Search results for "MUTATIONS"

showing 10 items of 205 documents

Myelodysplastic syndromes with 20q deletion: incidence, prognostic value and impact on response to azacitidine of ASXL1 chromosomal deletion and gene…

2021

In myelodysplastic syndromes (MDS), the 20q deletion [del(20q)] may cause deletion of the ASXL1 gene. We studied 153 patients with MDS and del(20q) to assess the incidence, prognostic value and impact on response to azacitidine (AZA) of ASXL1 chromosomal alterations and genetic mutations. Additionally, in vitro assay of the response to AZA in HAP1 (HAP1(WT)) and HAP1 ASXL1 knockout (HAP1(KN)) cells was performed. ASXL1 chromosomal alterations were detected in 44 patients (28 center dot 5%): 34 patients (22%) with a gene deletion (ASXL1(DEL)) and 10 patients (6 center dot 5%) with additional gene copies. ASXL1(DEL) was associated with a lower platelet count. The most frequently mutated genes…

MaleOncologyAntimetabolites Antineoplasticazacitidinemedicine.medical_specialtyAzacitidineASXL1Gene mutationInternal medicinemedicineHumansGeneChromosomal DeletionAged20q deletiongene mutationsAged 80 and overbusiness.industryIncidenceMyelodysplastic syndromesIncidence (epidemiology)Hazard ratioHematologyMiddle AgedPrognosismedicine.diseasemyelodysplastic syndromesConfidence intervalRepressor ProteinsMyelodysplastic SyndromesMutationAzacitidineFemaleChromosome Deletionbusinessmedicine.drugBritish Journal of Haematology
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The Insulin Receptor Substrate 1 (Irs1) in Intestinal Epithelial Differentiation and in Colorectal Cancer

2012

Colorectal cancer (CRC) is associated with lifestyle factors that affect insulin/IGF signaling, of which the insulin receptor substrate 1 (IRS1) is a key transducer. We investigated expression, localization and pathologic correlations of IRS1 in cancer-uninvolved colonic epithelium, primary CRCs with paired liver metastases and in vitro polarizing Caco2 and HT29 cells. IRS1 mRNA and protein resulted higher, relative to paired mucosa, in adenomas of familial adenomatous polyposis patients and in CRCs that overexpressed c-MYC, ß-catenin, InsRß, and IGF1R. Analysis of IRS1 immunostaining in 24 cases of primary CRC with paired colonic epithelium and hepatic metastasis showed that staining inten…

MalePathologyAnatomy and PhysiologySettore MED/06 - Oncologia MedicaMetastasisIntestinal mucosaInsulin Signaling CascadeMolecular Cell BiologyGastrointestinal CancersBasic Cancer ResearchInsulinIntestinal MucosaInsulin-like Growth FactorCOLON-CARCINOMA-CELLS; GROWTH-FACTOR RECEPTOR; BETA-CATENIN; FACTOR-I; IGF-I; NUCLEAR TRANSLOCATION; ADENOMATOUS POLYPOSIS; STEM-CELL; EXPRESSION; MUTATIONSMultidisciplinarybiologyChemistryQLiver NeoplasmsRCell PolarityCell DifferentiationSignaling CascadesGene Expression Regulation NeoplasticProtein Transportmedicine.anatomical_structureOncologyMedicineFemaleColorectal NeoplasmsHT29 CellsResearch ArticleSignal TransductionAdultendocrine systemmedicine.medical_specialtyColonScienceIRS1 IGF1R colorectal cancerEndocrine SystemGastroenterology and HepatologySignaling PathwaysFamilial adenomatous polyposisHT29 CellsmedicineHumansBiologyAgedInsulin-like growth factor 1 receptorEndocrine Physiologymedicine.diseasedigestive system diseasesEpitheliumIRS1Insulin receptorInsulin Receptor Substrate Proteinsbiology.proteinCancer researchCaco-2 CellsImmunostainingInsulin-Dependent Signal Transduction
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NEXMIF encephalopathy: an X-linked disorder with male and female phenotypic patterns

