Search results for "Predisposition"

showing 10 items of 771 documents

Shared genetic etiology between alcohol dependence and major depressive disorder

2018

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Male0301 basic medicineOncologyAlcoholism/geneticsMultifactorial Inheritancealcohol dependenceMedizinGenome-wide association study0302 clinical medicineRisk FactorsGermanyMedicineGenetics (clinical)Brief ReportRegression analysisAlcoholismPsychiatry and Mental healthpolygenic risk scoresMeta-analysisComputingMethodologies_DOCUMENTANDTEXTPROCESSINGRegression AnalysisMajor depressive disorderdisease comorbidityDepressive Disorder Major/geneticsmedicine.medical_specialtyBFPolymorphism Single Nucleotide03 medical and health sciencespsychiatric genomics consortiumInternal medicineGeneticsHumansGenetic Predisposition to Diseaseddc:610Biological PsychiatryDepressive Disorder Majormajor depressive disorderbusiness.industryAlcohol dependenceCase-control studymedicine.diseaseComorbidity030104 developmental biologySample size determinationCase-Control Studiesgenome-wide association studiesRC0321business030217 neurology & neurosurgeryGenome-Wide Association Study
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Homozygous Familial Hypercholesterolemia in Spain Prevalence and Phenotype-Genotype Relationship

2016

Background— Homozygous familial hypercholesterolemia (HoFH) is a rare disease characterized by elevated plasma levels of low-density lipoprotein cholesterol (LDL-C) and extremely high risk of premature atherosclerotic cardiovascular disease. HoFH is caused by mutations in several genes, including LDL receptor ( LDLR ), apolipoprotein B ( APOB ), proprotein convertase subtilisin/kexin type 9 ( PCSK9 ), and LDL protein receptor adaptor 1 ( LDLRAP1 ). No epidemiological studies have assessed HoFH prevalence or the clinical and molecular characteristics of this condition. Here, we aimed to characterize HoFH in Spain. Methods and Results— Data were collected from the Spanish Dyslipidemia Regist…

Male0301 basic medicineOncologyLdl receptor geneApolipoprotein BLipid-lowering therapyFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosity0302 clinical medicineAutosomal-dominant hypercholesterolemiaRisk FactorsEpidemiologyPrevalenceDiseaseRegistriesGenetics (clinical)Molecular EpidemiologybiologyhypercholesterolemiaHomozygoteDouble-blindMiddle AgedPhenotypeCardiovascular DiseasesApolipoprotein B-100allelesFemalelipids (amino acids peptides and proteins)Proprotein Convertase 9Cardiology and Cardiovascular MedicineMutationsAdultGenetic MarkersHeterozygotemedicine.medical_specialtyInhibitorAdolescentPlacebo-controlled trialHyperlipoproteinemia Type IIlipidsYoung Adult03 medical and health sciencesInternal medicineGeneticsmedicineHumansGenetic Predisposition to DiseaseAlleleAdaptor Proteins Signal TransducingRecessive hypercholesterolemiaPCSK9registriesCholesterol LDLApolipoprotein-bmedicine.disease030104 developmental biologyEndocrinologyReceptors LDLSpainMutationLDL receptorbiology.proteinmutationDyslipidemia
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Genome-Wide Association Study for Incident Myocardial Infarction and Coronary Heart Disease in Prospective Cohort Studies: The CHARGE Consortium

2016

Background Data are limited on genome-wide association studies (GWAS) for incident coronary heart disease (CHD). Moreover, it is not known whether genetic variants identified to date also associate with risk of CHD in a prospective setting. Methods We performed a two-stage GWAS analysis of incident myocardial infarction (MI) and CHD in a total of 64,297 individuals (including 3898 MI cases, 5465 CHD cases). SNPs that passed an arbitrary threshold of 5×10−6 in Stage I were taken to Stage II for further discovery. Furthermore, in an analysis of prognosis, we studied whether known SNPs from former GWAS were associated with total mortality in individuals who experienced MI during follow-up. Res…

