Search results for "Mutation"

showing 10 items of 2830 documents

Genome-Wide Estimation of the Spontaneous Mutation Rate of Human Adenovirus 5 by High-Fidelity Deep Sequencing

2016

Rates of spontaneous mutation determine the ability of viruses to evolve, infect new hosts, evade immunity and undergo drug resistance. Contrarily to RNA viruses, few mutation rate estimates have been obtained for DNA viruses, because their high replication fidelity implies that new mutations typically fall below the detection limits of Sanger and standard next-generation sequencing. Here, we have used a recently developed high-fidelity deep sequencing technique (Duplex Sequencing) to score spontaneous mutations in human adenovirus 5 under conditions of minimal selection. Based on >200 single-base spontaneous mutations detected throughout the entire viral genome, we infer an average mutatio…

0301 basic medicineAdenovirusesMutation rateGene Identification and AnalysisPathology and Laboratory MedicinePolymerase Chain ReactionMutation RateMedicine and Health Scienceslcsh:QH301-705.5GeneticsViral GenomicsInsertion MutationAdenovirus genomeMicrobial MutationHigh-Throughput Nucleotide SequencingGenomicsResistance mutation3. Good healthMedical MicrobiologyViral PathogensVirusesPathogensSequence AnalysisResearch Articlelcsh:Immunologic diseases. AllergySubstitution MutationImmunologyMicrobial GenomicsGenome ViralBiologyResearch and Analysis MethodsMicrobiologyDeep sequencingFrameshift mutation03 medical and health sciencesSequence Motif AnalysisVirologyGeneticsPoint MutationHumansMolecular Biology TechniquesSequencing TechniquesMicrobial PathogensMutation DetectionMolecular BiologySuppressor mutation030102 biochemistry & molecular biologyAdenoviruses HumanPoint mutationOrganismsBiology and Life SciencesVirology030104 developmental biologylcsh:Biology (General)MutationDynamic mutationParasitologyDNA viruseslcsh:RC581-607PLOS Pathogens
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Mutanome directed cancer immunotherapy

2015

Somatic mutations are important drivers of cancer development. Accumulating evidence suggests that a significant subset of mutations result in neo-epitopes recognized by autologous T cells and thus may constitute the Achilles' heel of tumor cells. T cells directed against mutations have been shown to have a key role in clinical efficacy of potent cancer immunotherapy modalities, such as adoptive transfer of autologous tumor infiltrating lymphocytes and immune checkpoint inhibitors. Whereas these findings strengthen the idea of a prominent role of neo-epitopes in tumor rejection, the systematic therapeutic exploitation of mutations was hampered until recently by the uniqueness of the reperto…

0301 basic medicineAdoptive cell transferSomatic cellT-Lymphocytesmedicine.medical_treatmentImmune checkpoint inhibitorsImmunology03 medical and health sciences0302 clinical medicineCancer immunotherapyAntigens NeoplasmNeoplasmsAnimalsHumansImmunology and AllergyMedicineClinical efficacybusiness.industryAutologous T-cellsImmune recognition030104 developmental biology030220 oncology & carcinogenesisTumor rejectionMutationImmunologyImmunotherapybusiness
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Dynamic clonal remodelling in breast cancer metastases is associated with subtype conversion

2019

Background: Changes in the clinical subtype (CS) and intrinsic subtype (IS) between breast cancer (BC) metastases and corresponding primary tumours have been reported. However, their relationship with tumour genomic changes remains poorly characterised. Here, we analysed the association between genomic remodelling and subtype conversion in paired primary and metastatic BC samples. Methods: A total of 57 paired primary and metastatic tumours from GEICAM/2009-03 (ConvertHER, NCT01377363) study participants with centrally assessed CS (n = 57) and IS (n = 46) were analysed. Targeted capture and next-generation sequencing of 202 genes on formalin-fixed paraffin-embedded samples was performed. Th…

