Search results for " mutations"

showing 10 items of 127 documents

Exploring by whole exome sequencing patients with initial diagnosis of Rubinstein-Taybi syndrome: the interconnections of epigenetic machinery disord…

2019

Rubinstein–Taybi syndrome (RSTS) is an autosomal-dominant neurodevelopmental disease affecting 1:125,000 newborns characterized by intellectual disability, growth retardation, facial dysmorphisms and skeletal abnormalities. RSTS is caused by mutations in genes encoding for writers of the epigenetic machinery: CREBBP (~ 60%) or its homologous EP300 (~ 10%). No causative mutation is identified in up to 30% of patients. We performed whole-exome sequencing (WES) on eight RSTS-like individuals who had normal high-resolution array CGH testing and were CREBBP- and EP300-mutation -negative, to identify the molecular cause. In four cases, we identified putatively causal variants in three genes (ASXL…

MaleGenetic Association StudieCompound heterozygosityWhole Exome SequencingArticleEpigenesis Genetic03 medical and health scienceswhole exome sequencing Rubinstein–Taybi syndrome epigenetic mutationsExome SequencingGeneticsmedicineHumansEpigeneticsEP300ChildGenetics (clinical)Exome sequencingGenetic Association Studies030304 developmental biologyGeneticsRubinstein-Taybi Syndrome0303 health sciencesComparative Genomic HybridizationbiologyRubinstein–Taybi syndrome030305 genetics & heredityInfant NewbornFaciesInfantmedicine.diseaseFacieCREB-Binding ProteinHuman geneticsRSTSKMT2APhenotypeChild PreschoolMutationbiology.proteinNeurodegenerative disordersFemaleHaploinsufficiencyE1A-Associated p300 ProteinHumanHuman genetics
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Prothrombotic gene variants as risk factors of acute myocardial infarction in young women

2012

Abstract Background Acute myocardial infarction (AMI) in young women represent an extreme phenotype associated with a higher mortality compared with similarly aged men. Prothrombotic gene variants could play a role as risk factors for AMI at young age. Methods We studied Factor V Leiden, FII G20210A, MTHFR C677T and beta-fibrinogen -455G>A variants by real-time PCR in 955 young AMI (362 females) and in 698 AMI (245 females) patients. The data were compared to those obtained in 909 unrelated subjects (458 females) from the general population of the same geographical area (southern Italy). Results In young AMI females, the allelic frequency of either FV Leiden and of FII G20210A was signif…

MaleHomocysteineMyocardial Infarctionlcsh:Medicinegene variantsprothrombotic gene variantsAMIchemistry.chemical_compoundGene FrequencyRisk FactorsgenderMyocardial infarctionMedicine(all)GeneticsYoung AMI Gender AMI Gene variants Mutations Prothrombotic variants Genetic predispositioneducation.field_of_studyprothrombotic variantsbiologyHomozygoteFactor VGeneral MedicineFemaleProthrombinyoung AMIAdultmedicine.medical_specialtyPopulationyoung AMI gender AMI gene variants mutations prothrombotic variants genetic predisposition.Polymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyInternal medicinemedicineFactor V LeidenGenetic predispositionHumansGenetic Predisposition to Diseasecardiovascular diseaseseducationAllele frequencyAgedBiochemistry Genetics and Molecular Biology(all)business.industryResearchlcsh:RFactor VThrombosismutationsmedicine.diseasechemistryMethylenetetrahydrofolate reductasebiology.proteinbusinessgenetic predispositionJournal of Translational Medicine
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Novel mutations of CETP gene in Italian subjects with hyeralphalipoproteinemia

2009

Abstract Cholesteryl ester transfer protein (CETP) is a plasma glycoprotein that catalyses the transfer of cholesteryl esters from HDL to the other plasma lipoproteins. Genetic deficiency of CETP is one of the known causes of elevation of plasma HDL-C (primary hyperalphalipoproteinemia, HALP). We sequenced CETP gene in a group of 24 Italian subjects with primary HALP (HDL-C>80 mg/dl) suspected to have CETP deficiency. Two unrelated subjects both coming from the same geographical district, were found to be heterozygous for a nucleotide substitution in exon 6 (c.544C>T) and another subject was found to be heterozygous for a C>T transition in exon 9 (c.802C>T). Both mutations introduce a prema…

