Search results for "MUTATION"

showing 10 items of 2830 documents

High risk of hepatocellular carcinoma in anti-HBe positive liver cirrhosis patients developing lamivudine resistance

2004

The emergence of drug-resistant virus in hepatitis B virus patients treated with lamivudine is well documented. However. its clinical impact in the long-term treatment of anti-HBe positive compensated cirrhotic patients is not well known. In this study, we treated 22 consecutive patients with anti-HBe compensated cirrhosis with lamivudine for a median period of 42 months. All patients responded to lamivudine, but viral breakthrough occurred in 13 patients (59%) between 9 and 42 months of therapy due to the emergence of a mutant strain. During the follow-up, 11 developed hepatocellular carcinoma. Of these, 10 occurred soon after the emergence of viral resistance, generally showing aggressive…

AdultLiver CirrhosisMaleHepatitis B virusmedicine.medical_specialtyCarcinoma HepatocellularCirrhosisLAMIVUDINEmedicine.disease_causeRisk AssessmentGastroenterologyVirusVirologyInternal medicineDrug Resistance ViralHumansMedicineHepatitis B e AntigensHEPATOCELLULAR CARCINOMAHepatitis B AntibodiesCIRRHOISIS; HEPATOCELLULAR CARCINOMA; LAMIVUDINE; HEPATITIS B; PRE-CORE MUTANTHepatitis B virusCirrhosiHepatologybusiness.industryCIRRHOISISLamivudineMiddle AgedHepatitis Bmedicine.diseaseHepatitis B Core AntigensViral BreakthroughPRE-CORE MUTANTInfectious DiseasesHepatocellular carcinomaRelative riskMutationHEPATITIS BReverse Transcriptase InhibitorsFemalePrecore mutantbusinessmedicine.drugJournal of Viral Hepatitis
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Vitamin D as an effective treatment in human uterine leiomyomas independent of mediator complex subunit 12 mutation.

2021

Objective To study whether vitamin D (VitD) inhibits cell proliferation and Wnt/β-catenin and transforming growth factor−β (TGFβ) signaling pathways in uterine leiomyomas independent of mediator complex subunit 12 (MED12) mutation status. Design Prospective study comparing leiomyoma vs. myometrial tissues and human uterine leiomyoma primary (HULP) cells treated with or without VitD and analyzed by MED12 mutation status. Setting Hospital and university laboratories. Patient(s) Women with uterine leiomyoma without any treatment (n = 37). Intervention(s) Uterine leiomyoma and myometrium samples were collected from women undergoing surgery because of symptomatic leiomyoma pathology. Main Outcom…

AdultMMP9MED12AndrologyWNT4medicineVitamin D and neurologyHumansProspective StudiesVitamin DneoplasmsCells CulturedCell ProliferationUterine leiomyomaMediator ComplexLeiomyomabusiness.industryWnt signaling pathwayMyometriumObstetrics and GynecologyMiddle Agedmusculoskeletal systemmedicine.diseasefemale genital diseases and pregnancy complicationsLeiomyomaTreatment OutcomeReproductive MedicineMutationUterine NeoplasmsFemalebusinessFertility and sterility
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Genetic screening for MC4R gene identifies three novel mutations associated with severe familiar obesity in a cohort of Spanish individuals

2019

Abstract MC4R gene is a hypothalamic satiety control mediator in which mutations cause a monogenic form of obesity. The aim of this study was to perform a genetic screening to identify variations in the entire region of MC4R gene. A total of 236 unrelated and severely obese patients (BMI ≥ 40 kg/m2) with Spanish ancestry and severe overweight familiar history have been enrolled into the study. Seven MC4R gene variants were identified in the heterozygous state in 21 patients. Coding variants p.Thr101Ile and p.Ala259Asp are new and variants p.Ser30Phe, p.Val103Ile and p.Ile251Leu were previously described. Two variants have been also observed in the promoter region of the MC4R gene; the c.-24…

AdultMale0301 basic medicineAdolescentObesity phenotypeIn silicoDNA Mutational AnalysisMutation MissenseOverweightBiologymedicine.disease_causePolymorphism Single NucleotideCohort StudiesYoung Adult03 medical and health sciences0302 clinical medicineGeneticsmedicineHumansGenetic Predisposition to DiseaseGenetic TestingGeneGenetic Association StudiesGeneticsMutationPromoterGeneral MedicineMiddle Agedmedicine.diseaseObesityObesity MorbidPedigree030104 developmental biologySpainCase-Control Studies030220 oncology & carcinogenesisCohortReceptor Melanocortin Type 4Femalemedicine.symptomGene
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Homozygous variants in the gene SCAPER cause syndromic intellectual disability

2019

The S-Phase Cyclin A Associated Protein In The ER (SCAPER) gene is a ubiquitously expressed gene with unknown function in the brain. Recently, biallelic SCAPER variants were described in four patients from three families with retinitis pigmentosa (RP) and intellectual disability (ID). Here, we expand the spectrum of pathogenic variants in SCAPER and report on 10 further patients from four families with ID, RP, and additional dysmorphic features carrying homozygous variants in SCAPER. The variants found comprise frameshift, nonsense, and missense variants as well as an intragenic homozygous deletion, which spans SCAPER exons 15 and 16 and introduces a frameshift and a premature stop codon. A…