0301 basic medicineAdultCancer ResearchSkin NeoplasmsBioinformaticsBone NeoplasmsBreast Neoplasmsmedicine.disease_causeMetastatic tumours03 medical and health sciences0302 clinical medicineBreast cancerBreast cancermedicineBiomarkers TumorHumansProspective StudiesPAM50AgedAged 80 and overMutationIntrinsic subtypebusiness.industryHuman epidermal growth factorBrain NeoplasmsClonal architectureHigh-Throughput Nucleotide SequencingClonal remodellingMiddle Agedmedicine.diseasePrognosisGene Expression Regulation Neoplastic030104 developmental biologyOncology030220 oncology & carcinogenesisLymphatic MetastasisCancer cellMutationCancer researchFemaleNeoplasm Recurrence LocalClinical subtypeHeterogeneitybusinessHormoneFollow-Up Studies
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Autosomal recessive hypercholesterolemia in Spain.

2017

Abstract Background and aims Autosomal recessive hypercholesterolemia (ARH) is a very rare disease, caused by mutations in LDL protein receptor adaptor 1 (LDLRAP1). It is characterized by high levels of low-density lipoprotein cholesterol (LDL-C) and increased risk of premature cardiovascular disease. We aimed to characterize ARH in Spain. Methods Data were collected from the Dyslipidemia Registry of the Spanish Atherosclerosis Society. A literature search was performed up to June 2017, and all diagnostic genetic studies for familial hypercholesterolemia of Spain were reviewed. Results Seven patients with ARH were identified, 6 true homozygous and one compound heterozygous with a novel muta…

0301 basic medicineAdultGenetic MarkersMalemedicine.medical_specialtyHeterozygoteHypercholesterolemiaDiseaseFamilial hypercholesterolemia030204 cardiovascular system & hematologyCompound heterozygosity03 medical and health sciences0302 clinical medicineInternal medicinemedicinePrevalenceHumansGenetic Predisposition to DiseaseRegistriesChildAdaptor Proteins Signal TransducingHypolipidemic Agentsbusiness.industryGenetic heterogeneityHomozygoteInfantCholesterol LDLMiddle Agedmedicine.diseaseAtherosclerosisUp-Regulation030104 developmental biologyEndocrinologyPhenotypeAutosomal Recessive HypercholesterolemiaSpainChild PreschoolCohortMutationDisease ProgressionFemaleCardiology and Cardiovascular MedicinebusinessDyslipidemiaRare diseaseAtherosclerosis
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Genome-wide association meta-analysis highlights light-induced signaling as a driver for refractive error

2018

Skin affections after sulfur mustard (SM) exposure include erythema, blister formation and severe inflammation. An antidote or specific therapy does not exist. Anti-inflammatory compounds as well as substances counteracting SM-induced cell death are under investigation. In this study, we investigated the benzylisoquinoline alkaloide berberine (BER), a metabolite in plants like berberis vulgaris, which is used as herbal pharmaceutical in Asian countries, against SM toxicity using a well-established in vitro approach. Keratinocyte (HaCaT) mono-cultures (MoC) or HaCaT/THP-1 co-cultures (CoC) were challenged with 100, 200 or 300 mM SM for 1 h. Post-exposure, both MoC and CoC were treated with 1…

0301 basic medicineAdultMaleCell typeResearchInstitutes_Networks_Beacons/MICRAIn silicotaittovirheetGenome-wide association studyRetinal Pigment EpitheliumBiologyBlindnessPolymorphism Single NucleotideSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]ArticleRetinaWhite People03 medical and health sciencesHIGH-GRADE MYOPIA ; RETINAL-PIGMENT EPITHELIUM ; SEROTONIN PATHWAY GENES ; FORM-DEPRIVATION MYOPIA ; COMMON VARIANTS ; OCULAR GROWTH ; RETINITIS-PIGMENTOSA ; GENOTYPE IMPUTATION ; MISSENSE MUTATIONS ; DOPAMINE-RECEPTORSAsian Peoplerefractive errorsRetinitis pigmentosaGeneticsmedicineMyopiaJournal ArticleHumansGenetic Predisposition to Disease610 Medicine & healthRegulation of gene expressionRetinaRetinal pigment epitheliummedicine.diseaseRefractive Errors030104 developmental biologymedicine.anatomical_structureManchester Institute for Collaborative Research on AgeingGene Expression Regulationgenetic factorsEye disorderFemalesense organsgeneettiset tekijätNeuroscienceGenome-Wide Association StudySignal Transduction
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Novel KIAA1033/WASHC4 mutations in three patients with syndromic intellectual disability and a review of the literature.

