Search results for "N2"

showing 10 items of 346 documents

ATNX2 is not a regulatory gene in Italian amyotrophic lateral sclerosis patients with C9ORF72 GGGGCC expansion

2015

Abstract There are indications that both familial amyotrophic lateral sclerosis (ALS) and sporadic ALS phenotype and prognosis are partly regulated by genetic and environmental factors, supporting the theory that ALS is a multifactorial disease. The aim of this article was to assess the role of ATXN2 intermediate length repeats in a large series of Italian and Sardinian ALS patients and controls carrying a pathogenetic C9ORF72 GGGGCC hexanucleotide repeat. A total of 1972 ALS cases were identified through the database of the Italian ALS Genetic consortium, a collaborative effort including 18 ALS centers throughout Italy. The study population included: (1) 276 Italian and 57 Sardinian ALS ca…

Male0301 basic medicineAgingC9ORF72Genetic Association Studie030105 genetics & heredityBiologySettore MED/03 - GENETICA MEDICA03 medical and health sciences0302 clinical medicineC9orf72medicineAlleleAmyotrophic lateral sclerosisAmyotrophic lateral sclerosiAgedAtaxin-2Regulator geneAmyotrophic lateral sclerosis; ATXN2; C9ORF72; Phenotype; Neuroscience (all); Medicine (all); Aging; Developmental Biology; Geriatrics and Gerontology; Neurology (clinical)GeneticsDNA Repeat ExpansionNeuroscience (all)ProteinMedicine (all)General NeuroscienceATXN2Middle AgedDNA Repeat Expansionmedicine.diseaseAmyotrophic lateral sclerosis3. Good healthC9orf72 ProteinAmyotrophic lateral sclerosis; ATXN2; C9ORF72; Phenotype; Neurology (clinical); Neuroscience (all); Aging; Developmental Biology; Geriatrics and GerontologyPhenotypeItalyPopulation studyFemaleSettore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyTrinucleotide repeat expansion030217 neurology & neurosurgeryHumanDevelopmental Biology
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Absence of germline CDKN2A mutation in Sicilian Patients with Familial Malignant Melanoma: could it be a population-specific genetic signature?

2015

Germline CDKN2A mutations have been described in 25% to 40% of melanoma families from several countries. Sicilian population is genetically different from the people of Europe and Northern Italy because of its historical background, therefore familial melanoma could be due to genes different from high-penetrance CDKN2A gene. Four hundred patients with cutaneous melanoma were observed in a 6-years period at the Plastic Surgery Unit of the University of Palermo. Forty-eight patients have met the criteria of the Italian Society of Human Genetics (SIGU) for the diagnosis of familial melanoma and were screened for CDKN2A and CDK4 mutations. Mutation testing revealed that none of the families car…

Male0301 basic medicineCancer ResearchMutation rateSettore MED/06 - Oncologia MedicaSettore MED/19 - Chirurgia Plasticap14ARFGermline0302 clinical medicineCDKN2ATumor Suppressor Protein p14ARFMedicineMelanomaSicilyfamilial melanomaGeneticseducation.field_of_studyMelanomaMiddle AgedGene Expression Regulation NeoplasticItalyOncologygermline mutation030220 oncology & carcinogenesisMolecular MedicineFemaleResearch PaperSignal TransductionAdultPopulation03 medical and health sciencesCDKN2Acutaneous melanomaGermline mutationp16INK4aHumansGenetic Predisposition to DiseaseeducationneoplasmsCyclin-Dependent Kinase Inhibitor p16Germ-Line MutationAgedPharmacologybusiness.industryGenetic heterogeneityp.R87W mutationmedicine.disease030104 developmental biologyMutationCutaneous melanomaCDKN2A; cutaneous melanoma; familial melanoma; germline mutation; p.R87W mutation; p14ARF; p16INK4a; Cancer Research; Oncology; Molecular Medicine; Pharmacologybusiness
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Expanding the β-III Spectrin-Associated Phenotypes toward Non-Progressive Congenital Ataxias with Neurodegeneration