Male0301 basic medicineOncologyPREDICTIONMyocardial Infarctionlcsh:MedicineGenome-wide association studyCoronary Artery DiseaseCardiovascular MedicineSUSCEPTIBILITY030204 cardiovascular system & hematologyCardiovascularBioinformaticsincident myocardial infarctionCohort StudiesCoronary artery diseaseMathematical and Statistical Techniques0302 clinical medicineDESIGNMedicine and Health Sciences2.1 Biological and endogenous factorsProspective StudiesMyocardial infarctionAetiologyCooperative Behaviorlcsh:ScienceProspective cohort studyRISKscreening and diagnosisMultidisciplinaryResearch Support Non-U.S. Gov'tSingle NucleotideGenomicsMiddle Aged3. Good healthMultidisciplinary SciencesDetectionCHROMOSOME 9P21Heart DiseaseResearch DesignCardiovascular DiseasesCARDIOVASCULAR-DISEASEPhysical SciencesScience & Technology - Other TopicsFemaleStatistics (Mathematics)4.2 Evaluation of markers and technologiesResearch ArticleCohort studymedicine.medical_specialtyGeneral Science & TechnologyCardiologySingle-nucleotide polymorphismResearch and Analysis MethodsGenome ComplexityPolymorphism Single Nucleotide03 medical and health sciencescoronary hearth diseaseInternal medicineMD MultidisciplinaryGenome-Wide Association StudiesGeneticsJournal ArticlemedicineHumansSNPGenetic Predisposition to DiseasePolymorphismStatistical MethodsHeart Disease - Coronary Heart DiseaseMETAANALYSISAgedGenetic associationta112Science & Technologybusiness.industryPreventionlcsh:RHuman GenomeBiology and Life SciencesComputational BiologyHuman GeneticsGenome AnalysisROTTERDAMmedicine.diseaseIntronsGood Health and Well Being030104 developmental biologyGenetic LociGenetics of Diseaselcsh:Q3111 BiomedicinebusinessMathematicsMeta-AnalysisGenome-Wide Association StudyPLOS ONE
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Overall survival in patients with BRAF-mutant melanoma receiving encorafenib plus binimetinib versus vemurafenib or encorafenib (COLUMBUS): a multice…

2018

Summary Background Encorafenib plus binimetinib and encorafenib alone improved progression-free survival compared with vemurafenib in patients with BRAF V600 -mutant melanoma in the COLUMBUS trial. Here, we report the results of the secondary endpoint of overall survival. Methods COLUMBUS was a two-part, randomised, open-label, phase 3 study done at 162 hospitals in 28 countries. Eligible patients were aged at least 18 years with histologically confirmed, locally advanced, unresectable, or metastatic cutaneous melanoma, or unknown primary melanoma, BRAF V600E or BRAF V600K mutation, an Eastern Cooperative Oncology Group (ECOG) performance status of 0 or 1, and were treatment naive or had pr…

Male0301 basic medicineOncologySkin NeoplasmsTime FactorsMedizinPhases of clinical researchGene mutationchemistry.chemical_compound0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsVemurafenibMelanomaAged 80 and overTrametinibSulfonamides10177 Dermatology ClinicBinimetinibMiddle AgedProgression-Free SurvivalPhenotypeOncologyTolerability030220 oncology & carcinogenesisDisease ProgressionFemale2730 Oncologymedicine.drugAdultProto-Oncogene Proteins B-rafmedicine.medical_specialty610 Medicine & healthYoung Adult03 medical and health sciencesInternal medicineBiomarkers TumormedicineHumansGenetic Predisposition to DiseaseProgression-free survivalProtein Kinase InhibitorsAgedPerformance statusbusiness.industry030104 developmental biologyVemurafenibchemistryMutationBenzimidazolesCarbamatesbusinessThe Lancet Oncology
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Shared Genetic Etiology of Obesity-Related Traits and Barrett's Esophagus/Adenocarcinoma: Insights from Genome-Wide Association Studies

2020

Abstract Background: Obesity is a major risk factor for esophageal adenocarcinoma (EA) and its precursor Barrett's esophagus (BE). Research suggests that individuals with high genetic risk to obesity have a higher BE/EA risk. To facilitate understanding of biological factors that lead to progression from BE to EA, the present study investigated the shared genetic background of BE/EA and obesity-related traits. Methods: Cross-trait linkage disequilibrium score regression was applied to summary statistics from genome-wide association meta-analyses on BE/EA and on obesity traits. Body mass index (BMI) was used as a proxy for general obesity, and waist-to-hip ratio (WHR) for abdominal obesity. …

Male0301 basic medicineOncologymedicine.medical_specialtyEsophageal NeoplasmsEpidemiologyQuantitative Trait LocieducationMedizinMEDLINEGenome-wide association studyAdenocarcinomaPolymorphism Single NucleotideRisk AssessmentLinkage DisequilibriumBody Mass IndexBarrett Esophagus03 medical and health sciencesSex Factors0302 clinical medicineMeta-Analysis as TopicRisk FactorsInternal medicineHumansMedicineGenetic Predisposition to DiseaseObesityEsophagusWaist-Hip Ratiobusiness.industryEsophageal cancermedicine.diseaseMedical researchObesityRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]030104 developmental biologymedicine.anatomical_structureOncology030220 oncology & carcinogenesisBarrett's esophagusDisease ProgressionAdenocarcinomaFemalebusinessGenome-Wide Association StudyCancer Epidemiology, Biomarkers & Prevention
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A Multi-Locus Genetic Risk Score for Primary Open-Angle Glaucoma (POAG) Variants Is Associated with POAG Risk in a Mediterranean Population: Inverse …