2021

Contains fulltext : 231688.pdf (Publisher’s version ) (Closed access) PURPOSE: Pathogenic variants in the X-linked gene NEXMIF (previously KIAA2022) are associated with intellectual disability (ID), autism spectrum disorder, and epilepsy. We aimed to delineate the female and male phenotypic spectrum of NEXMIF encephalopathy. METHODS: Through an international collaboration, we analyzed the phenotypes and genotypes of 87 patients with NEXMIF encephalopathy. RESULTS: Sixty-three females and 24 males (46 new patients) with NEXMIF encephalopathy were studied, with 30 novel variants. Phenotypic features included developmental delay/ID in 86/87 (99%), seizures in 71/86 (83%) and multiple comorbidi…

MalePediatricsmedicine.medical_specialtyINTELLECTUAL DISABILITYAutism Spectrum DisorderEncephalopathyNerve Tissue ProteinsILAE COMMISSIONMOSAICISMEpilepsy/geneticsCLASSIFICATIONEpilepsyBrain Diseases/geneticsGenes X-LinkedSeizuresIntellectual disabilityGenotypemedicineHumansdevelopmental and epileptic encephalopathyMYOCLONIAAtonic seizureGenetics (clinical)Brain Diseasesddc:618Neurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]KIAA2022business.industryMUTATIONSmedicine.diseasePhenotypeAutism Spectrum Disorder/geneticsGenes X-Linked/geneticsAutism spectrum disorderintellectual disabilityNEXMIFAutismepilepsyFemaleINACTIVATIONHuman medicineSeizures/geneticsbusinessPOSITION PAPERGenetics in Medicine
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TP53 in gastric cancer: mutations in the l3 loop and LSH motif DNA-binding domains of TP53 predict poor outcome.

2004

The aim of this study was to clarify whether specific p53 mutations may have biological relevance in terms of disease relapse or death in gastric carcinomas (GC). Resected specimens from a consecutive series of 62 patients with GC undergoing potentially curative surgery were prospectively studied. The mutational status of exons 5-8 of the p53 gene was investigated in 62 cases using the PCR-SSCP and sequencing. Presence of microsatellite instability (MSI) was evaluated in 56 cases by analyzing loci highly sensitive of MSI. Twenty mutations of p53 were detected in 17 of the 62 cases analyzed (27%). Ten mutations (50%) occurred in highly conserved domains. According to the p53 specific functio…

MalePhysiologyClinical BiochemistryBiologyBioinformaticsExonchemistry.chemical_compoundAge DistributionStomach NeoplasmsmedicineHumansCancer mutationsTP53Prospective StudiesProspective cohort studyGeneSurvival analysisPolymorphism Single-Stranded ConformationalAgedNeoplasm StagingCarcinomaMicrosatellite instabilityCell BiologyDNA-binding domainDNA NeoplasmExonsMiddle Agedmedicine.diseaseGenes p53PrognosisSurvival AnalysisProtein Structure TertiarychemistryItalyMutationCancer researchFemaleDNAFollow-Up StudiesMicrosatellite RepeatsJournal of cellular physiology
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Autoimmune polyendocrine syndrome type 1: an Italian survey on 158 patients

2021

Abstract Background Autoimmune Polyglandular Syndrome type 1 (APS-1) is a rare recessive inherited disease, caused by AutoImmune Regulator (AIRE) gene mutations and characterized by three major manifestations: chronic mucocutaneous candidiasis (CMC), chronic hypoparathyroidism (CH) and Addison’s disease (AD). Methods Autoimmune conditions and associated autoantibodies (Abs) were analyzed in 158 Italian patients (103 females and 55 males; F/M 1.9/1) at the onset and during a follow-up of 23.7 ± 15.1 years. AIRE mutations were determined. Results The prevalence of APS-1 was 2.6 cases/million (range 0.5–17 in different regions). At the onset 93% of patients presented with one or more component…

