Search results for "MUTATION"

showing 10 items of 2830 documents

Role of Colchicine Treatment in Tumor Necrosis Factor Receptor Associated Periodic Syndrome (TRAPS): Real-Life Data from the AIDA Network

2020

Objective. To analyze the potential role of colchicine monotherapy in patients with tumor necrosis factor receptor associated periodic syndrome (TRAPS) in terms of control of clinical and laboratory manifestations. Methods. Patients with TRAPS treated with colchicine monotherapy were retrospectively enrolled; demographic, clinical and therapeutic data were collected and statistically analysed after having clustered patients according to different times at disease onset, penetrance of mutations, dosage of colchicine, and different disease manifestations. Results. 24 patients (14 males; 15 with pediatric disease onset) treated with colchicine monotherapy were enrolled. Colchicine resulted in …

Male0301 basic medicineEye DiseasesTRAPSColchicineAIDA NetworkGene mutationGastroenterologyReceptors Tumor Necrosis Factorchemistry.chemical_compoundSettore MED/38 - Pediatria Generale E Specialistica0302 clinical medicineReceptorsPathologyRB1-214ColchicineAge of OnsetYoung adultChildAmyloidosisAmyloidosisSyndromeMiddle AgedColchicine tumor necrosis factor TRAPSInflamacióPenetrancePhenotypeChild PreschoolFemaleJoint DiseasesResearch ArticleAdultRiskmedicine.medical_specialtyAdolescentFeverArticle SubjectImmunologyAdolescent; Adult; Age of Onset; Amyloidosis; Child; Child Preschool; Colchicine; Exanthema; Eye Diseases; Female; Fever; Humans; Joint Diseases; Male; Middle Aged; Mutation; Myalgia; Phenotype; Receptors Tumor Necrosis Factor; Retrospective Studies; Risk; Syndrome; Young AdultLower riskYoung Adult03 medical and health sciencesInternal medicinemedicineHumansPreschoolRetrospective StudiesInflammation030203 arthritis & rheumatologybusiness.industryTRAPSRetrospective cohort studyMyalgiaCell BiologyExanthemamedicine.disease030104 developmental biologychemistryMutationAge of onsetColchicineTumor Necrosis FactorbusinessMediators of Inflammation
researchProduct

KCND3 potassium channel gene variant confers susceptibility to electrocardiographic early repolarization pattern

2019

BACKGROUND: The presence of an early repolarization pattern (ERP) on the surface ECG is associated with risk of ventricular fibrillation and sudden cardiac death. Family studies have shown that ERP is a highly heritable trait, but molecular genetic determinants are unknown. METHODS: To identify genetic susceptibility loci for ERP, we performed a GWAS and meta-analysis in 2,181 cases and 23,641 controls of European ancestry. RESULTS: We identified a genome-wide significant (P < 5 × 10(–8)) locus in the potassium voltage-gated channel subfamily D member 3 (KCND3) gene that was successfully replicated in additional 1,124 cases and 12,510 controls. A subsequent joint meta-analysis of the discov…

Male0301 basic medicineGenotypeHeart VentriclesGenome-wide association studyLocus (genetics)BiologyPolymorphism Single NucleotideWhite PeopleSudden cardiac deathElectrocardiography03 medical and health sciences0302 clinical medicineGenetic variationmedicineGenetic predispositionHumansSNPGWASGenetic Predisposition to DiseaseJ-POINT ELEVATIONS422LAlleleGENOME-WIDE ASSOCIATIONGeneMUTATIONAllelesMETAANALYSISGeneticsGeneral Medicinemedicine.diseaseddc:Death Sudden CardiacShal Potassium Channels030104 developmental biologyGenetic Loci030220 oncology & carcinogenesisVentricular FibrillationCORONARY-ARTERY-DISEASEFemaleVENTRICULAR-FIBRILLATIONClinical MedicineTranscriptomeGenome-Wide Association Study
researchProduct

Male breast cancer in BRCA1 and BRCA2 mutation carriers: pathology data from the Consortium of Investigators of Modifiers of BRCA1/2

2016

Background BRCA1 and, more commonly, BRCA2 mutations are associated with increased risk of male breast cancer (MBC). However, only a paucity of data exists on the pathology of breast cancers (BCs) in men with BRCA1/2 mutations. Using the largest available dataset, we determined whether MBCs arising in BRCA1/2 mutation carriers display specific pathologic features and whether these features differ from those of BRCA1/2 female BCs (FBCs). Methods We characterised the pathologic features of 419 BRCA1/2 MBCs and, using logistic regression analysis, contrasted those with data from 9675 BRCA1/2 FBCs and with population-based data from 6351 MBCs in the Surveillance, Epidemiology, and End Results (…

