Search results for "MUTATION"

showing 10 items of 2830 documents

Point mutations associated with Leber hereditary optic neuropathy in a Latvian population

2013

Purpose To study mutations associated with Leber hereditary optic neuropathy (LHON) in patients suspected of having this mitochondrial disorder in a Latvian population. Additional aims were to determine the heteroplasmy status of all non-synonymous polymorphisms identified in the current study and to identify the mitochondrial haplogroups of the studied participants because these factors may contribute to the manifestation of LHON. Methods Twelve patients, including patients in two families, were enrolled in the current study. LHON was suspected based on the findings of ophthalmologic examinations. In clinically affected individuals, the presence of all previously reported LHON-associated m…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesPolymorphism Geneticgenetic structuresnutritional and metabolic diseasesOptic Atrophy Hereditary LeberSequence Analysis DNAMiddle AgedDNA MitochondrialLatviaeye diseasesWhite PeopleMitochondriaPedigreeHaplotypesHumansPoint MutationFemaleResearch Article
researchProduct

One

2019

Neurofibromatosis type 1 (NF1) is an autosomal dominant disease with complete penetrance but high variable expressivity. NF1 is caused by loss-of-function mutations in the NF1 gene, a negative regulator of the RAS-MAPK pathway. The NF1 gene has one of the highest mutation rates in human disorders, which may explain the outbreak of independent de novo variants in the same family. Here, we report the co-occurrence of pathogenic variants in the NF1 and SPRED1 genes in six families with NF1 and Legius syndrome, using next-generation sequencing. In five of these families, we observed the co-occurrence of two independent NF1 variants. All NF1 variants were classified as pathogenic, according to t…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesSPRED1Neurofibromatosis 1Neurofibromin 1AdolescentCafe-au-Lait Spotsneurofibromatosis type 1eye diseasesArticlenervous system diseasesPedigreeLegius syndromePhenotypeNF1MutationHumansFemalede novo variantChildneoplasmsAdaptor Proteins Signal TransducingGenes
researchProduct

Subclinical hyperthyroidism due to a thyrotropin receptor (TSHR) gene mutation (S505R).

2006

Aim: To identify the molecular defect by which non-autoimmune subclinical hyperthyroidism was caused in a 6-mo-old infant who presented with weight loss. Methods: Congenital non-autoimmune hyperthyroidism is caused by activating germline mutations in the thyrotropin receptor (TSHR) gene. Therefore, the TSHR gene was sequenced directly from the patient's genomic DNA. Results: Molecular analysis revealed a heterozygous point mutation (S505R) in the TSHR gene as the underlying defect. Conclusion: A constitutively activating mutation in the TSHR gene has to be considered not only in patients with severe congenital non-autoimmune hyperthyroidism, but also in children with subclinical non-autoimm…

AdultMaleendocrine systemmedicine.medical_specialtyendocrine system diseasesAsymptomaticHyperthyroidismThyrotropin receptorTSHR Gene MutationGermline mutationInternal medicineMedicineMissense mutationHumansPoint MutationGeneSubclinical infectionbusiness.industryPoint mutationInfantReceptors ThyrotropinGeneral Medicineeye diseasesPedigreeEndocrinologyPediatrics Perinatology and Child HealthCancer researchFemalemedicine.symptombusinesshormones hormone substitutes and hormone antagonistsActa paediatrica (Oslo, Norway : 1992)
researchProduct

Congenital goitrous primary hypothyroidism in two German families caused by novel thyroid peroxidase (TPO) gene mutations.

2013

Congenital hypothyroidism occurs with a prevalence of approximately 1:3 500. Defects in thyroid hormone synthesis which lead to goitrous hypothyroidism account for 10-15% of these cases. Several genetic defects have been characterized and mutations in the thyroid peroxidase (TPO) gene are the most common cause for dyshormonogenesis.So far, more than 80 mutations in the TPO gene have been described, resulting in a variable decrease in TPO bioactivity. Clinically TPO defects manifest with congenital primary goitrous hypothyroidism.We here present 2 children with congenital primary hypothyroidism, who were identified to have compound heterozygous TPO mutations. They both shared the same novel …

AdultMaleendocrine systemmedicine.medical_specialtyendocrine system diseasesEndocrinology Diabetes and MetabolismMutation MissenseGene mutationmedicine.disease_causeCompound heterozygosityAutoantigensIodide Peroxidasefluids and secretionsEndocrinologyThyroid dyshormonogenesisThyroid peroxidaseInternal medicineGermanyIron-Binding ProteinsInternal MedicinemedicineCongenital HypothyroidismMissense mutationHumansFamilyMutationbiologybusiness.industryGoiterPrimary hypothyroidismInfant Newbornfood and beveragesGeneral MedicineExonsmedicine.diseaseCongenital hypothyroidismEndocrinologyembryonic structuresbiology.proteinFemalebusinessExperimental and clinical endocrinologydiabetes : official journal, German Society of Endocrinology [and] German Diabetes Association
researchProduct

Ten novel mutations found in Aniridia.