MaleTranscription FactorEndocrinology Diabetes and MetabolismAutoimmune hepatitisGene mutationGastroenterologyChronic mucocutaneous candidiasisEndocrinologyAddison DiseaseAutoimmune Polyglandular Syndrome type 1 (APS-1)PrevalenceMedicineChronic mucocutaneous candidiasisPolyendocrinopathies AutoimmuneCandidiasis Chronic MucocutaneouAddison’s disease AIRE gene mutations Autoimmune Polyglandular Syndrome type 1 (APS-1) Autoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED) Chronic hypoparathyroidism Chronic mucocutaneous candidiasis Interferon autoantibodiesCandidiasis Chronic MucocutaneousAIRE gene mutations; Addison’s disease; autoimmune polyglandular syndrome type 1 (APS-1); autoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED); chronic hypoparathyroidism; chronic mucocutaneous candidiasis; interferon autoantibodiesAutoimmune regulatorAutoantibodieItalyInterferon autoantibodieAddison's diseaseInterferon Type IOriginal ArticleFemaleChronic hypoparathyroidismHumanAdultmedicine.medical_specialtyAutoimmune GastritisHypoparathyroidismAddison’s diseaseAIRE gene mutationsInternal medicineInterferon autoantibodiesHumansMortalityAutoantibodiesAddison’s disease; AIRE gene mutations; Autoimmune Polyglandular Syndrome type 1 (APS-1); Autoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED); Chronic hypoparathyroidism; Chronic mucocutaneous candidiasis; Interferon autoantibodiesbusiness.industryChronic mucocutaneous candidiasiAIRE gene mutationAutoantibodymedicine.diseaseAutoimmune-poly-endocrine-candidiasis-ectodermal-dystrophy (APECED)Interferon autoantibodies.Autoimmune polyendocrine syndrome type 1MutationbusinessTranscription Factors
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Pan-cancer analysis of whole genomes

2020

Publisher's version (útgefin grein)

Maletert promoter mutationsCancer development and immune defence Radboud Institute for Molecular Life Sciences [Radboudumc 2]DNA Mutational AnalysisNormal tissuesystematic analysisGermlineTranscriptome0302 clinical medicineAetiologyCàncerCellular SenescenceCancer0303 health sciencesdna-damageMassive parallel sequencingPan cancerREARRANGEMENTSHigh-Throughput Nucleotide SequencingGenomicsSciences bio-médicales et agricolesTelomereCOMPREHENSIVE3. Good healthTERT PROMOTER MUTATIONSsignatures030220 oncology & carcinogenesisScience & Technology - Other TopicsErfðarannsóknirHuman:Informàtica::Aplicacions de la informàtica::Bioinformàtica [Àrees temàtiques de la UPC]EvolutionRNA SplicingGenomicsArticleEvolution MolecularStructural variationRC025403 medical and health sciencesSDG 3 - Good Health and Well-beingGeneticgenomicsSYSTEMATIC ANALYSISGeneticsGenomics--Databases.HumansGenetic TestingMolecular BiologySIGNATURESWhole genome sequencing1000 MultidisciplinaryChromothripsisScience & TechnologyRC0254 Neoplasms. Tumors. Oncology (including Cancer)Information DisseminationResearchInstitutes_Networks_Beacons/mcrcPreventionBiology and Life SciencesMolecularOncogenesCloud Computingmedicine.diseaseGenòmicaCompute cloudsMutation570 Life sciences; biologyCOMPREHENSIVE CHARACTERIZATIONGenèticaWhole Genome Sequencing--methodsBackground informationDNA Mutational Analysis ; Evolution ; Genetic / genetics ; Genome ; Genomics ; Germ-Line Mutation / genetics ; High-Throughput Nucleotide Sequencing ; Human / genetics ; Humans ; ICGC/TCGA Pan-Cancer Analysis of Whole Genomes ConsortiumMedizinGenomeWhole-genomeGenome mappingNeoplasms2.1 Biological and endogenous factorsPromoter Regions GeneticCàncer -- Aspectes genèticsTelomeraseGeneticsWomen's cancers Radboud Institute for Molecular Life Sciences [Radboudumc 17]MultidisciplinaryChromothripsisGenomeManchester Cancer Research Centregenomics cancer profiling3rd-DAS10124 Institute of Molecular Life SciencesWomen's cancers Radboud Institute for Health Sciences [Radboudumc 17]Multidisciplinary SciencesParallel sequencingICGC/TCGA Pan-Cancer Analysis of Whole Genomes ConsortiumFemaleprofilingMedical GeneticsEngineering sciences. TechnologyBiotechnologyGeneral Science & TechnologyThe Cancer Genome Atlas610 Medicine & healthComputational biologyQH426 GeneticsBiologyConsortium of the International Cancer Genome ConsortiumPromoter RegionsGermline mutationPan-cancer analysisKrabbameinsrannsóknirmedicinecancerddc:610QH426Germ-Line MutationMedicinsk genetikKrabbamein030304 developmental biologyCell ProliferationLANDSCAPEGenome Humancomprehensive characterizationPan-cancer analysis of whole genomesPoint mutationHuman GenomeCancerReproducibility of ResultsSOMATIC MUTATIONSEVOLUTIONCancer sequencing Chromothripsis telomereDNA-DAMAGEMutagenesisPATTERNS3111 BiomedicineCHARACTERIZATION
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Increase in transmitted resistance to non-nucleoside reverse transcriptase inhibitors among newly diagnosed HIV-1 infections in Europe