Male0301 basic medicineGenotype-phenotype correlationPathologygenotype-phenotype correlationsendocrine system diseasesSettore MED/06 - Oncologia MedicaFEATURESmale breast cancerGenotype-phenotype correlationsLogistic regressionHistologic grade610 Medical sciences MedicineBreast cancer0302 clinical medicineEpidemiologyMedicine and Health SciencesPathologypolycyclic compoundsskin and connective tissue diseasesPOPULATIONRISKeducation.field_of_studyBRCA1 ProteinMenSingle NucleotideMiddle Aged3. Good healthGRADE030220 oncology & carcinogenesisMale breast canceroncologyFemaleBreast NeoplasmResearch ArticleHumanAdultmedicine.medical_specialtyCARCINOMAGenotype–phenotype correlations3122 CancersPopulation610Breast NeoplasmsBRCA1/2; genotype-phenotype correlations; histologic grade; male breast cancer; pathology; cancer research; oncologyMale breast cancer BRCA1 BRCA2Polymorphism Single NucleotideCàncer de mamaBreast Neoplasms Male03 medical and health sciencesBreast cancerSDG 3 - Good Health and Well-beingBRCA1/2Journal ArticleCarcinomamedicineHumansGenetic Predisposition to DiseasePolymorphismeducationAgedNeoplasm StagingBRCA2 Proteinbusiness.industryOdds ratiohistologic grademedicine.diseaseConfidence intervalMale breast cancer030104 developmental biologyddc:161HomesMutationcancer researchpathologyBRCA1/2; Genotype-phenotype correlations; Histologic grade; Male breast cancer; Pathology; Adult; Aged; BRCA1 Protein; BRCA2 Protein; Breast Neoplasms; Breast Neoplasms Male; Female; Genetic Predisposition to Disease; Humans; Male; Middle Aged; Mutation; Neoplasm Staging; Polymorphism Single Nucleotide; Oncology; Cancer Researchbusiness
researchProduct

Early-infantile onset epilepsy and developmental delay caused by bi-allelic GAD1 variants

2020

Mice lacking GAD1 show neonatal mortality, but the human phenotype associated with GAD1 disruption is poorly characterized. Neuray et al. describe six patients with biallelic GAD1 mutations, presenting with early-infantile onset epilepsy, neurodevelopmental delay, muscle weakness and non-CNS manifestations.

Male0301 basic medicineGlutamate decarboxylaseMalalties cerebralsNeurotransmissorsNeurodevelopmental delayEpilepsy0302 clinical medicineMESH: ChildAge of OnsetChildcleft palateGAD1AcademicSubjects/SCI01870Glutamate DecarboxylaseGlutamate receptorMuscle weakness//purl.org/becyt/ford/3.1 [https]NeurotransmittersMESH: InfantHypotoniamuscle weakneCleft palateMESH: EpilepsyChild PreschoolMuscle Hypotonia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]//purl.org/becyt/ford/3 [https]FemaleBrain diseasesAbnormalitiesmedicine.symptomMultiplemedicine.drugcleft palate; epilepsy; GAD1; muscle weakness; neurodevelopmental delayMESH: Glutamate Decarboxylasemedicine.medical_specialtyMESH: Abnormalities MultipleMESH: MutationMESH: Age of OnsetBiologyInhibitory postsynaptic potentialGAD1 cleft palate epilepsy muscle weakness neurodevelopmental delay.gamma-Aminobutyric acidGAD1neurodevelopmental delay03 medical and health sciencesExcitatory synapseInternal medicinemedicineHumansAbnormalities MultiplePreschoolAllelesMESH: Neurodevelopmental Disordersmuscle weaknessMESH: HumansEpilepsyMESH: Muscle HypotoniaMESH: AllelesMESH: Child PreschoolInfantmedicine.diseaseMESH: MaleEpilèpsiaEditor's Choice030104 developmental biologyEndocrinologyNeurodevelopmental DisordersMutationepilepsyAcademicSubjects/MED00310Neurology (clinical)Cleft palate; Epilepsy; GAD1; Muscle weakness; Neurodevelopmental delay; Abnormalities Multiple; Age of Onset; Alleles; Child; Child Preschool; Epilepsy; Female; Glutamate Decarboxylase; Humans; Infant; Male; Muscle Hypotonia; Mutation; Neurodevelopmental DisordersMESH: Female[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology030217 neurology & neurosurgeryReports
researchProduct

Genomic and Metabolomic Profile Associated to Clustering of Cardio-Metabolic Risk Factors

2016

Background To identify metabolomic and genomic markers associated with the presence of clustering of cardiometabolic risk factors (CMRFs) from a general population. Methods and Findings One thousand five hundred and two subjects, Caucasian, > 18 years, representative of the general population, were included. Blood pressure measurement, anthropometric parameters and metabolic markers were measured. Subjects were grouped according the number of CMRFs (Group 1: <2; Group 2: 2; Group 3: 3 or more CMRFs). Using SNPlex, 1251 SNPs potentially associated to clustering of three or more CMRFs were analyzed. Serum metabolomic profile was assessed by 1H NMR spectra using a Brucker Advance DRX 600 spect…

