Search results for "AETIOLOGY"

showing 10 items of 94 documents

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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Global Functional Analyses of Cellular Responses to Pore-Forming Toxins

2011

Here we present the first global functional analysis of cellular responses to pore-forming toxins (PFTs). PFTs are uniquely important bacterial virulence factors, comprising the single largest class of bacterial protein toxins and being important for the pathogenesis in humans of many Gram positive and Gram negative bacteria. Their mode of action is deceptively simple, poking holes in the plasma membrane of cells. The scattered studies to date of PFT-host cell interactions indicate a handful of genes are involved in cellular defenses to PFTs. How many genes are involved in cellular defenses against PFTs and how cellular defenses are coordinated are unknown. To address these questions, we pe…

MAPK/ERK pathwayTranscription GeneticImmunology/Innate ImmunityMessengerInteractomeInfectious Diseases/Bacterial InfectionsRNA interference2.1 Biological and endogenous factorsAetiologyBiology (General)Genes HelminthCaenorhabditis elegansOligonucleotide Array Sequence AnalysisGenetics0303 health sciencesGenomebiologyReverse Transcriptase Polymerase Chain ReactionGenetics and Genomics/Functional Genomics030302 biochemistry & molecular biologyrespiratory systemCell biologyInfectious DiseasesMedical MicrobiologyRNA InterferenceSignal transductionDNA microarrayTranscriptionBiotechnologyResearch ArticleSignal TransductionPore Forming Cytotoxic ProteinsQH301-705.5Virulence FactorsMAP Kinase Signaling System1.1 Normal biological development and functioningBacterial ToxinsImmunologyMicrobiologyDNA-binding proteinCell Line03 medical and health sciencesBacterial ProteinsGeneticUnderpinning researchVirologyEscherichia coliHelminthGeneticsAnimalsHumansRNA MessengerCaenorhabditis elegansCaenorhabditis elegans ProteinsMolecular BiologyGene030304 developmental biologyGenome HelminthCell MembraneGenetics and GenomicsRC581-607biology.organism_classificationrespiratory tract diseasesTranscription Factor AP-1Emerging Infectious DiseasesGenesRNAParasitologyGeneric health relevanceRNA HelminthImmunologic diseases. AllergyPLoS Pathogens
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Transcriptomic metaanalyses of autistic brains reveals shared gene expression and biological pathway abnormalities with cancer

2019

Este es el artículo que se ha publicado de forma definitiva en: https://molecularautism.biomedcentral.com/articles/10.1186/s13229-019-0262-8 En este artículo también participa Joan Climent, Vera Pancaldi, Lourdes Fañanás, Celso Arango, Mara Parellada, Anaïs Baudot, Daniel Vogt, John L. Rubenstein, Alfonso Valencia y Rafael Tabarés-Seisdedos. Background: Epidemiological and clinical evidence points to cancer as a comorbidity in people with autism spectrum disorders (ASD). A significant overlap of genes and biological processes between both diseases has also been reported. Methods: Here, for the first time, we compared the gene expression profiles of ASD frontal cortex tissues and 22 cancer t…

Autism.AutismComorbidityBioinformaticsAutismo.lcsh:RC346-429Expresión génica.TranscriptomeAfectividad - Trastornos.0302 clinical medicineNeoplasmsGene expression2.1 Biological and endogenous factorsAetiologyCàncerCáncer - Aspectos genéticos.ComputingMilieux_MISCELLANEOUSCancer0303 health sciencesProstate CancerBrainAffective disorders.3. Good healthPsychiatry and Mental healthMental HealthSignal transductionSignal TransductionBiotechnologyUrologic DiseasesIntellectual and Developmental Disabilities (IDD)1.1 Normal biological development and functioningClinical SciencesBiologyASDBiological pathway03 medical and health sciencesDevelopmental NeuroscienceUnderpinning researchmental disordersGeneticsmedicineHumansAutistic DisorderIntellectual and Developmental DisabilitiesGeneMolecular Biologylcsh:Neurology. Diseases of the nervous systemPI3K/AKT/mTOR pathwayCancer - Genetic aspects.030304 developmental biologyResearchNeurosciencesMultimorbidityCancermedicine.diseaseExpressió gènicaHuman geneticsBrain DisordersMeta-analysisGene expression.AutismGene expressionAutisme[INFO.INFO-BI]Computer Science [cs]/Bioinformatics [q-bio.QM]TranscriptomeKidney cancer030217 neurology & neurosurgeryDevelopmental BiologyMolecular Autism
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Biomarkers in heart failure

2009

Nowadays, heart failure (HF) has an increasing prevalence, particularly in the elderly, and is becoming a clinical problem of epidemic proportion in terms of morbidity and mortality. Developing biological markers, that can aid in the diagnosis of HF and in the differentiation of congestive heart failure (CHF) from other causes of dyspnoea, will reduce the cost of health care. However, an ideal biomarker has not yet been identified. Potential markers of HF include neuro-hormonal mediators, markers of myocyte injury, and indicators of systemic inflammation. Among these, the BNP and NT-pro-BNP are the most widely studied and appear to be useful in patients with dyspnoea of unknown aetiology, a…

