Search results for "Gene mutation"

showing 10 items of 187 documents

Novel <b><i>VANGL1</i></b> Gene Mutations in 144 Slovakian, Romanian and German Patients with Neural Tube Defects

2012

Neural tube defects (NTDs) are a group of congenital malformations of the central nervous system occurring at an average rate of 1 per 1,000 human pregnancies worldwide. Numerous genetic and environmental factors are discussed to be relevant in their etiology. In mice, mutants in >200 genes including the planar cell polarity (PCP) pathway are known to cause NTDs, and recently, heterozygous mutations in the human <i>VANGL1</i> gene have been described in a small subset of patients with NTDs. We performed a <i>VANGL1</i> mutation analysis in 144 unrelated individuals with NTDs from Slovakia, Romania and Germany and identified 3 heterozygous missense mutations: c.613…

Geneticscongenital hereditary and neonatal diseases and abnormalitiesMutationbusiness.industryMutantCentral nervous systemNeural tubeGene mutationmedicine.disease_causemedicine.anatomical_structureGeneticsMutation testingmedicineMissense mutationbusinessGeneGenetics (clinical)Molecular Syndromology
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Epidemiological study of nonsyndromic hearing loss in Sicilian newborns

2007

Deafness is caused by a variety of facts, genetic and environmental. Regarding the acquired causes, deafness can be the consequence of prenatal infections, acoustic or cerebral trauma, and the use of ototoxic drugs. Deafness can be the only manifestation (nonsyndromic forms) or it may occur together with other phenotypic findings (syndromic forms). The majority of nonsyndromicdeafness has a genetic basis [Van Camp et al., 1997]. In recent years, deafness and hearing loss have assumed a clinical importance in the study of congenital disorders [Morton et al., 1991]. The clinical interest for hearing loss is supported by the social impact that this disorder has; if not treated, delays in the d…

GenotypeHearing lossHearing Loss SensorineuralDNA Mutational AnalysisNonsense mutationBiologyGene mutationConnexinsneonate deafness geneticExonNeonatal ScreeningGene Frequencyotorhinolaryngologic diseasesGeneticsmedicineHumansGenetic TestingSicilyGeneGenetics (clinical)Chromosome 13GeneticsSplice site mutationInfant NewbornGenetic VariationStop codonConnexin 26PhenotypeMutationmedicine.symptomAmerican Journal of Medical Genetics Part A
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Detection of DNA effects in human cells with the comet assay and their relevance for mutagenesis

1996

The single cell gel test (SCG-test or comet assay) is a rapid and sensitive method for measuring DNA damage and repair in individual cells. A wide variety of mutagens have been shown to cause DNA alterations detectable with the comet assay, but it is not yet clear whether a relationship exists between the DNA effects and the induction of mutations. We are therefore investigating in a cell culture system with human cells (MRC5CV1) the induction of DNA damage by environmental mutagens and the formation of mutations at the HPRT gene. In the present study we investigated benzo[a]pyrene (BP), an environmental mutagenic and carcinogenic polycyclic aromatic hydrocarbon, and its reactive metabolite…

Hypoxanthine PhosphoribosyltransferaseDNA repairDNA damageCytological TechniquesMutagenGene mutationToxicologymedicine.disease_causechemistry.chemical_compoundBenzo(a)pyrenemedicineHumansCell Line TransformedElectrophoresis Agar GelGeneticsCell DeathMutagenesisfood and beveragesGeneral MedicineMolecular biologyComet assaychemistryMutagenesisEnvironmental PollutantsDNAGenotoxicityDNA DamageToxicology Letters
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Biomarkers of Ineffective Erythropoiesis Predict Response to Luspatercept in Patients with Low or Intermediate-1 Risk Myelodysplastic Syndromes (MDS)…

