Search results for "Pedigree"

showing 10 items of 313 documents

Mutations in the Cone Photoreceptor G-Protein α-Subunit Gene GNAT2 in Patients with Achromatopsia

2002

Achromatopsia is an autosomal recessively inherited visual disorder that is present from birth and that features the absence of color discrimination. We here report the identification of five independent families with achromatopsia that segregate protein-truncation mutations in the GNAT2 gene, located on chromosome 1p13. GNAT2 encodes the cone photoreceptor-specific alpha-subunit of transducin, a G-protein of the phototransduction cascade, which couples to the visual pigment(s). Our results demonstrate that GNAT2 is the third gene implicated in achromatopsia.

Achromatopsiagenetic structuresMolecular Sequence DataColor Vision DefectsBiologymedicine.disease_causeRetinal Cone Photoreceptor CellsReportGNAT2 geneGeneticsmedicineHumansGenetics(clinical)TransducinGeneGenetics (clinical)GeneticsGNAT2Mutationmedicine.diseaseRod monocromacyeye diseasesPedigreeColor Vision DefectsMutationRetinal Cone Photoreceptor CellsAchromatopsiaTransducinsense organsVisual phototransductionThe American Journal of Human Genetics
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Congenital primary hypothyroidism with subsequent adenomatous goiter in a Turkish patient caused by a homozygous 10-bp deletion in the thyroid peroxi…

2006

Summary Objective  Congenital primary hypothyroidism occurs in 1 of 4000 births. Whereas the majority of the cases are due to developmental defects of the thyroid gland, 20% carry a defect in thyroid hormonogenesis. We report a Turkish boy who had goitrous hypothyroidism due to a mutation in the thyroid peroxidase (TPO) gene. Design  The TPO gene was sequenced directly from genomic DNA and cDNA which was transcribed from three RNA samples harvested from different parts of the patient's excised thyroid gland. Patient  The boy was thyroidectomized because of continuing growth of his thyroid gland and development of multiple nodes suspected of malignancy by ultrasound examination. Histopatholo…

AdenomaMaleThyroid Hormonesendocrine systemmedicine.medical_specialtyPathologyGoiterAdolescentTurkeyendocrine system diseasesEndocrinology Diabetes and Metabolismmedicine.medical_treatmentThyroid Function TestsBiologyIodide PeroxidaseThyroid function testsFrameshift mutationConsanguinityEndocrinologyThyroid peroxidaseInternal medicineCongenital HypothyroidismmedicineHumansIntracellular partmedicine.diagnostic_testHomozygoteThyroidThyroidectomyPrimary hypothyroidismmedicine.diseasePedigreeThyroxinemedicine.anatomical_structureEndocrinologyThyroidectomybiology.proteinGene DeletionGoiter NodularClinical Endocrinology
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Exome Sequencing Reveals VCP Mutations as a Cause of Familial ALS

2010

Summary Using exome sequencing, we identified a p.R191Q amino acid change in the valosin-containing protein ( VCP ) gene in an Italian family with autosomal dominantly inherited amyotrophic lateral sclerosis (ALS). Mutations in VCP have previously been identified in families with Inclusion Body Myopathy, Paget disease, and Frontotemporal Dementia (IBMPFD). Screening of VCP in a cohort of 210 familial ALS cases and 78 autopsy-proven ALS cases identified four additional mutations including a p.R155H mutation in a pathologically proven case of ALS. VCP protein is essential for maturation of ubiquitin-containing autophagosomes, and mutant VCP toxicity is partially mediated through its effect on…

Adenosine TriphosphataseMaleCell Cycle ProteinsUBQLN2Cohort Studies0302 clinical medicineReference ValuesValosin Containing ProteinCell Cycle ProteinReference ValueAmyotrophic lateral sclerosisExome sequencingAdenosine TriphosphatasesGenetics0303 health sciencesGeneral NeuroscienceExonsMiddle AgedPedigree3. Good healthMultisystem proteinopathyFemaleSettore MED/26 - NeurologiaCase-Control StudieChromosomes Human Pair 9HumanFrontotemporal dementiaNeuroscience(all)Valosin-containing proteinExonBiologyProtein degradationTARDBPArticle03 medical and health sciencesmedicineHumansAged030304 developmental biologyAmyotrophic lateral sclerosis familial ALS exome sequencingNeuroscience (all)business.industryAmyotrophic Lateral Sclerosismedicine.diseaseAmino Acid SubstitutionCase-Control StudiesMutationbiology.proteinCohort Studiebusiness030217 neurology & neurosurgeryAmyotrophic Lateral SclerosiNeuron
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A recurrent TP63 mutation causing EEC3 and Rapp–Hodgkin syndromes