2021

(1) Background: A non-progressive congenital ataxia (NPCA) phenotype caused by b-III spectrin (SPTBN2) mutations has emerged, mimicking spinocerebellar ataxia, autosomal recessive type 14 (SCAR14). The pattern of inheritance, however, resembles that of autosomal dominant classical spinocerebellar ataxia type 5 (SCA5). (2) Methods: In-depth phenotyping of two boys studied by a customized gene panel. Candidate variants were sought by structural modeling and protein expression. An extensive review of the literature was conducted in order to better characterize the SPTBN2-associated NPCA. (3) Results: Patients exhibited an NPCA with hypotonia, developmental delay, cerebellar syndrome, and cogni…

Male0301 basic medicineProbandPathologyProtein ConformationSequence Homology<i>SPTBN2 </i>geneb-III spectrin030105 genetics & heredityFluid-attenuated inversion recoveryCohort Studieslcsh:ChemistryNon-progressive congenital ataxia0302 clinical medicineβ-III spectrinSpectrin:enfermedades del sistema nervioso::enfermedades neurodegenerativas [ENFERMEDADES]Age of OnsetChildlcsh:QH301-705.5Spectroscopy:Otros calificadores::Otros calificadores::/genética [Otros calificadores]NeurodegenerationneurodegenerationNeurodegenerative Diseasesnon-progressive congenital ataxiaSyndromeGeneral MedicinePhenotypeHypotoniaComputer Science ApplicationsPhenotype:Nervous System Diseases::Neurodegenerative Diseases [DISEASES]Spinocerebellar ataxiamedicine.symptomSPTBN2 genemedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesCerebellar AtaxiaNeuroimagingBiologyCatalysisArticleInorganic Chemistry03 medical and health sciences:Nervous System Diseases::Central Nervous System Diseases::Brain Diseases::Cerebellar Diseases::Cerebellar Ataxia [DISEASES]:Other subheadings::Other subheadings::/genetics [Other subheadings]medicineHumansAmino Acid SequencePhysical and Theoretical ChemistryNeurodegenerationMolecular BiologyGenetic Association StudiesOrganic ChemistrySpectrinmedicine.diseaseHyperintensitySistema nerviós - Degeneració - Aspectes genèticslcsh:Biology (General)lcsh:QD1-999:enfermedades del sistema nervioso::enfermedades del sistema nervioso central::enfermedades cerebrales::enfermedades cerebelosas::ataxia cerebelosa [ENFERMEDADES]Mutation030217 neurology & neurosurgeryInternational Journal of Molecular Sciences
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Epigenetic changes in localized gastric cancer: the role of RUNX3 in tumor progression and the immune microenvironment

2016

// Marta Jessica Llorca-Cardenosa 1, * , Tania Fleitas 1, * , Maider Ibarrola-Villava 1 , Maria Pena-Chilet 1 , Cristina Mongort 2 , Carolina Martinez-Ciarpaglini 2 , Lara Navarro 2 , Valentina Gambardella 1 , Josefa Castillo 1 , Susana Rosello 1 , Samuel Navarro 2 , Gloria Ribas 1 , Andres Cervantes 1 1 Medical Oncology, Biomedical Research Institute INCLIVA, University of Valencia, Valencia, Spain 2 Department of Pathology, Biomedical Research Institute INCLIVA, University of Valencia, Valencia, Spain * These authors contributed equally to this work Correspondence to: Gloria Ribas, email: gribas@incliva.es Andres Cervantes, email: andres.cervantes@uv.es Keywords: RUNX3, ARID1A, gastric ca…

