinical, pathologic, and genetic features of massive soft tissue neurofibromas in a Sicilian patient

2008

Abstract CONTEXT: Lipase maturation factor 1 (LMF1) gene is a novel candidate gene in severe hypertriglyceridemia. Lmf1 is involved in the maturation of lipoprotein lipase (LPL) and hepatic lipase in endoplasmic reticulum. To date only one patient with severe hypertriglyceridemia and related disorders was found to be homozygous for a nonsense mutation in LMF1 gene (Y439X). OBJECTIVE: The objective of the study was to investigate LMF1 gene in hypertriglyceridemic patients in whom mutations in LPL, APOC2, and APOA5 genes had been excluded. RESULTS: The resequencing of LMF1 gene led to the discovery of a novel homozygous nonsense mutation in one patient with severe hypertriglyceridemia and rec…

Nonsynonymous substitutionMalecongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyHeterozygoteNeurofibromatosis 1BiopsyDNA Mutational AnalysisMutation MissenseSoft Tissue NeoplasmsDermatologymassive soft tissue neurofibromas NeurofibromatosisBiologymedicine.disease_causeFrameshift mutationExonGenes Neurofibromatosis 1medicineSettore MED/35 - Malattie Cutanee E VenereeMissense mutationHumansNeurofibromatosisFrameshift MutationGeneSicilyGeneticsMutationHeterozygote advantageGeneral MedicineExonsMiddle Agedmedicine.diseasenervous system diseasesGene Expression Regulation NeoplasticButtocks
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Novel P53 mutations detected by FAMA in colorectal cancers

2006

Background The aim of the study was to identify p53 gene mutations by FAMA (fluorescence-assisted mismatch analysis) in colorectal cancers. Patients and methods Analytical scanning of the p53 gene (exons 5–9) was performed in colon cancer samples from 44 consecutive patients by FAMA. FAMA is a semiautomatic scanning approach based on the chemical cleavage of the mismatch in fluorescently labeled heteroduplex DNA, obtained from the combination of a normal and a mutated allele. FAMA has already shown optimal levels of diagnostic accuracy and sensitivity in detecting gene mutations (nucleotide substitutions, insertions/deletions) both at the germline and somatic level. The peculiar feature of …

Oncologymedicine.medical_specialtyMutantDNA Mutational AnalysisMutation MissenseGene mutationmedicine.disease_causeExonInternal medicinemedicineMissense mutationHumansKey words: colon cancer p53 mutations FAMAAlleleGeneMutationbusiness.industryHematologyDNA NeoplasmExonsGenes p53Molecular biologyOncologybusinessColorectal NeoplasmsHeteroduplex
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C21orf2 is mutated in recessive early-onset retinal dystrophy with macular staphyloma and encodes a protein that localises to the photoreceptor prima…

2015

Background/aim We have noted a phenotype of early-onset retinal dystrophy with macular staphyloma but without high myopia. The aim of this study is to report the underlying genetic mutations and the subcellular localisation of the gene product in the retina. Methods Retrospective case series (2012–2015); immunohistochemical analyses of mammalian retina for in situ protein localisation. Results All three probands were first noted to have decreased vision at 3–6 years old which worsened over time. At ages 39, 37 and 12 years old, all had similar retinal findings: dystrophic changes (retinal pigment epithelium mottling, vessel narrowing), macular staphyloma (despite only mild myopia or high hy…

Pathologygenetic structuresSus scrofaPolymerase Chain ReactionPhotoreceptor cellchemistry.chemical_compoundConsanguinityMiceChildFrameshift MutationGeneticsmedicine.diagnostic_testMagnetic Resonance ImagingSensory SystemsTissue DonorsPedigreemedicine.anatomical_structureFemaleRetinal DystrophiesTomography Optical CoherenceDilatation PathologicAdultmedicine.medical_specialtyBlotting WesternMolecular Sequence DataMutation MissenseGenes RecessiveBiologyRetinaCellular and Molecular NeuroscienceRetinal DystrophiesmedicineElectroretinographyAnimalsHumansAmino Acid SequencePhotoreceptor Connecting CiliumRetrospective StudiesRetinaRetinal pigment epitheliumDystrophyProteinsRetinalmedicine.diseaseeye diseasesOphthalmologyCiliopathyCytoskeletal Proteinschemistrysense organsElectroretinographyThe British journal of ophthalmology
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Novel alpha-galactosidase A mutation in a female with recurrent strokes.