2015

Abstract Background: Luspatercept is a fusion protein (modified activin receptor IIB-IgG Fc) being investigated for the treatment of anemias with ineffective erythropoiesis. MDS patients have increased Smad2/3 signaling in the bone marrow, leading to ineffective erythropoiesis. Luspatercept inhibits Smad2/3 signaling and promotes late-stage erythroid differentiation, thereby correcting ineffective erythropoiesis. Aims: This completed, 3-month, phase 2, multicenter, open-label study evaluated the effects of luspatercept on anemia in patients with low/int-1 risk MDS (IPSS classification). Study outcomes include erythroid response of increased hemoglobin (Hb) in low transfusion burden (LTB) pa…

Ineffective erythropoiesisOncologymedicine.medical_specialtyAnemiaImmunologyPopulationGene mutationmedicine.disease_causeLower riskBiochemistry03 medical and health sciences0302 clinical medicineInternal medicineMedicineeducationLenalidomideeducation.field_of_studybusiness.industryMyelodysplastic syndromesCell BiologyHematologymedicine.disease3. Good healthSurgery030220 oncology & carcinogenesisAbsolute neutrophil countbusiness030215 immunologymedicine.drugBlood
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CFTR p.Arg117His associated with CBAVD and other CFTR-related disorders

2013

International audience; BACKGROUND:The high frequency of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) gene mutation p.Arg117His in patients with congenital bilateral absence of the vas deferens (CBAVD) and in newborns screened for CF has created a dilemma.METHODS:Phenotypic and genotypic data were retrospectively collected in 179 non-newborn French individuals carrying p.Arg117His and a second CFTR mutation referred for symptoms or family history, by all French molecular genetics laboratories, referring physicians, CF care centres and infertility clinics.RESULTS:97% of the patients had the intronic T7 normal variant in cis with p.Arg117His. 89% patients were male, wit…

InfertilityMalemedicine.medical_specialtyHeterozygoteCystic FibrosisOffspring[SDV]Life Sciences [q-bio]Cystic Fibrosis Transmembrane Conductance RegulatorGene mutationCompound heterozygosityAsymptomaticCystic fibrosis03 medical and health sciences0302 clinical medicineVas DeferensMale Urogenital DiseasesMutation RateInternal medicinePrenatal DiagnosisGenotypeGeneticsmedicineHumansFamily historyChildSweatGenetics (clinical)Infertility Male030304 developmental biology0303 health sciencesbusiness.industryInfant NewbornInfantmedicine.disease3. Good healthPhenotype030228 respiratory systemChild PreschoolImmunologyMutationFemalemedicine.symptombusiness
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Driver mutations and differential sensitivity to targeted therapies: a new approach to the treatment of lung adenocarcinoma

2010

The adenocarcinoma of the lung has recently shown peculiar molecular characteristics, which relate with both carcinogenesis and response to targeted drugs. Several molecular alterations have been defined as "driver mutations". These are responsible for both the initiation and maintenance of the malignancy. The epidermal growth factor receptor (EGFR) pathway is the main regulator of cell function and cancer development. It has a widely defined role in the occurrence of driver mutations. Up till now EGFR gene mutations, KRAS gene mutations and EML4-ALK fusion genes are the most widely recognized alterations involved in both the biology and the clinical management of lung adenocarcinoma. In th…

Lung NeoplasmsOncogene Proteins FusionSettore MED/06 - Oncologia MedicaEGFRGene ExpressionAdenocarcinomaGene mutationmedicine.disease_causeProto-Oncogene Proteins p21(ras)Phosphatidylinositol 3-KinasesPredictive Value of TestsProto-Oncogene ProteinsAntineoplastic Combined Chemotherapy ProtocolsmedicineAdenocarcinoma of the lungHumansRadiology Nuclear Medicine and imagingMolecular Targeted TherapyEpidermal growth factor receptorTyrosine kinase inhibitorsMutationbiologybusiness.industryDriver mutationGeneral MedicineProtein-Tyrosine KinasesPrognosismedicine.diseaseErbB ReceptorsTreatment OutcomeOncologyMutationImmunologyras ProteinsCancer researchbiology.proteinAdenocarcinomaKRASCarcinogenesisbusinessTyrosine kinaseAlgorithmsCancer Treatment Reviews
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Cell of origin markers identify different prognostic subgroups of lung adenocarcinoma