Male0301 basic medicineHeredityPhysiologylcsh:MedicinePhysiologyBlood Pressure030204 cardiovascular system & hematologyBioinformaticsBiochemistry0302 clinical medicineGlucose MetabolismRisk FactorsPolymorphism (computer science)GenotypeMedicine and Health SciencesMetaboliteslcsh:Scienceeducation.field_of_studyMultidisciplinaryFatty AcidsGenomicsMiddle AgedLipidsGenetic MappingPhysiological ParametersCardiovascular DiseasesPhysical SciencesCarbohydrate MetabolismResearch ArticleAdultGenetic MarkersGenotypePermutationFADS2PopulationVariant GenotypesSingle-nucleotide polymorphismBiologyPolymorphism Single Nucleotide03 medical and health sciencesMetabolomicsMetabolic DiseasesGeneticsmedicineHumansMetabolomicsGenetic Predisposition to DiseaseObesityeducationGenotypingAgedDiscrete Mathematicslcsh:RBody WeightBiology and Life SciencesLipid Metabolismmedicine.diseaseObesityMetabolism030104 developmental biologyCombinatoricslcsh:QMathematicsPLOS ONE
researchProduct

Heterozygous HMGB1 loss-of-function variants are associated with developmental delay and microcephaly

2021

International audience; 13q12.3 microdeletion syndrome is a rare cause of syndromic intellectual disability. Identification and genetic characterization of patients with 13q12.3 microdeletion syndrome continues to expand the phenotypic spectrum associated with it. Previous studies identified four genes within the approximately 300 Kb minimal critical region including two candidate protein coding genes: KATNAL1 and HMGB1. To date, no patients carrying a sequence-level variant or a single gene deletion in HMGB1 or KATNAL1 have been described. Here we report six patients with loss-of-function variants involving HMGB1 and who had phenotypic features similar to the previously described 13q12.3 m…

Male0301 basic medicineHeterozygoteMicrocephalyAdolescentDNA Copy Number VariationsLanguage delay[SDV]Life Sciences [q-bio]KaryotypeInheritance Patternschemical and pharmacologic phenomena030105 genetics & heredityBiologydysmorphic featuresloss of function mutation03 medical and health sciencesExome SequencingIntellectual disabilityGeneticsmedicineHumansGenetic Predisposition to DiseaseHMGB1 ProteinChildGeneGenetic Association StudiesIn Situ Hybridization FluorescenceGenetics (clinical)Loss functionGeneticsHMGB1FaciesExonsdevelopmental disabilitiesMicrodeletion syndromemedicine.diseasePhenotypePhenotype030104 developmental biologyChild PreschoolMicrocephalyFemaleHaploinsufficiency
researchProduct

Fifteen years of research on oral-facial-digital syndromes: from 1 to 16 causal genes

2017

Oral–facial–digital syndromes (OFDS) gather rare genetic disorders characterised by facial, oral and digital abnormalities associated with a wide range of additional features (polycystic kidney disease, cerebral malformations and several others) to delineate a growing list of OFDS subtypes. The most frequent, OFD type I, is caused by a heterozygous mutation in theOFD1gene encoding a centrosomal protein. The wide clinical heterogeneity of OFDS suggests the involvement of other ciliary genes. For 15 years, we have aimed to identify the molecular bases of OFDS. This effort has been greatly helped by the recent development of whole-exome sequencing (WES). Here, we present all our published and …

Male0301 basic medicineHeterozygoteciliopathieOral facial digital[SDV]Life Sciences [q-bio][ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyBiologyCiliopathiesCentriole elongation03 medical and health sciencesIntraflagellar transportGenotypeGeneticsPolycystic kidney diseasemedicineHumansAbnormalities Multiple[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyFunctional studies[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyGene*oral-facial-digital syndromesGenetics (clinical)ComputingMilieux_MISCELLANEOUSEncephaloceleGeneticsPolycystic Kidney Diseases[ SDV ] Life Sciences [q-bio]*ciliopathiesProteinsMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6][SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyOrofaciodigital Syndromesmedicine.disease030104 developmental biologyFaceMutationciliopathiesoral-facial-digital syndromesFemaleRetinitis PigmentosaRare cancers Radboud Institute for Health Sciences [Radboudumc 9]Ciliary Motility Disorders
researchProduct

Microsomal triglyceride transfer protein gene mutations in Turkish children: A novel mutation and clinical follow up.