2014

Background: One out of ten newly diagnosed patients in Europe was infected with a virus carrying a drug resistant mutation. We analysed the patterns over time for transmitted drug resistance mutations (TDRM) using data from the European Spread program.Methods: Clinical, epidemiological and virological data from 4317 patients newly diagnosed with HIV-1 infection between 2002 and 2007 were analysed. Patients were enrolled using a pre-defined sampling strategy.Results: The overall prevalence of TDRM in this period was 8.9% (95% CI: 8.1-9.8). Interestingly, significant changes over time in TDRM caused by the different drug classes were found. Whereas nucleoside resistance mutations remained con…

Malevirus strainResistanceHIV InfectionsDrug resistanceTHERAPYNucleoside Reverse Transcriptase InhibitorANTIRETROVIRAL DRUG-RESISTANCE0302 clinical medicineMedical microbiologyGenotypeMedicine and Health SciencesPrevalenceHIV Infection030212 general & internal medicineUNITED-KINGDOMPhylogeny0303 health sciencesCommunicable diseaseTransmission (medicine)adultvirus mutationUPDATED RECOMMENDATIONSvirus transmission3. Good healthEuropeInfectious Diseasesfemalerisk factorvirus resistanceFemaleNAIVE PATIENTSSOCIETY-USA PANELResearch ArticleHumanAdultmedicine.medical_specialtyGenotypeAnti-HIV AgentsVirusArticle03 medical and health sciencesSDG 3 - Good Health and Well-beingmaleMOLECULAR EPIDEMIOLOGYDrug Resistance Viralmedicineproteinase inhibitorHumansTransmissioncontrolled studyhumanmolecular phylogeny030304 developmental biologynonhumanMUTATIONSbusiness.industryAnti-HIV Agentnucleotide sequencenonnucleoside reverse transcriptase inhibitorHuman immunodeficiency virus 1 infectionVirologymajor clinical studyunindexed sequenceParasitology3121 General medicine internal medicine and other clinical medicineMutationHIV-1business
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Combinatorial Gray codes for classes of pattern avoiding permutations

2007

The past decade has seen a flurry of research into pattern avoiding permutations but little of it is concerned with their exhaustive generation. Many applications call for exhaustive generation of permutations subject to various constraints or imposing a particular generating order. In this paper we present generating algorithms and combinatorial Gray codes for several families of pattern avoiding permutations. Among the families under consideration are those counted by Catalan, Schr\"oder, Pell, even index Fibonacci numbers and the central binomial coefficients. Consequently, this provides Gray codes for $\s_n(\tau)$ for all $\tau\in \s_3$ and the obtained Gray codes have distances 4 and 5.