Heart Failuremedicine.medical_specialtybusiness.industryUnknown aetiologymedicine.diseaseSystemic inflammationHeart failureHealth caremedicineBiomarker (medicine)HumansIn patientMyocyte injurymedicine.symptomBiomarkers heart failurebusinessIntensive care medicineRisk assessmentBiomarkers
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Genetic association analysis identifies variants associated with disease progression in primary sclerosing cholangitis

2018

ObjectivePrimary sclerosing cholangitis (PSC) is a genetically complex, inflammatory bile duct disease of largely unknown aetiology often leading to liver transplantation or death. Little is known about the genetic contribution to the severity and progression of PSC. The aim of this study is to identify genetic variants associated with PSC disease progression and development of complications.DesignWe collected standardised PSC subphenotypes in a large cohort of 3402 patients with PSC. After quality control, we combined 130 422 single nucleotide polymorphisms of all patients—obtained using the Illumina immunochip—with their disease subphenotypes. Using logistic regression and Cox proportiona…

Male0301 basic medicineOncologyCandidate geneCholangitismedicine.medical_treatmentMedizinTrasplantament hepàticGenome-wide association studyKaplan-Meier EstimateLIVER FIBROSISLiver transplantationBioinformaticsSclerosingOral and gastrointestinalPrimary sclerosing cholangitis; genetics; liver transplantationCohort StudiesACTIVATION0302 clinical medicineMED/12 - GASTROENTEROLOGIAMULTIPLE2.1 Biological and endogenous factorsEPIDEMIOLOGYgeneticsAetiologyCIRRHOSISliver transplantationBilious diseases and biliousnessPrimary sclerosing cholangitisLiver Diseasedigestive oral and skin physiologyGastroenterologySingle NucleotidePrimary sclerosing cholangitiMiddle Aged3. Good healthULCERATIVE-COLITISDisease ProgressionFemale030211 gastroenterology & hepatologyAdultmedicine.medical_specialtyCholangitis SclerosingChronic Liver Disease and CirrhosisClinical SciencesMalalties del tracte biliarSingle-nucleotide polymorphismHEPATIC STELLATE CELLSPolymorphism Single NucleotideInternational PSC Study GroupArticlePrimary sclerosing cholangitisPaediatrics and Reproductive Medicine03 medical and health sciencesRare DiseasesClinical ResearchInternal medicineGeneticsmedicineHumansPolymorphismGENOME-WIDE ASSOCIATIONAlleleDigestive Diseases - (Gallbladder)Survival analysisProportional Hazards ModelsMALIGNANCYThe UK PSC ConsortiumTransplantationGastroenterology & Hepatologybusiness.industryProportional hazards modelmedicine.diseaseRISK LOCILogistic Models030104 developmental biology3121 General medicine internal medicine and other clinical medicinegeneticHepatic transplantationThrombospondinsDigestive DiseasesbusinessGenèticaGut
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Acquired BRAF inhibitor resistance: A multicenter meta-analysis of the spectrum and frequencies, clinical behaviour, and phenotypic associations of r…

2015

BackgroundAcquired resistance to BRAF inhibitors (BRAFi) is a near-universal phenomenon caused by numerous genetic and non-genetic alterations. In this study, we evaluated the spectrum, onset, pattern of progression, and subsequent clinical outcomes associated with specific mechanisms of resistance.MethodsWe compiled clinical and genetic data from 100 patients with 132 tissue samples obtained at progression on BRAFi therapy from 3 large, previously published studies of BRAFi resistance. These samples were subjected to whole-exome sequencing and/or polymerase chain reaction-based genetic testing.ResultsAmong 132 samples, putative resistance mechanisms were identified in 58%, including NRAS o…

OncologyNeuroblastoma RAS viral oncogene homologMaleCancer ResearchSkin NeoplasmsTime FactorsResistanceDNA Mutational AnalysisDrug ResistanceMedizinKaplan-Meier EstimateBioinformaticsmedicine.disease_causeRisk Factors2.1 Biological and endogenous factorsAetiologyVemurafenibMelanomaCancerMutationTumorDabrafenibMelanomaAcquiredMiddle AgedPhenotypeEuropePhenotypeTreatment OutcomeSpliceOncologyMeta-analysisPublic Health and Health ServicesDisease ProgressionFemalemedicine.drugSignal TransductionProto-Oncogene Proteins B-rafmedicine.medical_specialtyOncology and CarcinogenesisNRASAntineoplastic AgentsBiologyDisease-Free SurvivalArticleBRAFMEK1Clinical ResearchInternal medicineGeneticsmedicineBiomarkers TumorHumansGenetic Predisposition to DiseaseOncology & CarcinogenesisProtein Kinase InhibitorsProportional Hazards ModelsProportional hazards modelAustraliaDabrafenibmedicine.diseaseMAPKUnited StatesMeta-analysisVemurafenibDrug Resistance NeoplasmMutationNeoplasmBiomarkersEuropean journal of cancer (Oxford, England : 1990)
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Axons take a dive

