Search results for " mutation"

showing 10 items of 1212 documents

Antihistamine-resistant Angioedema in Women with Negative Family History: Estrogens and F12 Gene Mutations

2013

Abstract Background In women with sporadic recurrent angioedema with an unknown cause who are unresponsive to antihistamines and have normal C1 inhibitor activity and a negative family history of angioedema, it is unclear whether they have idiopathic angioedema or hereditary angioedema with normal C1 inhibitor, and what impact exogenous estrogens have on their angioedema. Methods A cohort of 147 women was analyzed for F12 exon 9 mutations and for the influence of oral contraceptives, hormonal replacement therapy, and pregnancy on their angioedema. Results A total of 142 women had idiopathic angioedema unresponsive to antihistamines. Five women had an F12 mutation and thereby hereditary angi…

medicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentGene mutationC1-inhibitorimmune system diseasesInternal medicinemedicineHereditary Angioedema Type IIIcardiovascular diseasesFamily historyskin and connective tissue diseasesbiologyAngioedemabusiness.industryfood and beveragesGeneral Medicinemedicine.diseaseDermatologyEndocrinologyEstrogenHereditary angioedemabiology.proteinAntihistaminemedicine.symptombusinessThe American Journal of Medicine
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Neonatal Respiratory Insufficiency Caused by an (Homozygous) ABCA3-Stop Mutation: a Systematic Evaluation of Therapeutic Options

2014

Background Autosomal recessive ABCA3 (ATP-binding cassette protein A3) gene mutations have been associated with neonatal respiratory distress and pediatric interstitial lung disease. The clinical course of the disease depends on the underlying mutations. Therefore, knowledge of course, symptoms and treatment of the disease is important. Patient and methods A term newborn suffered from progressive respiratory insufficiency, which led to death at the age of 4.8 months. The girl developed interstitial lung disease. Infections as well as structural and functional disorders of the lung were systematically excluded. A homozygous c.4681C > T (Arg 1561 Stop) mutation of the ABCA3 gene was identifie…

medicine.medical_specialtymedicine.medical_treatmentGenes RecessiveDiseaseGene mutationABCA3Fatal OutcomeAdrenal Cortex HormonesInternal medicinemedicineHumansLung transplantationTreatment FailureIntensive care medicineChromosome AberrationsRespiratory Distress Syndrome NewbornLungbiologybusiness.industryHomozygoteInfant NewbornInterstitial lung diseaseInfantHydroxychloroquinemedicine.diseasePathophysiologymedicine.anatomical_structureMutationPediatrics Perinatology and Child HealthCodon Terminatorbiology.proteinATP-Binding Cassette TransportersFemaleMacrolidesLung Diseases InterstitialRespiratory InsufficiencybusinessHydroxychloroquinemedicine.drugKlinische Pädiatrie
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Magnetic Resonance Imaging Derived Biomarkers of IDH Mutation Status and Overall Survival in Grade III Astrocytomas

2020

The evaluation of the isocitrate dehydrogenase (IDH) mutation status in the glioma decision-making process has diagnostic, prognostic and therapeutic implications. The aim of this study was to evaluate whether conventional magnetic resonance imaging (MRI) and apparent diffusion coefficient (ADC) can noninvasively predict the most common IDH mutational status (R132H) in GIII-astrocytomas and the overall survival (OS). Hence, twenty-two patients (9-F, 13-M) with a histological diagnosis of GIII-astrocytoma and evaluation of IDH-mutation status (12-wild type, 10-mutant) were retrospectively evaluated. Imaging studies were reviewed for the morphological feature and mean ADC values (ADCm). Stati…

medicine.medical_specialtyoverall survivalClinical BiochemistryradiogenomicsRadiogenomicsGastroenterologyArticle03 medical and health sciences0302 clinical medicineGliomaInternal medicinemedicineOverall survivalEffective diffusion coefficientdiffusion weighted imaging (DWI)apparent diffusion coefficient (ADC)lcsh:R5-920medicine.diagnostic_testbusiness.industryanaplastic astrocytomaMagnetic resonance imagingmedicine.diseaseExact testIsocitrate dehydrogenaseisocitrate dehydrogenase (IDH) mutation030220 oncology & carcinogenesisHuman medicinelcsh:Medicine (General)businessanaplastic astrocytomas030217 neurology & neurosurgeryAnaplastic astrocytomaDiagnostics
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F9 missense mutations impairing factor IX activation are associated with pleiotropic plasma phenotypes.