AdultMale0301 basic medicineAdolescentmedia_common.quotation_subjectCyclin ANonsenseGene Expression030105 genetics & heredityFrameshift mutationConsanguinityMice03 medical and health sciencesExonNeural Stem CellsIntellectual DisabilityRetinitis pigmentosaGene expressionGeneticsmedicineAnimalsHumansMissense mutationFamilyChildGeneGenetics (clinical)media_commonCerebral CortexNeuronsGeneticsbiologyHomozygoteSyndromemedicine.diseasePedigree030104 developmental biologyMutationbiology.proteinFemaleCarrier ProteinsRetinitis PigmentosaAmerican Journal of Medical Genetics Part A
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MicroRNAs expression associated with aggressive clinicopathological features and poor prognosis in primary cutaneous melanomas

2020

Several studies have focused on identifying microRNAs involved in the pathogenesis of melanoma. However, its association with clinicopathological features has been scarcely addressed. The aim of this study is to identify microRNAs expression profiles related to aggressive clinicopathological and molecular features, and to analyze the association with melanoma survival. A retrospective and observational study was performed in a series of 179 formalin-fixed paraffin embedded primary cutaneous melanomas. First, a screening analysis on a discovery set (n = 22) using miRNA gene chip array (Affymetrix, Santa Clara, California, USA) was performed. Differentially expressed microRNAs were detected e…

AdultMale0301 basic medicineCancer ResearchPoor prognosisSkin NeoplasmsTERT mutationsDermatologyBiologyPathogenesisBreslow Thickness03 medical and health sciences0302 clinical medicinemicroRNAmelanomamedicineHumansMelanomaMitosisSurvival analysisAgedMelanomaMicroRNA Expression ProfileMiddle AgedPrognosismedicine.diseasemicroRNAsMicroRNAs030104 developmental biologyOncology030220 oncology & carcinogenesisCancer researchFemaleprognosisclinicopathological featuresMelanoma Research
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Identification of a novel LMF1 nonsense mutation responsible for severe hypertriglyceridemia by targeted next-generation sequencing

2016

Background Severe hypertriglyceridemia (HTG) may result from mutations in genes affecting the intravascular lipolysis of triglyceride (TG)-rich lipoproteins. Objective The aim of this study was to develop a targeted next-generation sequencing panel for the molecular diagnosis of disorders characterized by severe HTG. Methods We developed a targeted customized panel for next-generation sequencing Ion Torrent Personal Genome Machine to capture the coding exons and intron/exon boundaries of 18 genes affecting the main pathways of TG synthesis and metabolism. We sequenced 11 samples of patients with severe HTG (TG>885 mg/dL–10 mmol/L): 4 positive controls in whom pathogenic mutations had pre…

AdultMale0301 basic medicineCandidate geneEndocrinology Diabetes and MetabolismDNA Mutational AnalysisNonsense mutationPanel-based NGS sequencing030204 cardiovascular system & hematologyBiologymedicine.disease_causeDNA sequencing03 medical and health sciencessymbols.namesakeExon0302 clinical medicineNutrition and DieteticInternal MedicinemedicineHumansGeneHypertriglyceridemiaSanger sequencingGeneticsMutationNutrition and DieteticsLMF1 geneNonsense mutationHigh-Throughput Nucleotide SequencingInfantMembrane ProteinsIon semiconductor sequencingMiddle AgedIon torrent PGM sequencingPhenotype030104 developmental biologyChild PreschoolsymbolsFemaleCardiology and Cardiovascular MedicineJournal of Clinical Lipidology
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Further delineation of a rare recessive encephalomyopathy linked to mutations in GFER thanks to data sharing of whole exome sequencing data

2017

Background Alterations in GFER gene have been associated with progressive mitochondrial myopathy, congenital cataracts, hearing loss, developmental delay, lactic acidosis and respiratory chain deficiency in 3 siblings born to consanguineous Moroccan parents by homozygosity mapping and candidate gene approach (OMIM#613076). Next generation sequencing recently confirmed this association by the finding of compound heterozygous variants in 19-year-old girl with a strikingly similar phenotype, but this ultra-rare entity remains however unknown from most of the scientific community. Materials and methods Whole exome sequencing was performed as part of a "diagnostic odyssey" for suspected mitochon…