2016

The ectrodactyly, ectodermal dysplasia, and cleft lip/palate syndrome 3 (EEC3; OMIM #604292), the Rapp-Hodgkin syndrome (RHS), and various other syndromes are caused by mutations in the TP63 gene, which encodes a p53-like transcription factor. Here, we report on a woman aged 37 years and her daughter aged 3 years with the previously reported c.1028G>A (p.Arg343Gln) mutation in exon 8 of TP63. The mother lacked ectrodactyly, indicating a diagnosis of RHS, whereas the girl presented with all three major features (ectrodactyly, ectodermal dysplasia, clefting) and different minor features (including small and brittle nails, and recurrent conjunctivitis believed to be because of stenotic and blo…

Adult0301 basic medicineHeterozygoteEctodermal dysplasiamedicine.medical_specialtyEctrodactylyFoot Deformities CongenitalCleft Lipmedia_common.quotation_subjectmedicine.disease_causePathology and Forensic MedicineFingers030207 dermatology & venereal diseases03 medical and health sciencesExon0302 clinical medicineEctodermal DysplasiaTP63medicineHumansAlleleAllelesGenetics (clinical)media_commonDaughterMutationbusiness.industryTumor Suppressor ProteinsFaciesExonsGeneral Medicinemedicine.diseaseDermatologyPenetrancePedigreeCleft PalatePhenotype030104 developmental biologyAmino Acid SubstitutionChild PreschoolMutationPediatrics Perinatology and Child HealthFemaleAnatomybusinessHand Deformities CongenitalTranscription FactorsClinical Dysmorphology
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Development of primary early-onset colorectal cancers due to biallelic mutations of the FANCD1/BRCA2 gene

2013

International audience; Fanconi anaemia (FA) is characterized by progressive bone marrow failure, congenital anomalies, and predisposition to malignancy. In a minority of cases, FA results from biallelic FANCD1/BRCA2 mutations that are associated with early-onset leukaemia and solid tumours. Here, we describe the clinical and molecular features of a remarkable family presenting with multiple primary colorectal cancers (CRCs) without detectable mutations in genes involved in the Mendelian predisposition to CRCs. We unexpectedly identified, despite the absence of clinical cardinal features of FA, a biallelic mutation of the FANCD1/BRCA2 corresponding to a frameshift alteration (c.1845_1846del…

AdultBiallelic MutationRNA Splicing[SDV]Life Sciences [q-bio]DNA Mutational AnalysisBiologymedicine.disease_causeArticleFrameshift mutationGeneticsmedicineHumansMissense mutationAge of OnsetGeneAllelesGenetics (clinical)BRCA2 ProteinGeneticsMutationPoint mutationComputational BiologyChromosome BreakageBRCA2 ProteinPedigree3. Good healthAmino Acid SubstitutionMutationFemaleRNA Splice SitesChromosome breakageColorectal NeoplasmsEuropean Journal of Human Genetics
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Aceruloplasminaemia: a family with a novel mutation and long-term therapy with deferasirox.

2014

Ceruloplasmin is a member of the multicopper oxidase family that plays a major role in the transport of iron in the body. Aceruloplasminaemia (ACP) is a rare disease and is clinically identified by iron overload in liver, pancreas, brain, and other organs, and by microcytic anaemia. So far, the iron chelator deferasirox was given for therapy only up to 6 months due to side effects. Here, we describe a novel mutation leading to ACP and report for the first time a long-term therapy, that is, 2 years with deferasirox. ACP was diagnosed in 3 siblings using clinical and biochemical characteristics, HFE and ceruloplasmin mutational analysis, liver biopsy, brain-, liver-, and heart-MRI. For iron d…

AdultBlood GlucoseMalemedicine.medical_specialtyEndocrinology Diabetes and MetabolismIronClinical BiochemistryCarbohydrate metabolismBiochemistryBenzoatesEndocrinologyInsulin resistanceHepcidinInternal medicineGermanyMedicineHumansChelating Agentsbiologymedicine.diagnostic_testbusiness.industryBiochemistry (medical)DeferasiroxCeruloplasminNeurodegenerative DiseasesGeneral MedicineTriazolesmedicine.diseaseIron Metabolism DisordersMagnetic Resonance ImagingPedigreeDeferasiroxEndocrinologymedicine.anatomical_structureTreatment OutcomeLiverLiver biopsyMutationbiology.proteinFemaleChromosomes Human Pair 3businessCeruloplasminPancreasmedicine.drugRare diseaseHormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme
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Retinoblastoma epidemiology: Does the evidence matter?