Male0301 basic medicineRUNX3immune microenvironmentBiologyEpigenesis Genetic03 medical and health sciences0302 clinical medicineStomach NeoplasmsCDKN2ABiomarkers TumorTumor MicroenvironmentmedicineHumansEpigeneticsPromoter Regions GeneticAgedAged 80 and overTumor microenvironmentgastric cancerMicrosatellite instabilityCancerMethylationDNA MethylationMiddle AgedPrognosismedicine.diseaseARID1Adigestive system diseasesSurvival RateCore Binding Factor Alpha 3 Subunit030104 developmental biologyOncologyTumor progressionCase-Control Studies030220 oncology & carcinogenesisDNA methylationImmunologyCancer researchCpG IslandsFemaleMicrosatellite InstabilityFollow-Up StudiesResearch Papergene methylationOncotarget
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Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease

2013

Eleven susceptibility loci for late-onset Alzheimer&apos;s disease (LOAD) were identified by previous studies; however, a large portion of the genetic risk for this disease remains unexplained. We conducted a large, two-stage meta-analysis of genome-wide association studies (GWAS) in individuals of European ancestry. In stage 1, we used genotyped and imputed data (7,055,881 SNPs) to perform meta-analysis on 4 previously published GWAS data sets consisting of 17,008 Alzheimer&apos;s disease cases and 37,154 controls. In stage 2, 11,632 SNPs were genotyped and tested for association in an independent set of 8,572 Alzheimer&apos;s disease cases and 11,312 controls. In addition to the APOE locu…

MaleApolipoprotein Eepidemiology [Alzheimer Disease]SORL1Medizingenetics [Alzheimer Disease]Genome-wide association studySingle-nucleotide polymorphismBiologyPolymorphism Single NucleotideArticlePICALMCohort StudiesAlzheimer Diseaseddc:570PSEN2GeneticsmedicineHumansGenetic Predisposition to DiseaseAge of OnsetBiologyAgedGenetic associationAged 80 and overGeneticsMiddle Agedmedicine.diseaseGenetic LociCase-Control StudiesFemaleHuman medicineAlzheimer's diseasestatistics & numerical data [Genome-Wide Association Study]Genome-Wide Association StudyNature Genetics
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TGF-β Signaling Pathways in Different Compartments of the Lower Airways of Patients With Stable COPD

2017

Background: The expression and localization of transforming growth factor-β (TGF-β) pathway proteins in different compartments of the lower airways of patients with stable COPD is unclear. We aimed to determine TGF-β pathway protein expression in patients with stable COPD. Methods: The expression and localization of TGF-β pathway components was measured in the bronchial mucosa and peripheral lungs of patients with stable COPD (n = 44), control smokers with normal lung function (n = 24), and control nonsmoking subjects (n = 11) using immunohistochemical analysis. Results: TGF-β1, TGF-β3, and connective tissue growth factor expression were significantly decreased in the bronchiolar epithelium…

MaleCCN2 connective tissue growth factorSmad Proteinsairway inflammationCritical Care and Intensive Care MedicineTRAP-1 transforming growth factor-β receptor-associated binding proteinPulmonary Disease Chronic ObstructiveLAP latency-associated peptideSMAD small mother against decapentaplegicBAMBI CTGF SMAD TGF-B airway inflammation autoimmunityLungTGF transforming growth factorLLC large latent complexBAMBI CTGF SMAD TGF-β Airway Inflammation AutoimmunityautoimmunityMiddle Agedrespiratory systemLTBP latent transforming growth factor-β binding proteinImmunohistochemistryTGIF 5′-TG-3′-interacting factorECM extracellular matrixTGFBI transforming growth factor-β-induced proteinFemaleCardiology and Cardiovascular MedicinePI3K phosphoinositide 3-kinaseSignal TransductionTGF-βPulmonary and Respiratory MedicineTGF-βR TGF-β receptorSocio-culturaleBronchiRespiratory MucosaArticleTGF-BTransforming Growth Factor beta1Transforming Growth Factor beta3Macrophages AlveolarHumansAgedBAMBI; CTGF; SMAD; TGF-β; airway inflammation; autoimmunityBAMBIMembrane ProteinsCTGFBMP bone morphogenetic proteinBAMBI; CTG; SMAD; TGF-β; airway inflammation; autoimmunityCTGBAMBI bone morphogenetic proteins and activin membrane-bound inhibitorrespiratory tract diseasesairway inflammation; autoimmunity; BAMBI; CTGF; SMAD; TGF-β; Pulmonary and Respiratory Medicine; Critical Care and Intensive Care Medicine; Cardiology and Cardiovascular MedicineCase-Control StudiesBiomarkersMAPK mitogen-activated protein kinaseSMAD
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation.