2019

In 2011, KIAA1033/WASHC4 was associated with autosomal recessive intellectual disability (ARID) in a large consanguineous family comprising seven affected individuals with moderate ID and short stature. Since then, no other cases of KIAA1033 variants have been reported. Here we describe three additional patients (from two unrelated families) with syndromic ID due to compound heterozygous KIAA1033 variants ascertained by exome sequencing (ES). Two sisters, aged 4 and 5.5 years, had a stop-gain and a missense variants, each inherited from one parent (p.(Gln442*) and p.(Asp1048Gly)). Both had learning disabilities, macrocephaly, dysmorphic features, skeletal anomalies, and subependymal heterot…

0301 basic medicineAdultMaleMicrocephaly030105 genetics & heredityCompound heterozygosityShort stature03 medical and health sciencesKIAA0196Intellectual DisabilityIntellectual disabilityGeneticsMedicineMissense mutationHumansGenetics (clinical)Exome sequencingGeneticsbusiness.industryMacrocephalyInfant NewbornIntracellular Signaling Peptides and Proteinsmedicine.diseasePedigreeProtein Subunits030104 developmental biologyPhenotypeChild PreschoolMutationFemalemedicine.symptombusinessAmerican journal of medical genetics. Part AREFERENCES
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Effect of ABC transporter expression and mutational status on survival rates of cancer patients

2020

ATP-binding cassette (ABC) transporters mediate multidrug resistance in cancer. In contrast to DNA single nucleotide polymorphisms in normal tissues, the role of mutations in tumors is unknown. Furthermore, the significance of their expression for prediction of chemoresistance and survival prognosis is still under debate. We investigated 18 tumors by RNA-sequencing. The mutation rate varied from 27,507 to 300885. In ABCB1, three hotspots with novel mutations were in transmembrane domains 3, 8, and 9. We also mined the cBioPortal database with 11,814 patients from 23 different tumor entities. We performed Kaplan-Meier survival analyses to investigate the effect of ABC transporter expression …

0301 basic medicineAdultMaleMutation rateNonsense mutationSingle-nucleotide polymorphismATP-binding cassette transporterRM1-950BiologyMultidrug resistanceP-glycoproteinPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineNeoplasmsmedicineMissense mutationHumansSurvival analysisAgedCancerPharmacologyAged 80 and overPrognostic factorSequence Analysis RNACancerABCB5General MedicineMiddle AgedSurvival analysismedicine.diseaseMolecular Docking SimulationSurvival Rate030104 developmental biologyABC transporters030220 oncology & carcinogenesisMutationCancer researchATP-Binding Cassette TransportersFemaleTherapeutics. PharmacologyBiomedicine & Pharmacotherapy
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Genetics of Wilson disease and Wilson-like phenotype in a clinical series from eastern Spain.

2019

Wilson's disease (WD) is an autosomal recessive disorder caused by ATP7B mutations. Subjects with only one mutation may show clinical signs and individuals with biallelic changes may remain asymptomatic. We aimed to achieve a conclusive genetic diagnosis for 34 patients clinically diagnosed of WD. Genetic analysis comprised from analysis of exons to WES (whole exome sequencing), including promoter, introns, UTRs (untranslated regions), besides of study of large deletions/duplications by MLPA (multiplex ligation-dependent probe amplification). Biallelic ATP7B mutations were identified in 30 patients, so that four patients were analyzed using WES. Two affected siblings resulted to be compound…