1998

Aniridia (AN) is a sight-threatening congenital ocular disorder characterized by iris hypoplasia, corneal pannus, foveal and optic nerve hypoplasia, cataract formation, and glaucoma. In two-thirds of the patients, AN is inherited in an autosomal dominant fashion with almost complete penetrance but variable expression. The remaining cases are sporadic. Aniridia has been shown to be associated with mutations in the PAX6 gene, located on chromosome 11p13, telomeric to the Wilms' tumor predisposition gene (WT1). This paper describes 14 mutations in the PAX6 gene in patients with AN. Among these 14 mutations, 10 have been unpublished until now. They result most probably in haploinsufficiency and…

AdultMalegenetic structuresAdolescentPAX6 Transcription FactorDNA Mutational AnalysisMolecular Sequence DataBiologyPolymerase Chain ReactionVariable ExpressionGeneticsmedicineHumansPaired Box Transcription FactorsAmino Acid SequenceChildEye ProteinsGeneAniridiaGenetics (clinical)Polymorphism Single-Stranded ConformationalGeneticsHomeodomain ProteinsOptic nerve hypoplasiaInfantMiddle Agedmedicine.diseasePenetranceeye diseasesDNA-Binding ProteinsRepressor ProteinsAniridiaChild PreschoolMutationHomeoboxFemalesense organsPAX6HaploinsufficiencyTranscription FactorsHuman mutation
researchProduct

PTCH-1 and MDM2 expression in ameloblastoma from a West African sub-population: implication for chemotherapeutics

2015

INTRODUCTION: ameloblastoma is a slow growing, painless odontogenic swelling which can attain sizes that result in severe deformities of the craniofacial complex. It is the most commonly encountered odontogenic tumor in Nigeria. Surgical intervention is currently the method of treatment; however identification of altered molecular pathways may inform chemotherapeutic potential. The Protein Patched homolog 1 (PTCH-1) is overexpressed in ameloblastoma. Also, mutation in the MDM2 gene can reduce the tumor suppressor function of p53 and promote ameloblastoma growth. No study however has characterized the molecular profile of African cases of ameloblastoma with a view to developing chemotherapeu…

AdultMalemdm2Pathologymedicine.medical_specialtyPopulationNigeriaPathology and Forensic MedicinePTCH-1 MdM2 ameloblastoma chemotherapeuticsameloblastomaptch-1HumansMedicineRadiology Nuclear Medicine and imagingDentistry (miscellaneous)ddc:610educationAmeloblastomaStellate reticulumProtein Patched Homolog 1education.field_of_studylcsh:R5-920biologybusiness.industryResearchlcsh:Public aspects of medicinechemotherapeuticsOdontogenic tumorProto-Oncogene Proteins c-mdm2lcsh:RA1-1270General Medicinemedicine.diseaseJaw NeoplasmsGene Expression Regulation NeoplasticPatched-1 ReceptorWest africanstomatognathic diseasesMutationMonoclonalCancer researchbiology.proteinMdm2FemaleSurgeryOral SurgeryAntibodybusinesslcsh:Medicine (General)The Pan African Medical Journal
researchProduct

Association between the MHC class I gene HFE polymorphisms and longevity: a study in Sicilian population.

2001

Classes I and II human leukocyte antigens (HLA) genes encode highly polymorphic heterodimeric glycoproteins involved in the control of immune responses. The HLA class I gene HFE seemingly no longer participates in immunity because it has lost its ability to bind peptides and it has acquired the ability to form complex with the receptor for iron-binding transferrin by regulating iron uptake by intestinal cells. Thus, it indirectly regulates immune responses too, because iron availability plays a role in specific and non-specific immune responses. The distribution of HFE polymorphisms in Sicilian centenarians and nonagenarians was studied to evaluate if HFE alleles might be represented differ…

AdultMalemedia_common.quotation_subjectImmunologyPopulationLongevityGenes MHC Class IHuman leukocyte antigenBiologyCompound heterozygositymedicine.disease_causeGene FrequencyHLA AntigensGeneticsmedicineHumansAlleleeducationHemochromatosis ProteinAllele frequencySicilyGenetics (clinical)Allelesmedia_commonAgedGeneticsAged 80 and overeducation.field_of_studyMutationPolymorphism GeneticHaplotypeHistocompatibility Antigens Class ILongevityMembrane ProteinsMiddle AgedHaplotypesFemaleGenes and immunity
researchProduct

Treatment of Fabry's Disease With Migalastat: Outcome From a Prospective Observational Multicenter Study (FAMOUS).