2014

The Ewing sarcoma family of tumors (EFT) is a group of highly malignant small round blue cell tumors occurring in children and young adults. We report here the largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines). Using a combination of whole genome sequencing and targeted sequencing approaches, we discover that EFT has a very low mutational burden (0.15 mutations/Mb) but frequent deleterious mutations in the cohesin complex subunit STAG2 (21.5% tumors, 44.4% cell lines), homozygous deletion of CDKN2A (13.8% and 50%) and mutations of TP53 (6.2% and 71.9%). We additionally note an increased prevalence of the BRCA2 K3326X polymorphism in EFT patient samples (7.3%) compared …

MaleCancer ResearchCell Cycle Proteinsmedicine.disease_causeFusion geneCDKN2AMedicine and Health Sciences2.1 Biological and endogenous factorsAetiologyChildGenetics (clinical)CancerPediatricMutationTissue microarrayTumorGenomeSarcomasHigh-Throughput Nucleotide SequencingAntigens NuclearSarcomaNeoplasm ProteinsOncologyChild PreschoolFemaleSarcomaResearch ArticleBiotechnologyHumanAdultPediatric Research Initiativelcsh:QH426-470Cohesin complexAdolescentPediatric CancerEwing SarcomaSarcoma EwingBiologyDisease-Free SurvivalFrameshift mutationCell LineGermline mutationRare DiseasesCell Line TumorEwingCancer GeneticsmedicineGeneticsHumansNuclearGenetic TestingAntigensPreschoolMolecular BiologyEcology Evolution Behavior and SystematicsGenome HumanHuman GenomeBiology and Life SciencesCancers and NeoplasmsInfantmedicine.diseaselcsh:GeneticsOrphan DrugMutationCancer researchGene DeletionDevelopmental Biology
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Alternating Hemiplegia of Childhood: neurological comorbidities and intrafamilial variability.

2022

Abstract Background Alternating of Childhood (AHC) is an uncommon and complex disorder characterized by age of onset before 18 months with recurrent hemiplegia of one or either sides of the body or quadriplegia. The disorder is mainly caused by mutations in ATP1A3 gene, and to a lesser extent in ATP1A2 gene. In AHC neurological co-morbidities are various and frequently reported including developmental delay, epilepsy, tonic or dystonic spells, nystagmus,autonomic manifestations with intrafamilial variability. Case presentation Clinical and genetic findings of a couple of twins (Family 1: Case 1 and Case 2) and a couple of siblings (Family 2: Case 3 and Case 4) coming from two different Ital…

MaleEpilepsyAlternating hemiplegia of childhood (AHC)Alternating hemiplegia of childhood (AHC) Case report Comorbidities Epilepsy GRIN2AMutation MissenseInfantHemiplegiaNeurology Behaviour and DevelopmentGRIN2AComorbiditiesCase reportMutationHumansSodium-Potassium-Exchanging ATPaseChildItalian journal of pediatrics
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ATXN2 trinucleotide repeat length correlates with risk of ALS