AdultMale0301 basic medicineHeterozygoteCandidate geneAdolescentdata sharingMitochondrial diseaseCompound heterozygosityBioinformaticsYoung Adult03 medical and health sciencesMitochondrial myopathyMitochondrial EncephalomyopathiesExome SequencingGeneticsHumansMedicineGenetic Predisposition to DiseaseOxidoreductases Acting on Sulfur Group Donorswhole-exome sequencingChildExomeCytochrome ReductasesGenetics (clinical)Exome sequencing[SDV.GEN]Life Sciences [q-bio]/Geneticsbusiness.industryGFERDisease gene identificationmedicine.diseasePedigree3. Good health030104 developmental biologymitochondrial conditionMutationCongenital cataractsFemale[ SDV.GEN ] Life Sciences [q-bio]/GeneticsbusinessClinical Genetics
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Increased structural white and grey matter network connectivity compensates for functional decline in early multiple sclerosis

2016

Background: The pathology of multiple sclerosis (MS) consists of demyelination and neuronal injury, which occur early in the disease; yet, remission phases indicate repair. Whether and how the central nervous system (CNS) maintains homeostasis to counteract clinical impairment is not known. Objective: We analyse the structural connectivity of white matter (WM) and grey matter (GM) networks to understand the absence of clinical decline as the disease progresses. Methods: A total of 138 relapsing–remitting MS patients (classified into six groups by disease duration) and 32 healthy controls were investigated using 3-Tesla magnetic resonance imaging (MRI). Networks were analysed using graph the…

AdultMale0301 basic medicineMultiple SclerosisModularity (biology)DiseaseGrey matterBiologyNerve Fibers MyelinatedYoung Adult03 medical and health sciences0302 clinical medicineImage Processing Computer-AssistedmedicineHumansGray MatterMultiple sclerosisMiddle Agedmedicine.diseaseNetwork dynamicsWhite MatterPathology of multiple sclerosisWhite (mutation)Diffusion Tensor Imaging030104 developmental biologymedicine.anatomical_structureNeurologyFemaleNeurology (clinical)Nerve NetAdaptationNeuroscience030217 neurology & neurosurgeryDemyelinating DiseasesMultiple Sclerosis Journal
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A meta-analysis of 120 246 individuals identifies 18 new loci for fibrinogen concentration

2015

Genome-wide association studies have previously identified 23 genetic loci associated with circulating fibrinogen concentration. These studies used HapMap imputation and did not examine the X-chromosome. 1000 Genomes imputation provides better coverage of uncommon variants, and includes indels. We conducted a genome-wide association analysis of 34 studies imputed to the 1000 Genomes Project reference panel and including similar to 120 000 participants of European ancestry (95 806 participants with data on the X-chromosome). Approximately 10.7 million single-nucleotide polymorphisms and 1.2 million indels were examined. We identified 41 genome-wide significant fibrinogen loci ; of which, 18 …

AdultMale0301 basic medicineNetherlands Twin Register (NTR)Single-nucleotide polymorphismGenome-wide association studyBiologyPolymorphism Single NucleotideWhite People03 medical and health sciencesINDEL MutationGenetics/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_Humans1000 Genomes ProjectInternational HapMap ProjectIndelMolecular BiologyGenetics (clinical)ComputingMilieux_MISCELLANEOUSAgedGenetic associationAged 80 and overGeneticsAssociation Studies ArticlesFibrinogen[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyGeneral MedicineMiddle AgedGenetic architecture030104 developmental biologyGenetic LociFemaleGENOME-WIDE ASSOCIATION ; C-REACTIVE PROTEIN ; CARDIOVASCULAR-DISEASE ; CIRCULATING FIBRINOGEN ; GENETIC ARCHITECTURE ; VARIANTS ; DESIGN ; HEMOSTASIS ; RESOURCE ; HEALTHImputation (genetics)Genome-Wide Association Study
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Phenotype and natural history of inherited neuropathies caused byHSJ1c.352+1G>A mutation

2015

Mutations in the HSJ1 ( Heat-Shock Protein J1 ) gene, also called DNAJB2 (DnaJ (Hsp40) homologue, subfamily B, member 2), have been recently described as a cause of hereditary neuropathies. The HSJ1 c.352+1G>A mutation in homozygote state has been reported as the causative mutation in a single family with autosomal recessive distal hereditary motor neuropathy (dHMN).1 Since then, two other families with different HSJ1 mutations have been described: one with a dHMN phenotype and the other with a Charcot-Marie-Tooth disease type 2 (CMT2) phenotype.2 We identified the HSJ1 c.352+1G>A mutation in 10 patients who underwent long-lasting follow-up. We describe their phenotype and clinical evolutio…

AdultMale0301 basic medicineNeural ConductionCell Cycle ProteinsNeurological examinationDisease03 medical and health sciencessymbols.namesake0302 clinical medicineCharcot-Marie-Tooth DiseasemedicineHumansGeneHeat-Shock ProteinsExome sequencingAdaptor Proteins Signal TransducingGenetic testingGeneticsSanger sequencingmedicine.diagnostic_testbusiness.industryNuclear ProteinsMiddle AgedPhenotypePsychiatry and Mental healthPhenotype030104 developmental biologySpainMutationMutation (genetic algorithm)symbolsFemaleSurgeryNeurology (clinical)Hereditary Sensory and Motor Neuropathybusiness030217 neurology & neurosurgeryJournal of Neurology, Neurosurgery & Psychiatry
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