2017

Primary open-angle glaucoma (POAG) is a leading cause of blindness worldwide. The genetics of POAG are complex, and population-specific effects have been reported. Although many polymorphisms associated with POAG risk have been reported, few studies have analyzed their additive effects. We investigated, in a southern European Mediterranean population, the association between relevant POAG polymorphisms, identified by initial genome-wide association studies (GWASs) and POAG risk, both separately and as an aggregated multi-locus genetic risk score (GRS). Also, bearing in mind that oxidative stress is a factor increasingly recognized in the pathogenesis of POAG, we analyzed the potential assoc…

Male0301 basic medicineOncologyprimary open-angle glaucomagenetic structuresmedicine.medical_treatmentvitamin CGenome-wide association studyAscorbic Acidvitamin EBioinformaticslcsh:Chemistry0302 clinical medicineRisk FactorsGenotypeVitamin EGWASgeneticsVitamin Clcsh:QH301-705.5Spectroscopyeducation.field_of_studyMediterranean RegionGeneral MedicineMiddle AgedGenetic risk scoreComputer Science ApplicationsnutritionFemalePrimary open-angle glaucomaGlaucoma Open-Anglemedicine.medical_specialtyGenotypePopulationgenetic risk scoreArticleCatalysisInorganic Chemistry03 medical and health sciencesInternal medicineGeneticsmedicineHumansGenetic Predisposition to DiseasePhysical and Theoretical ChemistryeducationMolecular BiologyNutritionAgedGenetic associationPolymorphism Geneticbusiness.industryVitamin EfungiOrganic Chemistryprimary open-angle glaucoma; genetics; GWAS; nutrition; vitamin C; vitamin E; genetic risk scoreCase-control studyAscorbic acideye diseasesConfidence interval030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Genetic LociCase-Control Studies030221 ophthalmology & optometrybusinessGenome-Wide Association StudyInternational Journal of Molecular Sciences
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Molecular properties underlying regional vulnerability to Alzheimer’s disease pathology

2018

Amyloid deposition and neurofibrillary degeneration in Alzheimer's disease specifically affect discrete neuronal systems, but the underlying mechanisms that render some brain regions more vulnerable to Alzheimer's disease pathology than others remain largely unknown. Here we studied molecular properties underlying these distinct regional vulnerabilities by analysing Alzheimer's disease-typical neuroimaging patterns of amyloid deposition and neurodegeneration in relation to regional gene expression profiles of the human brain. Graded patterns of brain-wide vulnerability to amyloid deposition and neurodegeneration in Alzheimer's disease were estimated by contrasting multimodal amyloid-sensiti…

Male0301 basic medicinePathologyphysiology [Amyloidogenic Proteins]genetics [Transcriptome]genetics [Alzheimer Disease]Cohort StudiesTranscriptomepathology [Alzheimer Disease]metabolism [Amyloidogenic Proteins]methods [Magnetic Resonance Imaging]0302 clinical medicinepathology [Brain]Gene expressiongenetics [Genetic Predisposition to Disease]Aged 80 and overmethods [Positron-Emission Tomography]NeurodegenerationBrainNeurofibrillary TanglesHuman brainMagnetic Resonance Imagingmetabolism [Neurofibrillary Tangles]medicine.anatomical_structureFemalemethods [Neuroimaging]Alzheimer's Disease Neuroimaging InitiativeAmyloidmedicine.medical_specialtyAmyloidmetabolism [Amyloid beta-Peptides]Amyloidogenic ProteinsNeuroimagingtau ProteinsBiology03 medical and health sciencesAlzheimer DiseasemedicineHumansDementiaGenetic Predisposition to Diseaseddc:610metabolism [Amyloid]AgedAmyloid beta-PeptidesCyclin-dependent kinase 5medicine.diseasemetabolism [tau Proteins]030104 developmental biologyPositron-Emission Tomographypathology [Neurofibrillary Tangles]Neurology (clinical)Transcriptome030217 neurology & neurosurgeryBrain
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The landscape of epilepsy-related GATOR1 variants

2019

Purpose:\ud \ud To define the phenotypic and mutational spectrum of epilepsies related to DEPDC5, NPRL2 and NPRL3 genes encoding the GATOR1 complex, a negative regulator of the mTORC1 pathway.\ud \ud Methods:\ud \ud We analyzed clinical and genetic data of 73 novel probands (familial and sporadic) with epilepsy-related variants in GATOR1-encoding genes and proposed new guidelines for clinical interpretation of GATOR1 variants.\ud \ud Results:\ud \ud The GATOR1 seizure phenotype consisted mostly in focal seizures (e.g., hypermotor or frontal lobe seizures in 50%), with a mean age at onset of 4.4 years, often sleep-related and drug-resistant (54%), and associated with focal cortical dysplasia…