0301 basic medicineAdultMaleNerve Tissue Proteins030105 genetics & heredityBiologymedicine.disease_causeCompound heterozygosityGenetic analysis03 medical and health sciencesExonHepatolenticular DegenerationExome SequencingGeneticsmedicineHumansGenetic Predisposition to DiseaseMultiplex ligation-dependent probe amplificationGenetic TestingGenetics (clinical)Exome sequencingGeneticsMutationExonsmedicine.diseaseWilson's disease030104 developmental biologyPhenotypeCopper-Transporting ATPasesSpainMutationFemaleCongenital disorder of glycosylationClinical geneticsREFERENCES
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Molecular diagnosis of PIK3CA-related overgrowth spectrum (PROS) in 162 patients and recommendations for genetic testing.

2017

Postzygotic activating mutations of PIK3CA cause a wide range of mosaic disorders collectively referred to as PIK3CA-related overgrowth spectrum (PROS). We describe the diagnostic yield and characteristics of PIK3CA sequencing in PROS. We performed ultradeep next-generation sequencing (NGS) of PIK3CA in various tissues from 162 patients referred to our clinical laboratory and assessed diagnostic yield by phenotype and tissue tested. We identified disease-causing mutations in 66.7% (108/162) of patients, with mutant allele levels as low as 1%. The diagnostic rate was higher (74%) in syndromic than in isolated cases (35.5%; P = 9.03 × 10−5). We identified 40 different mutations and found stro…

0301 basic medicineAdultMalePathologymedicine.medical_specialtyAdolescentGenotypeClass I Phosphatidylinositol 3-KinasesPrenatal diagnosisBioinformaticsmedicine.disease_causeDNA sequencing03 medical and health sciencesYoung Adult0302 clinical medicinePrenatal DiagnosisGenotypemedicineHumansGenetic Predisposition to DiseaseGenetic TestingAlleleChildGenetics (clinical)AllelesGenetic Association StudiesGrowth DisordersGenetic testingMutationmedicine.diagnostic_testbusiness.industryMosaicismInfant NewbornDisease ManagementHigh-Throughput Nucleotide SequencingInfantSequence Analysis DNAPhenotype030104 developmental biologyPhenotypeAmino Acid SubstitutionChild PreschoolMutationAllelic heterogeneityFemalebusiness030217 neurology & neurosurgeryGenetics in medicine : official journal of the American College of Medical Genetics
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The Amount of Melanin Influences p16 Loss in Spitzoid Melanocytic Lesions: Correlation With CDKN2A Status by FISH and MLPA.

2019

AIMS The risk assessment of spitzoid lesions is one of the most difficult challenges in dermatopathology practice. In this regard, the loss of p16 expression and the homozygous deletion of CDKN2A, have been pointed in the literature as reliable indicators of high risk. However, these findings are poorly reproducible, and the molecular bases underlying the loss of p16 expression remain unclear. We aimed to identify the underlying events causing loss of CDKN2A/p16 in spitzoid tumors. MATERIALS AND METHODS We evaluated the immunohistochemical expression of p16, and the presence of CDKN2A genetic alterations detected through fluorescence in situ hybridization (FISH) and multiplex ligation-depen…

0301 basic medicineAdultMalePathologymedicine.medical_specialtyHistologySkin NeoplasmsPathology and Forensic MedicineMelanin03 medical and health sciencesYoung Adult0302 clinical medicineCDKN2ANevus Epithelioid and Spindle CellmedicineBiomarkers TumorNevusHumansMultiplex ligation-dependent probe amplificationneoplasmsMelanomaCyclin-Dependent Kinase Inhibitor p16In Situ Hybridization FluorescenceMelaninsmedicine.diagnostic_testbusiness.industryMelanomamedicine.diseaseImmunohistochemistryGene Expression Regulation NeoplasticMedical Laboratory Technology030104 developmental biology030220 oncology & carcinogenesisMutationImmunohistochemistryMelanocytesFemaleDermatopathologybusinessMultiplex Polymerase Chain ReactionFluorescence in situ hybridizationApplied immunohistochemistrymolecular morphology : AIMM
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