2016

Abetalipoproteinemia (ABL; OMIM 200100) is a rare autosomal recessive disease that affects the absorption of dietary fats and fat soluble vitamins. Here, we describe the clinical and genetic characteristics of three patients with ABL. Two patients (patients 1 and 2) who were carriers of the c.398-399delAA mutation (previously known mutation) had developmental delay and hepatic steatosis developed at the age of five in patient 1. Patient 3 was the carrier of a novel mutation (g.10886-10902delAAGgtaagtttgtgttg in intron 3 and c.506A>T exon 5) in microsomal triglyceride transfer protein (MTP) gene and had hepatic steatosis.

Male0301 basic medicineHeterozygotemedicine.medical_specialtySettore MED/09 - Medicina InternaTurkeyDevelopmental delayDevelopmental DisabilitiesTurkish030204 cardiovascular system & hematologyHepatic steatosimedicine.disease_causeMicrosomal triglyceride transfer protein03 medical and health sciencesExon0302 clinical medicineInternal medicineHumansMedicineGeneGenetic Association StudiesGeneticsMutationABLbiologyAbetalipoproteinemiaDevelopmental delayHepatic steatosisMicrosomal triglyceride transfer proteinTurkishbusiness.industryIntronGastroenterologyInfantAbetalipoproteinemiaMicrosomal triglyceride transfer proteinmedicine.diseaseIntronsAbetalipoproteinemiaFatty Liver030104 developmental biologyEndocrinologyMutationbiology.proteinFemaleSteatosisCarrier ProteinsbusinessFollow-Up Studies
researchProduct

Imatinib dose escalation versus sunitinib as a second line treatment in KIT exon 11 mutated GIST: a retrospective analysis

2015

We retrospectively reviewed data from 123 patients (KIT exon 11 mutated) who received sunitinib or dose-escalated imatinib as second line. All patients progressed on imatinib (400 mg/die) and received a second line treatment with imatinib (800 mg/die) or sunitinib (50 mg/die 4 weeks on/2 off or 37.5 mg/day). Deletion versus other KIT 11 mutation was recorded, correlated with clinical benefits. 64% received imatinib, 36% sunitinib. KIT exon 11 mutation was available in 94 patients. With a median follow-up of 61 months, median time to progression (TTP) in patients receiving sunitinib and imatinib was 10 (95% CI 9.7–10.9) and 5 months (95% CI 3.6–6.7) respectively (P = 0.012). No difference wa…

Male0301 basic medicineIndolesTime FactorsGIST; exon 11; imatinib; second line; sunitinibGastroenterologyExon 11Exon0302 clinical medicineSecond linehemic and lymphatic diseasesSunitinibMedicineAged 80 and overGiSTSunitinibExonsMiddle AgedProto-Oncogene Proteins c-kitOncology030220 oncology & carcinogenesisDisease ProgressionImatinib MesylateFemaleResearch PaperGISTmedicine.drugAdultmedicine.medical_specialtyGastrointestinal Stromal TumorsAntineoplastic AgentsDisease-Free Survival03 medical and health sciencesInternal medicineHumansPyrrolesAgedRetrospective StudiesSecond lineSecond line treatmentDose-Response Relationship Drugbusiness.industryRetrospective cohort studyImatinibSurgery030104 developmental biologyImatinib mesylateMutationImatinibbusinessOncotarget
researchProduct

Bi-allelic LoF NRROS Variants Impairing Active TGF-β1 Delivery Cause a Severe Infantile-Onset Neurodegenerative Condition with Intracranial Calcifica…

2020

Negative regulator of reactive oxygen species (NRROS) is a leucine-rich repeat-containing protein that uniquely associates with latent transforming growth factor beta-1 (TGF- β1) and anchors it on the cell surface; this anchoring is required for activation of TGF-β1 in macrophages and microglia. We report six individuals from four families with bi-allelic variants in NRROS. All affected individuals had neurodegenerative disease with refractory epilepsy, developmental regression, and reduced white matter volume with delayed myelination. The clinical course in affected individuals began with normal development or mild developmental delay, and the onset of seizures occurred within the first ye…

Male0301 basic medicineInflammationBiologyintracranial calcificationneuroinflammationTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineReportTGF-β1NRROSGeneticsmedicineHumansAllelesGenetics (clinical)NeuroinflammationBrain DiseasesMicrogliaMacrophagesNeurodegenerationneurodegenerationCalcinosisGenetic VariationInfantNeurodegenerative Diseasesmedicine.diseaseNFKB1Latent TGF-beta binding proteinHEK293 Cells030104 developmental biologymedicine.anatomical_structureLatent TGF-beta Binding ProteinsImmunologyKnockout mouseFemaleMicrogliamutationmedicine.symptomDevelopmental regression030217 neurology & neurosurgeryThe American Journal of Human Genetics
researchProduct