Mathematics::CombinatoricsFibonacci numberPattern avoiding permutationsGeneral Computer ScienceOrder (ring theory)Generating algorithms94B25Gray codesCombinatorial algorithms05A05; 94B25; 05A15Theoretical Computer ScienceCombinatoricsSet (abstract data type)Constraint (information theory)Gray codePermutation05A05ComputingMethodologies_SYMBOLICANDALGEBRAICMANIPULATIONFOS: MathematicsMathematics - CombinatoricsCombinatorics (math.CO)05A15Binomial coefficientComputer Science(all)MathematicsTheoretical Computer Science
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Targeting Cavity-Creating p53 Cancer Mutations with Small-Molecule Stabilizers: the Y220X Paradigm

2020

We have previously shown that the thermolabile, cavity-creating p53 cancer mutant Y220C can be reactivated by small-molecule stabilizers. In our ongoing efforts to unearth druggable variants of the p53 mutome, we have now analyzed the effects of other cancer-associated mutations at codon 220 on the structure, stability, and dynamics of the p53 DNA-binding domain (DBD). We found that the oncogenic Y220H, Y220N, and Y220S mutations are also highly destabilizing, suggesting that they are largely unfolded under physiological conditions. A high-resolution crystal structure of the Y220S mutant DBD revealed a mutation-induced surface crevice similar to that of Y220C, whereas the corresponding pock…

Models Molecular0301 basic medicineMutantCarbazolesDruggabilityCancer therapyAntineoplastic Agents01 natural sciencesBiochemistryDNA-binding proteinStructure-Activity Relationship03 medical and health sciencesProtein DomainsHumansCancer mutationsThermolabileQD0415Protein Stability010405 organic chemistryChemistryArticlesGeneral MedicineSmall moleculeAffinities0104 chemical sciences030104 developmental biologyGene Expression RegulationMutationBiophysicsMolecular MedicineMutant ProteinsDrug Screening Assays AntitumorTumor Suppressor Protein p53CrystallizationProtein BindingQD0241ACS Chemical Biology
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Genomic determinants of protein folding thermodynamics in prokaryotic organisms.

2004

Here we investigate how thermodynamic properties of orthologous proteins are influenced by the genomic environment in which they evolve. We performed a comparative computational study of 21 protein families in 73 prokaryotic species and obtained the following main results. (i) Protein stability with respect to the unfolded state and with respect to misfolding are anticorrelated. There appears to be a trade-off between these two properties, which cannot be optimized simultaneously. (ii) Folding thermodynamic parameters are strongly correlated with two genomic features, genome size and G+C composition. In particular, the normalized energy gap, an indicator of folding efficiency in statistical…

Models MolecularProtein DenaturationProtein FoldingProtein familyArchaeal ProteinsThermodynamicsdeleterious mutationsthermophilic proteinsBiologymonte-carlo algorithmGenomeNegative selectionBacterial ProteinsStructural BiologyMolecular evolutionGenome ArchaealevolutionbuchneraMolecular BiologyGenome sizeGeneticsPrincipal Component Analysisacid side-chainsBacteriaSequence Homology Amino Acidreplica approachComputational BiologystabilityGenetic codeArchaeaPRI BioscienceFolding (chemistry)endosymbiotic bacteriacation-pi interactionsThermodynamicsProtein foldingHydrophobic and Hydrophilic InteractionsGenome BacterialJournal of molecular biology
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