2012

Abstract Anderson–Fabry disease (AFD) is an X-linked inborn error of glycosphingolipid catabolism resulting from the deficient activity of the lysosomal exoglycohydrolase, a-galactosidase A. The complete genomic and cDNA sequences of the human alpha-galactosidase A gene have been determined and to date, several disease-causing alpha-galactosidase A mutations have been identified, including missense mutations, small deletions/insertions, splice mutations, and large gene rearrangements We report a case of a 56-year-old woman with recurrent cryptogenic strokes. Ophthalmological examination revealed whorled opacities of the cornea (cornea verticillata) and dilated tortuous conjunctival vessels.…

Pathologymedicine.medical_specialtyHeterozygoteClinical BiochemistryMolecular Sequence DataMutation MissenseBiologymedicine.disease_causeExonRecurrencemedicineMissense mutationHumansCornea verticillataAmino Acid SequenceGeneMutationBase SequencePoint mutationGeneral MedicineSequence Analysis DNAMiddle Agedmedicine.diseaseFabry diseaseMolecular biologyAngiokeratomaPedigreeStrokealpha-GalactosidaseFabry DiseaseFemalemedicine.symptomClinical biochemistry
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Y179C, F486L and N550H are BRCA1 variants that may be associated with breast cancer in a Sicilian family: results of a 5-year GOIM (Gruppo Oncologico…

2006

Background Over 600 different pathogenic mutations have been identified in the BRCA1 gene. Nevertheless, numerous missense mutations of unknown biological function still exist. Understanding of biological significance of these mutations should help in genetic counselling to carriers and their families. Patients and methods A total of 104 patients with breast and/or ovarian cancer whose genetic counselling answered the criteria of the American Society of Clinical Oncology (ASCO 2003), were prospectively screened for mutations in all coding exons of the BRCA1 gene by automatic direct sequencing. Results During these mutational screening procedures one case presented three mutations classified…

ProbandAdultmedicine.medical_specialtyProtein ConformationGenetic counselingGenes BRCA1Mutation MissenseBreast NeoplasmsGenetic CounselingExonBreast cancermedicineMissense mutationHumansProspective StudiesGeneSicilyScreening proceduresGerm-Line MutationGynecologyGeneticsFamily HealthOvarian Neoplasmsbusiness.industryBRCA1 ProteinGenetic VariationHematologyDNA NeoplasmExonsmedicine.diseasePedigreeOncologyFemalebusinessOvarian cancerAnnals of oncology : official journal of the European Society for Medical Oncology
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No evidence of ATP1A2 involvement in 12 multiplex Italian families with benign familial infantile seizures

2005

A missense mutation in the gene encoding the alpha(2) Subunit of the Na+,K+ ATPase pump (ATP1A2) was found in a family with both familial hemiplegic migraine (FHM) and Benign Familial Infantile Seizures (BFIC). As it is still unclear whether ATP1A2 is responsible for pure BFIC syndromes, we checked mutations of the ATP1A2 gene in probands of 12 Italian multiplex families with pure BFIC, who were negative for mutations in the SCN2A gene. We screened the ATP1A2 gene by denaturing high performance liquid chromatography (D-HPLC) and direct sequencing of DNA fragments showing an aberrant elution pattern. We found one exonic variant and five intronic variants, none leading to significant amino ac…

ProbandBenign NeonatalMigraine DisordersMutation MissenseBenign familial infantile convulsionsBiologymedicine.disease_causeDenaturing high performance liquid chromatographyBenign familial infantile convulsions; Epilepsy; Familial hemiplegic migraine; Genetics; Epilepsy Benign Neonatal; Exons; Family Health; Humans; Infant; Introns; Italy; Migraine Disorders; Sodium-Potassium-Exchanging ATPase; Mutation MissenseExonATP1A2GeneticsmedicineHumansMissense mutationGeneFamilial hemiplegic migraineFamilial hemiplegic migraineFamily HealthGeneticsMutationEpilepsyGeneral NeuroscienceInfantExonsmedicine.diseaseEpilepsy Benign NeonatalIntronsItalyMutationBenign familial infantile convulsionMissenseSodium-Potassium-Exchanging ATPaseNeuroscience Letters
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Genome-wide variant calling in reanalysis of exome sequencing data uncovered a pathogenic TUBB3 variant.

2021

Almost half of all individuals affected by intellectual disability (ID) remain undiagnosed. In the Solve-RD project, exome sequencing (ES) datasets from unresolved individuals with (syndromic) ID (n = 1,472 probands) are systematically reanalyzed, starting from raw sequencing files, followed by genome-wide variant calling and new data interpretation. This strategy led to the identification of a disease-causing de novo missense variant in TUBB3 in a girl with severe developmental delay, secondary microcephaly, brain imaging abnormalities, high hypermetropia, strabismus and short stature. Interestingly, the TUBB3 variant could only be identified through reanalysis of ES data using a genome-wi…

ProbandExome sequencingAdolescentDevelopmental Disabilitieslnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Mutation MissenseComputational biologyBiologyGenomeExonAll institutes and research themes of the Radboud University Medical CenterTubulinIntellectual DisabilitySolve-RDExome SequencingGeneticsCoding regionMissense mutationHumansTUBB3GeneGenetics (clinical)Exome sequencingSequence (medicine)Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]ERN ITHACABrainMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]General MedicineGenome-wide variant callingStrabismusFaceMicrocephalyFemaleEuropean journal of medical genetics
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Additive effect of mutations in LDLR and PCSK9 genes on the phenotype of familial hypercholesterolemia.