2017

We investigated a CAG trinucleotide repeat expansion in the ATXN2 gene in amyotrophic lateral sclerosis (ALS). Two new case-control studies, a British dataset of 1474 ALS cases and 567 controls, and a Dutch dataset of 1328 ALS cases and 691 controls were analyzed. In addition, to increase power, we systematically searched PubMed for case-control studies published after 1 August 2010 that investigated the association between ATXN2 intermediate repeats and ALS. We conducted a meta-analysis of the new and existing studies for the relative risks of ATXN2 intermediate repeat alleles of between 24 and 34 CAG trinucleotide repeats and ALS. There was an overall increased risk of ALS for those carry…

MaleExpansion0301 basic medicineAgingATXN2 geneSettore MED/03 - GENETICA MEDICA0302 clinical medicineTrinucleotide RepeatsGenetic Report AbstractAmyotrophic lateral sclerosisAtaxin-2GeneticsCAGGeneral NeuroscienceATXN2Triplet3. Good healthFemalePsychologyNeurovetenskaperRiskNeuroscience(all)Age of onsetClinical Neurology03 medical and health sciencesSCA2Trinucleotide repeatJournal ArticlemedicineHumansAlleleAllelesGenetic Association StudiesAmyotrophic lateral sclerosiIntermediate expansionNeuroscience (all)NeurosciencesExponential riskCase-control studyAmyotrophic lateral sclerosismedicine.diseaseClinical neurologyAgeing030104 developmental biologyCase-Control StudiesHuman medicineNeurology (clinical)ALSGeriatrics and GerontologyAge of onsetTrinucleotide Repeat ExpansionTrinucleotide repeat expansionALS; ATXN2; Age of onset; Amyotrophic lateral sclerosis; CAG; Expansion; Exponential risk; Intermediate expansion; Risk; SCA2; Trinucleotide repeat; TripletNeuroscience030217 neurology & neurosurgeryMeta-AnalysisDevelopmental BiologyNeurobiology of Aging
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Risk Profiles and Penetrance Estimations in Multiple Endocrine Neoplasia Type 2A Caused by Germline RET Mutations Located in Exon 10

2010

Multiple endocrine neoplasia type 2 is characterized by germline mutations in RET. For exon 10, comprehensive molecular and corresponding phenotypic data are scarce. The International RET Exon 10 Consortium, comprising 27 centers from 15 countries, analyzed patients with RET exon 10 mutations for clinical-risk profiles. Presentation, age-dependent penetrance, and stage at presentation of medullary thyroid carcinoma (MTC), pheochromocytoma, and hyperparathyroidism were studied. A total of 340 subjects from 103 families, age 4-86, were registered. There were 21 distinct single nucleotide germline mutations located in codons 609 (45 subjects), 611 (50), 618 (94), and 620 (151). MTC was present…

MalePHEOCHROMOCYTOMAendocrine system diseasesMEDULLARY-THYROID CARCINOMAAdrenal Gland NeoplasmsMultiple Endocrine Neoplasia Type 2aPenetrancemedicine.disease_causePHENOTYPEGermlineExon0302 clinical medicinemedullary thyroid carcinomaMEN2BMEN2AChildGenetics (clinical)GeneticsAged 80 and overMutationHyperparathyroidismLife SciencesExonsMiddle AgedCARRIERSPenetranceCANCERPROPHYLACTIC THYROIDECTOMY3. Good healthgenotype-phenotypeFAMILYMEN2030220 oncology & carcinogenesisChild PreschoolFemaleAdultAdolescent030209 endocrinology & metabolismMultiple endocrine neoplasia type 2BiologyPheochromocytoma03 medical and health sciencesYoung AdultGermline mutationGeneticsmedicineHumansThyroid NeoplasmsCodonGerm-Line MutationAgedNeoplasm StagingProto-Oncogene Proteins c-retCancerHIRSCHSPRUNG-DISEASEPROTOONCOGENEmedicine.diseaseGENECarcinoma NeuroendocrineCancer researchRETHuman Mutation
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