MaleHyperlipoproteinemiasMessengerDNA Mutational Analysismedicine.disease_causeExonFamilial hyperalphalipoproteinemiaChlorocebus aethiopsCETP activity; CETP gene mutations; Familial hyperalphalipoproteinemia; HDL size; Adolescent; Adult; Aged; Animals; Biomarkers; COS Cells; Cercopithecus aethiops; Cholesterol Ester Transfer Proteins; Cholesterol HDL; DNA Mutational Analysis; European Continental Ancestry Group; Female; Humans; Hyperlipoproteinemias; Italy; Male; Middle Aged; Phenotype; RNA Messenger; Transfection; Up-Regulation; Young Adult; Mutation; Cardiology and Cardiovascular MedicineGeneticsMutationTransition (genetics)biologyCETP activityMiddle AgedUp-RegulationCholesterolPhenotypeItalyCOS CellsRNA splicingFemaleFamilial hyperalphalipoproteinemia; CETP gene mutations; CETP activity; HDL sizelipids (amino acids peptides and proteins)Cardiology and Cardiovascular MedicineAdultHDLAdolescentEuropean Continental Ancestry GroupSocio-culturaleHDL sizeTransfectionWhite PeopleCercopithecus aethiopsYoung AdultCETP gene mutationsCholesterylester transfer proteinmedicineAnimalsHumansRNA MessengerGeneAgedCholesterol HDLIntroncetpCholesterol Ester Transfer Proteinscarbohydrates (lipids)biology.proteinRNAmutationBiomarkersMinigene
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Molecular surveillance of pandemic influenza A(H1N1) viruses circulating in Italy from May 2009 to February 2010: association between haemagglutinin …

2010

Haemagglutinin sequences of pandemic influenza A(H1N1) viruses circulating in Italy were examined, focusing on amino acid changes at position 222 because of its suggested pathogenic relevance. Among 169 patients, the D222G substitution was detected in three of 52 (5.8%) severe cases and in one of 117 (0.9%) mild cases, whereas the D222E mutation was more frequent and evenly distributed in mild (31.6%) and severe cases (38.4%). A cluster of D222E viruses among school children confirms reported human-to-human transmission of viruses mutated at amino acid position 222.

MaleMolecular surveillance; Pandemic influenza A(H1N1); Haemagglutinin mutations; Italy from May 2009 to February 2010pandemic influenzasurveillance of pandemic influenza A(H1N1); Molecular surveillance; pandemic influenzaEpidemiologyvirusesHaemagglutinin mutationssurveillance of pandemic influenza A(H1N1)Settore MED/42 - Igiene Generale E Applicatamedicine.disease_causeSeverity of Illness IndexInfluenza A Virus H1N1 SubtypePandemic influenza A(H1N1)PandemicInfluenza A VirusA(H1N1)ChildMutationReverse Transcriptase Polymerase Chain ReactionTransmission (medicine)Adolescent; Adult; Age Distribution; Aged; Amino Acid Substitution; Child; Child Preschool; Female; Hemagglutinins; Humans; Infant; Influenza A Virus H1N1 Subtype; Influenza Human; Italy; Male; Middle Aged; Mutation; Population Surveillance; Reverse Transcriptase Polymerase Chain Reaction; Severity of Illness Index; Sex Distribution; Young Adult; PandemicsMiddle AgedItaly from May 2009 to February 2010Molecular surveillance; pandemic influenza; A(H1N1); Italy; haemagglutinin mutationsHemagglutininsMolecular surveillanceItalyChild PreschoolPopulation SurveillanceFemaleHumanAdultAdolescentBiologyDisease clusterDisease courseYoung AdultAge DistributionVirologyInfluenza HumanmedicineHumansH1N1 SubtypeSex DistributionPreschoolhaemagglutinin mutationsPandemicsAgedMolecular epidemiologyPublic Health Environmental and Occupational HealthPandemic influenzaInfantVirologyInfluenzaMutational analysisAmino Acid SubstitutionMutationEurosurveillance
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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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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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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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