2006

Patients homozygous or Compound heterozygous for LDLR mutations or double heterozygous for LDLR and apo B R3500Q mutation have higher LDL-C levels. more extensive xanthomatosis and more severe premature coronary disease (pCAD) than simple heterozygotes for mutations in either these genes or for missense mutations in PCSK9 gene. It is not known whether combined mutations in LDLR and PKCS9 are associated with such a severe phenotype. We sequenced Apo B and PCSK9 genes in two patients with the clinical diagnosis of homozygous FH who were heterozygous for LDLR gene mutations. Proband Z.P. (LDL-C 13.39 mmol/L and pCAD) was heterozygous for an LDLR mutation (p.E228K) inherited from her father (LD…

ProbandLDLR geneAdultMaleSettore MED/09 - Medicina InternaApolipoprotein BFamilial hypercholesterolemia (FH); Autosomal dominant hypercholesterolemia 3 (ADH3); LDLR gene; PCSK9 gene; Premature coronary artery diseasePremature coronary artery diseaseLDLR PCSK9Mutation MissenseFamilial hypercholesterolemiaCompound heterozygositymedicine.disease_causeHyperlipoproteinemia Type IIFamilial hypercholesterolemia (FH) Autosomal dominant hypercholesterolemia 3 (ADH3) LDLR gene PCSK9 gene Premature coronary artery diseaseFamilial hypercholesterolemia (FH)medicineMissense mutationHumansCells CulturedGeneticsMutationbiologybusiness.industrySerine EndopeptidasesHeterozygote advantageMiddle Agedmedicine.diseaseAutosomal dominant hypercholesterolemia 3 (ADH3)PedigreePhenotypeSettore MED/03 - Genetica MedicaAmino Acid SubstitutionReceptors LDLPCSK9 geneLDL receptorbiology.proteinlipids (amino acids peptides and proteins)FemaleProprotein ConvertasesProprotein Convertase 9Cardiology and Cardiovascular MedicinebusinessAtherosclerosis
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BBS1 Mutations in a Wide Spectrum of Phenotypes Ranging From Nonsyndromic Retinitis Pigmentosa to Bardet-Biedl Syndrome

2012

OBJECTIVE: To investigate the involvement of the Bardet-Biedl syndrome (BBS) gene BBS1 p.M390R variant in nonsyndromic autosomal recessive retinitis pigmentosa (RP). METHODS: Homozygosity mapping of a patient with isolated RP was followed by BBS1 sequence analysis. We performed restriction fragment length polymorphism analysis of the p.M390R allele in 2007 patients with isolated RP or autosomal recessive RP and in 1824 ethnically matched controls. Patients with 2 BBS1 variants underwent extensive clinical and ophthalmologic assessment. RESULTS: In an RP proband who did not fulfill the clinical criteria for BBS, we identified a large homozygous region encompassing the BBS1 gene, which carrie…

ProbandMaleBBS1Genetics and epigenetic pathways of disease [NCMLS 6]DNA Mutational AnalysisEvaluation of complex medical interventions Genomic disorders and inherited multi-system disorders [NCEBP 2]GenotypeEthnicityPrevalenceIsraelGeneticseducation.field_of_studyRetinitis Pigmentosa/diagnosisMiddle AgedDisease gene identificationPedigreeEuropePhenotypeFemaleMicrotubule-Associated ProteinsRetinitis PigmentosaAdultcongenital hereditary and neonatal diseases and abnormalitiesCanadaPopulationCanada/epidemiologyMicroscopy AcousticMutation MissenseEthnic GroupsDNA/geneticsBiologyEurope/epidemiologyGenomic disorders and inherited multi-system disorders [IGMD 3]Bardet-Biedl Syndrome/diagnosisBardet–Biedl syndromeRetinitis pigmentosamedicineElectroretinographyHumansAlleleeducationBardet-Biedl SyndromeIsrael/epidemiologyAllelesDNAMicrotubule-Associated Proteins/geneticsmedicine.diseaseOphthalmoscopyOphthalmologyGenetics and epigenetic pathways of disease Genomic disorders and inherited multi-system disorders [NCMLS 6]
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ATP1A2 mutations in 11 families with familial hemiplegic migraine.

2005

Abstract Familial hemiplegic migraine (FHM) is an autosomal dominant form of migraine with aura. The disease is caused by mutations of at least three genes among which two have been identified, CACNA1A and ATP1A2. Very few mutations have been identified so far in ATP1A2. We screened the coding sequence of ATP1A2 in 26 unrelated FHM probands in whom CACNA1A screening was negative. A total of eight different mutations were identified in 11 of the probands (41%), including six missense mutations, one small deletion leading to a frameshift, and one in frame deletion. All were novel mutations. Two mutations were recurrent, in three and two families, respectively. Genotyping of 94 relatives of th…

ProbandMaleMigraine with AuraMolecular Sequence DataMutation MissenseBiologymedicine.disease_causeFrameshift mutationATP1A2GeneticsmedicineMissense mutationAnimalsHumansAmino Acid SequenceGenotypingGenetics (clinical)Familial hemiplegic migraineGeneticsFamily HealthMutationPolymorphism GeneticSequence Homology Amino AcidExonsmedicine.diseaseMigraine with auraPedigreeMutationFemalemedicine.symptomSodium-Potassium-Exchanging ATPase
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