2022

Background Circulating dysfunctional factor IX (FIX) might modulate distribution of infused FIX in hemophilia B (HB) patients. Recurrent substitutions at FIX activation sites (R191-R226, >300 patients) are associated with variable FIX activity and antigen (FIXag) levels. Objectives To investigate the (1) expression of a complete panel of missense mutations at FIX activation sites and (2) contribution of F9 genotypes on the FIX pharmacokinetics (PK). Methods We checked FIX activity and antigen and activity assays in plasma and after recombinant expression of FIX variants and performed an analysis of infused FIX PK parameters in patients (n = 30), mostly enrolled in the F9 Genotype and PK HB …

medicine.medical_specialtypharmacogenetics.Mutation MissenseSocio-culturaleAlpha (ethology)aemophilia Brecombinant proteinsHemophilia Blaw.inventionFactor IXAntigenlawInternal medicineGenotypemedicineMissense mutationHumansHaemophilia BpharmacokineticBeta (finance)Factor IXpharmacogeneticsChemistryHematologymedicine.diseaseEndocrinologyPhenotypefactor IX activation; hemophilia B; pharmacogenetics; pharmacokinetics; recombinant proteinsRecombinant DNAFemalefactor IX activationBlood Coagulation Testspharmacokineticsrecombinant proteinmedicine.drugJournal of thrombosis and haemostasis : JTH
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Amplicon-based high-throughput pooled sequencing identifies mutations in CYP7B1 and SPG7 in sporadic spastic paraplegia patients

2011

Hereditary spastic paraplegia (HSP) is a neurodegenerative disorder defined clinically by progressive lower limb spasticity and weakness. HSP is a genetically highly heterogeneous condition with at least 46 gene loci identified so far, involving X-linked, autosomal recessive (AR) and autosomal dominant inheritance. For correct diagnosis, molecular testing is essential because clinical parameters by themselves are not reliable to differentiate HSP forms. The purpose of this study was to establish amplicon-based high-throughput genotyping for AR-HSP. A sample of 187 index cases with apparently sporadic or recessive spastic paraplegia were analyzed by applying an array-based amplification stra…

methods [High-Throughput Nucleotide Sequencing]GenotypeHereditary spastic paraplegiaDNA Mutational AnalysisMolecular Sequence DataSPG7 protein humanCytochrome P450 Family 7diagnosis [Paraplegia]Biologymedicine.disease_causegenetics [Paraplegia]Cohort Studiesgenetics [Metalloendopeptidases]03 medical and health sciences0302 clinical medicineGenetic variationGenotypeGeneticsmedicineHumansddc:610Genetic TestingGenotypingGenetics (clinical)CYP7B1 protein human030304 developmental biologyGenetic testingParaplegiaGenetics0303 health sciencesMutationBase SequenceParapleginmedicine.diagnostic_testgenetics [Steroid Hydroxylases]Genetic VariationHigh-Throughput Nucleotide SequencingMetalloendopeptidasesmethods [DNA Mutational Analysis]Ampliconmedicine.diseasegenetics [Genetic Variation]3. Good healthMutationSteroid HydroxylasesATPases Associated with Diverse Cellular Activities030217 neurology & neurosurgeryClinical Genetics
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FUNCTIONAL EFFECT OF NOVEL AMINO ACID VARIANTS OF APOLIPOPROTEIN B IN FAMILIAL HYPOBETALIPOPROTEINEMIA

2011

Introduction. Familial Hypobetalipoproteinemia (FHBL) is a codominant disorder characterized by reduced plasma levels of LDL-C and apolipoprotein (apo) B. In 50% of cases FHBL is due to mutations in APOB gene resulting in truncated apoBs of various size. Some mutations in APOB gene resulting in non-conservative amino acid substitutions were reported to cause FHBL. In vitro, these mutations induce the retention of the mutant apoB in the endoplasmic reticulum (ER) and impair the secretion of apoB-containing lipoproteins. In two FHBL subjects we identified two novel amino acid variants (Thr26_27delinsAsn and Tyr102Cys) located in the N-terminal 1000 amino acids of mature apoB. Methods. To inve…

missense mutationsSettore MED/09 - Medicina InternaFHBL
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A SUMOylation-defective MITF germline mutation predisposes to melanoma and renal carcinoma

2011

International audience; So far, no common environmental and/or phenotypic factor has been associated with melanoma and renal cell carcinoma (RCC). The known risk factors for melanoma include sun exposure, pigmentation and nevus phenotypes; risk factors associated with RCC include smoking, obesity and hypertension. A recent study of coexisting melanoma and RCC in the same patients supports a genetic predisposition underlying the association between these two cancers. The microphthalmia-associated transcription factor (MITF) has been proposed to act as a melanoma oncogene; it also stimulates the transcription of hypoxia inducible factor (HIF1A), the pathway of which is targeted by kidney canc…

multidisciplinary sciencesMESH : Germ-Line MutationSUMO proteinurologic and male genital diseasesmedicine.disease_causeMESH : Neoplasm Invasiveness[ SDV.CAN ] Life Sciences [q-bio]/CancerMESH : Carcinoma Renal Cell0302 clinical medicineGene FrequencyCell MovementMESH: Germ-Line MutationMESH : Cell MovementMESH : Gene FrequencyMESH: Cell MovementComputingMilieux_MISCELLANEOUSGenetics0303 health sciencesMultidisciplinaryMESH: SumoylationMelanomaMESH : SumoylationMESH: Genetic Predisposition to Diseaserenal carcinomaMESH: Carcinoma Renal CellMicrophthalmia-associated transcription factorMESH : Microphthalmia-Associated Transcription Factor3. Good healthgermline mutation030220 oncology & carcinogenesisMESH: Microphthalmia-Associated Transcription Factorscience and technologyMESH: MelanomasumoMESH : Melanoma[SDV.CAN]Life Sciences [q-bio]/CancerBiology03 medical and health sciencesGermline mutationmelanomaMESH: Gene FrequencyGenetic predispositionmedicineHumansGenetic Predisposition to DiseaseNeoplasm InvasivenessCarcinoma Renal CellneoplasmsTranscription factorGerm-Line Mutation030304 developmental biologyMicrophthalmia-Associated Transcription FactorMESH: HumansMESH : HumansSumoylationMESH: Neoplasm Invasivenessmedicine.diseaseHIF1Acancer cellsCancer researchMESH : Genetic Predisposition to DiseaseCarcinogenesis
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Does δ-sarcoglycan-associated autosomal-dominant cardiomyopathy exist?