2019

Fabry's disease (FD) is an X-linked lysosomal storage disorder caused by the deficient activity of the lysosomal enzyme alpha-galactosidase A (alpha-Gal A) leading to intracellular accumulation of globotriaosylceramide (Gb3). Patients with amenable mutations can be treated with migalastat, a recently approved oral pharmacologic chaperone to increase endogenous alpha-Gal A activity. We assessed safety along with cardiovascular, renal, and patient-reported outcomes and disease biomarkers in a prospective observational multicenter study after 12 months of migalastat treatment under real-world conditions. Fifty-nine (28 females) patients (34 (57.6%) pretreated with enzyme replacement therapy) w…

AdultMalemedicine.medical_specialty1-DeoxynojirimycinTime FactorsGlobotriaosylceramideRenal function030226 pharmacology & pharmacyGastroenterologyVentricular Function Left03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineMigalastatGermanymedicineClinical endpointHumansPharmacology (medical)Genetic Predisposition to DiseaseProspective StudiesPharmacologySphingolipidsVentricular Remodelingbusiness.industryEnzyme replacement therapyMiddle Agedmedicine.diseaseFabry's diseaseFabry diseaseBlood pressureTreatment Outcomechemistry030220 oncology & carcinogenesisalpha-GalactosidaseMutationFabry DiseaseFemaleGlycolipidsbusinessBiomarkersGlomerular Filtration RateClinical pharmacology and therapeutics
researchProduct

Clinical outcome of HBeAg-negative chronic hepatitis B in relation to virological response to lamivudine.

2004

The effect of lamivudine treatment on the outcome of patients with hepatitis B e antigen (HBeAg)-negative chronic hepatitis is unclear. In a retrospective multicenter study, we have analyzed the virological events observed during lamivudine therapy in patients with HBeAg-negative chronic hepatitis and evaluated the correlation between virological response and clinical outcomes. Among 656 patients (mean age 49.1 years) included in the database, 54% had chronic hepatitis, 30% had Child-Turcotte-Pugh (CTP) A cirrhosis, and 16% had CTP B/C cirrhosis. On therapy (median 22 months, range 1–66), a virological response was obtained in 616 patients (93.9%). The rate of maintained virological respons…

AdultMalemedicine.medical_specialtyANTIVIRAL TREATMENTHepatitis B virusCirrhosisCarcinoma Hepatocellularmedicine.medical_treatmentEpatite cronica da Virus B trattamento antiviraleLAMIVUDINE; ANTIVIRAL TREATMENT; CHRONIC HEPATITIS B; TREATMENT RESISTANCECHRONIC HEPATITIS BLiver transplantationGastroenterologyLiver diseaseHepatitis B ChronicInternal medicineMedicineHumansHepatitis B e AntigensAgedRetrospective StudiesHepatologybusiness.industryIncidenceLiver NeoplasmsTREATMENT RESISTANCELamivudineHepatologyMiddle Agedmedicine.diseaseSurgeryLiver TransplantationSurvival RateTreatment OutcomeHBeAgLamivudineHepatocellular carcinomaMultivariate AnalysisMutationReverse Transcriptase InhibitorsFemalebusinessViral loadmedicine.drugHepatology (Baltimore, Md.)
researchProduct

Influence of CYP3A5 and ABCB1 gene polymorphisms and other factors on tacrolimus dosing in Caucasian liver and kidney transplant patients

2011

Tacrolimus is a substrate of cytochrome P4503A (CYP3A) enzymes as well as of the drug transporter ABCB1. We have investigated the possible influence of CYP3A5 and ABCB1 single nucleotide polymorphisms (SNPs) and other factors (e.g. albumin, hematocrit and steroids) on tacrolimus blood levels achieved in a population of Caucasian liver (n=51) and kidney (n=50) transplant recipients. At 1, 3 and 6 months after transplantation, tacrolimus doses (mg/kg/day) and trough blood levels (C0) were recorded and the weight-adjusted tacrolimus dosage (mg/kg/day) was calculated. Polymerase chain reaction followed by restriction fragment length polymorphism analysis was used for genotyping CYP3A5*1 and *3 …

AdultMalemedicine.medical_specialtyATP Binding Cassette Transporter Subfamily BGenotypemedicine.medical_treatmentDNA Mutational AnalysisPopulationSingle-nucleotide polymorphismLiver transplantationBiologyKidneyPolymorphism Single NucleotideGastroenterologyBiomarkers PharmacologicalTacrolimusWhite PeopleGene FrequencyInternal medicineGeneticsmedicineCytochrome P-450 CYP3AHumansDrug Dosage CalculationsATP Binding Cassette Transporter Subfamily B Member 1educationAllele frequencyAllelesKidney transplantationAgededucation.field_of_studyKidney metabolismGeneral MedicineMiddle Agedmedicine.diseaseKidney TransplantationTacrolimusLiver TransplantationTransplantationsurgical procedures operativeItalyLiverImmunologySettore BIO/14 - FarmacologiaPharmacogenetics CYP3A5 ABCB1 TacrolimusTransplant patientsFemaleImmunosuppressive AgentsPolymorphism Restriction Fragment LengthInternational Journal of Molecular Medicine
researchProduct