2007

It has been proposed that retinoblastoma is 'caused' by two sequential mutations affecting the RB1 gene, but this is a rather outdated view of cancer aetiology that does not take into account a large amount of new acquisitions such as chromosomal and epigenetic alterations. Retinoblastoma remains probably the only cancer in which the rather simplistic 'two hit' mutational model is still considered of value, although cancer is known to be associated with genomic and microsatellite instability, defects of the DNA mismatch repair system, alterations of DNA methylation and hystone acethylation/deacethylation, and aneuploidy. Moreover, as it is shown herein, the predictions made by the 'two hit'…

AdultCancer ResearchAdolescentRetinal NeoplasmsRetinoblastoma Aneuploidy Two hit theoryDiseaseBiologyAge DistributionChromosome instabilitymedicineHumansEpigeneticsAge of OnsetChildGerm-Line MutationGeneticsRetinoblastomaRetinoblastomaMicrosatellite instabilityCancerInfantMiddle Agedmedicine.diseasePedigreeSettore BIO/18 - GeneticaOncologyChild PreschoolDNA methylationDNA mismatch repair
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X-Linked Dilated Cardiomyopathy.

1995

We report on a family with a severe form of X-linked dilated cardiomyopathy (DCM). Two brothers, the elder requiring heart transplantation, and a maternal cousin presented elevated creatine kinase levels, increased right ventricular diameters and electrocardiographic abnormalities. All complained of exertional cramping myalgia, but none had muscle weakness or a pathological electromyogram. Muscle biopsies of these individuals revealed a mild myopathic picture with atrophic type I and hypertrophic type II fibers. Immunofluorescence using N- and C-terminal antibodies (dys-2, dys-3) against the dystrophin protein showed preserved, but reduced intensity of staining of the sarcolemmal membranes.…

AdultCardiomyopathy DilatedGenetic MarkersMaleX ChromosomeGenetic LinkageBiopsyMyosinsImmunofluorescencePolymerase Chain ReactionGeneral Biochemistry Genetics and Molecular BiologyDystrophinExonHistory and Philosophy of ScienceWestern blotmedicineHumansRNA MessengerMuscle SkeletalDNA PrimersSequence DeletionSouthern blotRecombination Geneticbiologymedicine.diagnostic_testMyocardiumGeneral NeuroscienceChromosome MappingDilated cardiomyopathyExonsmusculoskeletal systemmedicine.diseaseMolecular biologyPedigreeAlternative Splicingbiology.proteinFemaleCreatine kinaseLod ScoreAntibodyDystrophinAnnals of the New York Academy of Sciences
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A mutation in myotilin causes spheroid body myopathy

2005

Background: Spheroid body myopathy (SBM) is a rare, autosomal dominant, neuromuscular disorder, which has only been previously reported in a single large kindred. Identification of the mutated gene in this disorder may provide insight regarding abnormal neuromuscular function. Methods: The authors completed a detailed clinical evaluation on an extensive kindred diagnosed with SBM. Genome-wide linkage analysis was performed to localize the disease gene to a specific chromosomal region. Further marker genotyping and screening of a positional, functional candidate gene were completed to detect the disease-causing mutation. Pathologic analysis of muscle biopsy was performed on three individuals…

AdultGenetic MarkersMaleCandidate genePathologymedicine.medical_specialtyDNA Mutational AnalysisMuscle ProteinsChromosome DisordersBiologyExonMuscular DiseasesmedicineHumansPoint MutationMyotilinConnectinGenetic Predisposition to DiseaseGenetic TestingMuscular dystrophyMuscle SkeletalMyopathyAgedGenes DominantAged 80 and overInclusion BodiesGeneticsMuscle biopsymedicine.diagnostic_testMicrofilament ProteinsChromosome MappingExonsMiddle Agedmedicine.diseasePedigreeCytoskeletal ProteinsMutationChromosomal regionbiology.proteinChromosomes Human Pair 5FemaleTitinNeurology (clinical)medicine.symptomNeurology
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Restless legs syndrome: Epidemiological and clinicogenetic study in a South Tyrolean population isolate.

2006

Genetic contributions to restless legs syndrome (RLS) have been consistently recognized from population and family studies. To determine the clinical and genetic features of RLS in a population isolate and explore linkage to three previously described susceptibility loci on chromosomes 12q, 14q, and 9p, respectively, an isolated population in the South Tyrolean Alps was identified and 530 adults participated in the study. Using a two-step strategy, 47 patients with idiopathic RLS were ascertained. The prevalence in the population was 8.9%. Twenty-eight patients (59.6%) had at least one affected first-degree relative and were classified as hereditary cases. In a single extended pedigree, lin…

AdultGenetic MarkersMalemedicine.medical_specialtyPopulationFamily studiesLocus heterogeneityGermanyRestless Legs SyndromeSurveys and Questionnairesmental disordersEpidemiologymedicineHumansRestless legs syndromeeducationLinkage (software)Geneticseducation.field_of_studyPolymorphism Geneticbusiness.industryChromosome MappingReproducibility of Resultsmedicine.diseaseSurgeryPedigreeNeurologyItalyHomogeneousSusceptibility locusFemaleNeurology (clinical)business
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