2009

In this study we clinically and genetically characterize a consanguineous family with a homozygous novel missense mutation in the delta-sarcoglycan gene and a second delta-sarcoglycan mutation that has previously been reported to cause severe autosomal-dominant dilated cardiomyopathy. We identified a novel missense mutation in exon 6 (p.A131P) of the delta-sarcoglycan gene, which in a homozygous state leads to the clinical picture of a limb girdle muscular dystrophy. In four heterozygous carriers for the mutation, aged 3-64 years, a second sequence variant in exon 6 (p.S151A) of the delta-sarcoglycan gene was detected on the other allele. This second missense change had previously been repo…

musculoskeletal diseasesAdultCardiomyopathy DilatedMalemedicine.medical_specialtyAdolescentBiopsyDNA Mutational AnalysisCardiomyopathyMutation MissenseCompound heterozygosityArticleExonConsanguinityElectrocardiographyYoung AdultInternal medicineSarcoglycansGeneticsMedicineMissense mutationHumansMuscular dystrophyChildGenetics (clinical)Genes DominantGeneticsFamily Healthbusiness.industryMusclesMyocardiumDilated cardiomyopathyMiddle Agedmedicine.diseasePedigreeEndocrinologyEchocardiographyChild PreschoolMutation (genetic algorithm)FemalebusinessLimb-girdle muscular dystrophy
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Abnormalities in alpha-dystroglycan expression in MDC1C and LGMD2I muscular dystrophies

2004

We recently identified mutations in the fukutin related protein (FKRP) gene in patients with congenital muscular dystrophy type 1C (MDC1C) and limb girdle muscular dystrophy type 2I (LGMD2I). The sarcolemma of these patients typically displays an immunocytochemical reduction of alpha-dystroglycan. In this report we extend these observations and report a clear correlation between the residual expression of alpha-dystroglycan and the phenotype. Three broad categories were identified. Patients at the severe end of the clinical spectrum (MDC1C) were compound heterozygote between a null allele and a missense mutation or carried two missense mutations and displayed a profound depletion of alpha-d…

musculoskeletal diseasesAdultPathologymedicine.medical_specialtyNonsense mutationBlotting WesternDNA Mutational AnalysisMedizinCompound heterozygosityPolymerase Chain ReactionMuscular DystrophiesPathology and Forensic MedicineFetusDystroglycanmedicineMissense mutationHumansPentosyltransferasesMuscular dystrophyChildDystroglycansMuscle SkeletalGeneticsFukutin-related proteinMembrane GlycoproteinsbiologyProteinsmedicine.diseasemusculoskeletal systemImmunohistochemistryCytoskeletal ProteinsPhenotypeMutationbiology.proteinCongenital muscular dystrophyLimb-girdle muscular dystrophyRegular Articles
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Phenotypic spectrum and genomics of undiagnosed arthrogryposis multiplex congenital

2022

BackgroundArthrogryposis multiplex congenita (AMC) is characterised by congenital joint contractures in two or more body areas. AMC exhibits wide phenotypic and genetic heterogeneity. Our goals were to improve the genetic diagnosis rates of AMC, to evaluate the added value of whole exome sequencing (WES) compared with targeted exome sequencing (TES) and to identify new genes in 315 unrelated undiagnosed AMC families.MethodsSeveral genomic approaches were used including genetic mapping of disease loci in multiplex or consanguineous families, TES then WES. Sanger sequencing was performed to identify or validate variants.ResultsWe achieved disease gene identification in 52.7% of AMC index pati…

musculoskeletal diseasesArtrogriposi múltiple congènitaSettore BIO/18 - GENETICAhuman geneticsneuromuscular diseasesGenomicsBiologyCONTRACTURESCLASSIFICATIONdiseasessymbols.namesakeDiagnòsticGene mappingarthrogryposis multiplex congenitaExome SequencingOF-FUNCTION MUTATIONSGeneticsMedicine and Health SciencesgenomicsHumansGenetics (clinical)Exome sequencingArthrogryposisSanger sequencingGeneticsArthrogryposis multiplex congenitaGenetic heterogeneitySPINAL MUSCULAR-ATROPHYProteinsnervous system malformationsDYSTROPHYDisease gene identificationGENEHuman geneticsPedigreeETIOLOGYPhenotypesymbolsneuromuscularGenèticaTranscription Factors
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