2014

In the walls of the lateral ventricles of the adult mammalian brain, neural stem cells (NSCs) and ependymal (E1) cells share the apical surface of the ventricular-subventricular zone (V-SVZ). In a recent article, we show that supraependymal serotonergic (5HT) axons originating from the raphe nuclei in mice form an extensive plexus on the walls of the lateral ventricles where they contact E1 cells and NSCs. Here we further characterize the contacts between 5HT supraependymal axons and E1 cells in mice, and show that suprependymal axons tightly associated to E1 cells are also present in the walls of the human lateral ventricles. These observations raise interesting questions about the functio…

Ependymal Cell1.1 Normal biological development and functioningBiologySerotonergicArticleLateral ventriclesDevelopmental NeuroscienceUnderpinning research2.1 Biological and endogenous factorshumanAetiologyneural stem cellsPlexusNeurogenesisNeurosciencesependymal cellsAnatomyStem Cell ResearchNeural stem cellserotoninsupraependymal axonsadult neurogenesisnervous systemNeurologicalSerotoninRaphe nucleiNeuroscienceDevelopmental BiologyNeurogenesis
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Placental DNA methylation signatures of maternal smoking during pregnancy and potential impacts on fetal growth.

2021

We would like to thank all the families that participated in these studies for their generous contribution. Detailed acknowledgements and funding can be found in Sup plementary Material.

EpigenomicsMaternal smokingPlacentaGeneral Physics and AstronomyReproductive health and childbirthBioinformaticsLow Birth Weight and Health of the NewbornEpigenesis GeneticFetal DevelopmentPregnancyInfant MortalityFetal growth2.1 Biological and endogenous factorsAetiologyPediatricMultidisciplinaryQSmokingCord bloodDNA methylationEpigeneticsFemalemedicine.symptomScience1.1 Normal biological development and functioningInflammationFetus -- Trastorns del creixementBiologyGeneral Biochemistry Genetics and Molecular BiologyArticleGenetic HeterogeneityGeneticPretermUnderpinning researchTobaccomedicineGeneticsHumansEpigeneticsConditions Affecting the Embryonic and Fetal PeriodsNucleotide MotifsPregnancyHormone activitydNaMGeneral ChemistryEpigenomeDNA MethylationPerinatal Period - Conditions Originating in Perinatal Periodmedicine.diseaseEmbarassades -- Consum de tabacGood Health and Well BeingRisk factorsEpigenesis
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Reduced In Vivo Aortic Uptake of Radiolabeled Oxidation-Specific Antibodies Reflects Changes in Plaque Composition Consistent With Plaque Stabilizati…

2004

Objective— Labeled oxidation-specific antibodies (Ox-AB) detect, quantify, and noninvasively image lipid-rich atherosclerotic lesions. However, it is unknown whether Ox-AB detect plaque stabilization. Methods and Results— The aortic uptake of intravenously injected 125 I-MDA2 (Ox-AB to malondialdehyde [MDA]–low-density lipoprotein [LDL]) was quantitated in: (1) LDL receptor−/− mice with established atherosclerosis continued on Western diet (Progression) or switched to chow (Regression) or chow+vitamins E and C (Regression-VIT) for 6 months; and (2) Watanabe rabbits (3- to 57-months old) with naturally evolved atherosclerotic lesions. In mice, the Progression group had more extensive athero…

AgingPathologyArteriosclerosisCardiorespiratory Medicine and HaematologyCardiovascularIodine RadioisotopesMiceEpitopeschemistry.chemical_compoundAntibody SpecificityMalondialdehydeReceptorsMonoclonal2.1 Biological and endogenous factorsMacrophageAetiologyradionuclideAortaFibrous capAntibodies MonoclonalimagingMalondialdehydeImmunohistochemistryLipoproteins LDLMutant StrainsHeart Diseasemedicine.anatomical_structurelipids (amino acids peptides and proteins)RabbitsCardiology and Cardiovascular MedicineOxidation-ReductionBlood vesselmedicine.medical_specialtyoxidationLipoproteinsClinical SciencesBiologyAntibodiesLDLIn vivomedicine.arterymedicineAnimalsHeart Disease - Coronary Heart DiseaseAortaAtherosclerosisMice Mutant StrainsReceptors LDLRadioimmunodetectionCardiovascular System & HematologychemistryImmunostainingLipoproteinArteriosclerosis, Thrombosis, and Vascular Biology
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2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases…

2015

Guidelines summarize and evaluate all available evidence on a particular issue at the time of the writing process, with the aim of assisting health professionals in selecting the best management strategies for an individual patient with a given condition, taking into account the impact on outcome, as well as the risk–benefit ratio of particular diagnostic or therapeutic means. Guidelines and recommendations should help health professionals to make decisions in their daily practice. However, the final decisions concerning an individual patient must be made by the responsible health professional(s) in consultation with the patient and caregiver as appropriate.

PericardiocentesiPrognosiMyopericarditiTamponadeConstrictive pericarditiPericardial effusionPericarditiTherapyAetiologyGuidelinePericardiumDiagnosi
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