Male0301 basic medicineProbandDEPDC5SUDEP030105 genetics & heredityBioinformaticsLoss of Function Mutation/geneticsEpilepsyINDEL MutationLoss of Function MutationmTORC1 pathwayGenetics(clinical)ChildGenetics (clinical)Multiprotein Complexes/geneticsBrugada SyndromeDNA Copy Number VariationBrugada syndromeINDEL Mutation/geneticsGTPase-Activating ProteinsNPRL3SeizureDEPDC5PhenotypePedigree3. Good healthBrugada Syndrome/geneticsChild PreschoolFemaleHumanSignal TransductionDNA Copy Number VariationsAdolescentSeizures/complicationsMechanistic Target of Rapamycin Complex 1/geneticsDNA Copy Number Variations/geneticsMechanistic Target of Rapamycin Complex 1Tumor Suppressor Proteins/geneticsArticleFocal cortical dysplasia03 medical and health sciencesSeizuresGTPase-Activating Proteins/geneticsmedicineHumansGenetic Predisposition to DiseaseDEPDC5; Focal cortical dysplasia; Genetic focal epilepsy; mTORC1 pathway; SUDEPGenetic focal epilepsyEpilepsy/complicationsRepressor Proteins/geneticsEpilepsybusiness.industryGTPase-Activating ProteinTumor Suppressor ProteinsInfant NewbornCorrectionInfantRepressor ProteinCortical dysplasiamedicine.diseaseddc:616.8Repressor Proteins030104 developmental biologyFrontal lobe seizures[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsMultiprotein ComplexesMultiprotein ComplexeSignal Transduction/geneticsHuman medicinebusiness
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Exonic Mosaic Mutations Contribute Risk for Autism Spectrum Disorder

2017

AbstractGenetic risk factors for autism spectrum disorder (ASD) have yet to be fully elucidated. Postzygotic mosaic mutations (PMMs) have been implicated in several neurodevelopmental disorders and overgrowth syndromes. We systematically evaluated PMMs by leveraging whole-exome sequencing data on a large family-based ASD cohort, the Simons Simplex Collection. We found evidence that 11% of published single nucleotide variant (SNV)de novomutations are potentially PMMs. We then developed a robust SNV PMM calling approach that leverages complementary callers, logistic regression modeling, and additional heuristics. Using this approach, we recalled SNVs and found that 22% ofde novomutations like…

Male0301 basic medicineProbandZygoteautism spectrum disorderSYNGAP1Biologypostzygoticmedicine.disease_causeArticleGermlineCohort Studies03 medical and health sciencessplicing0302 clinical medicineNeurodevelopmental disorderGermline mutationDatabases GeneticGeneticsmedicineHumansMissense mutationGenetic Predisposition to DiseaseChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsGenetics (clinical)030304 developmental biologyGenetics0303 health sciencesMutationneurodevelopmentsomaticGenetic VariationExonsmedicine.disease030104 developmental biologymosaicism[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsAutism spectrum disorderCHD2AutismFemalemutation030217 neurology & neurosurgeryexome
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Gluten Degrading Enzymes for Treatment of Celiac Disease

2020

Celiac disease (CeD) affects about 1% of most world populations. It presents a wide spectrum of clinical manifestations, ranging from minor symptoms to mild or severe malabsorption, and it may be associated with a wide variety of autoimmune diseases. CeD is triggered and maintained by the ingestion of gluten proteins from wheat and related grains. Gluten peptides that resist gastrointestinal digestion are antigenically presented to gluten specific T cells in the intestinal mucosa via HLA-DQ2 or HLA-DQ8, the necessary genetic predisposition for CeD. To date, there is no effective or approved treatment for CeD other than a strict adherence to a gluten-free diet, which is difficult to maintain…

Male0301 basic medicineProteasesGlutensDrug CompoundingT-Lymphocytesenzyme therapylcsh:TX341-641ReviewBiologyDiet Gluten-Free03 medical and health sciences0302 clinical medicineAntigenIntestinal mucosaglutenasewheatHLA-DQ AntigensEnzyme StabilityGenetic predispositionHumansGenetic Predisposition to Diseaseenteric coatingSubtilisinsendopeptidasechemistry.chemical_classificationNutrition and Dieteticstreatmentfungiautoimmunitynutritional and metabolic diseasesGlutendigestive system diseasesGlutamine030104 developmental biologyEnzymeBiochemistrychemistryglutenProteolysisFemale030211 gastroenterology & hepatologyProlyl OligopeptidasesSubtilisinslcsh:Nutrition. Foods and food supplyceliac diseaseFood ScienceNutrients
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