2018

Strong prognostic markers able to stratify lung adenocarcinoma (ADC) patients are lacking. We evaluated whether a six-immunohistochemical markers panel (TTF1, SP-A, Napsin A, MUC5AC, CDX2 and CK5), defining the putative neoplastic “cell of origin,” allows to identify prognostic subgroups among lung ADC. We screened a large cohort of ADC specimens (2003–2013) from Torino Institutional Repository identifying: (i) marker positivity by immunohistochemistry, (ii) main morphological appearance by light microscopy, (iii) presence of “hotspot” mutations of candidate genes by Sequenom technology. To evaluate possible predictors of survival and time to recurrence, uni- and multivariable-adjusted comp…

Lung adenocarcinomaMorphologyAdultMale0301 basic medicineOncologyBiomarkers; Genetic mutations; Immunohistochemistry; Lung adenocarcinoma; Morphology; Survival analysisPathologymedicine.medical_specialtyCandidate geneCell of originsix-immunohistochemical markers panel (TTF1 SP-A Napsin A MUC5AC CDX2 and CK5)Adenocarcinoma of LungKaplan-Meier Estimategenetic mutationsGene mutationBiologymedicine.disease_causeadenocarcinoma (ADC)survival analysisPathology and Forensic Medicine03 medical and health sciences0302 clinical medicineInternal medicinemorphologyBiomarkers TumormedicineHumansCDX2Survival analysisAgedbiomarkers; genetic mutations; immunohistochemistry; lung adenocarcinoma; morphology; survival analysisbiomarkersSurvival analysisMiddle Agedrespiratory systemPrognosislung adenocarcinomamedicine.diseaseImmunohistochemistryGenetic mutations030104 developmental biology030220 oncology & carcinogenesisimmunohistochemistryAdenocarcinomaImmunohistochemistryFemaleKRASBiomarkersHuman Pathology
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High Rate of Recurrent De Novo Mutations in Developmental and Epileptic Encephalopathies

2017

Item does not contain fulltext Developmental and epileptic encephalopathy (DEE) is a group of conditions characterized by the co-occurrence of epilepsy and intellectual disability (ID), typically with developmental plateauing or regression associated with frequent epileptiform activity. The cause of DEE remains unknown in the majority of cases. We performed whole-genome sequencing (WGS) in 197 individuals with unexplained DEE and pharmaco-resistant seizures and in their unaffected parents. We focused our attention on de novo mutations (DNMs) and identified candidate genes containing such variants. We sought to identify additional subjects with DNMs in these genes by performing targeted sequ…

Male0301 basic medicineCandidate genemedicine.medical_specialtymedical geneticsglycosylationNonsense mutationGenome-wide association studyGene mutationBiologySensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]Articlesevere intellectual disability03 medical and health sciencesEpilepsy0302 clinical medicinechildrenRecurrenceSeizuresGenetic linkageIntellectual Disability[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyJournal ArticleGeneticsmedicineHumansChilddisordersGenetics (clinical)Genetic associationGeneticsBrain DiseasesdiseaseEpilepsycis-prenyltransferaseGenome Humanstructural basismedicine.diseasediphosphate synthase030104 developmental biologyChild PreschoolMutationMedical geneticsFemalenogo-b receptor030217 neurology & neurosurgery[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyGenome-Wide Association StudyMeta-Analysis
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Role of Colchicine Treatment in Tumor Necrosis Factor Receptor Associated Periodic Syndrome (TRAPS): Real-Life Data from the AIDA Network

2020

Objective. To analyze the potential role of colchicine monotherapy in patients with tumor necrosis factor receptor associated periodic syndrome (TRAPS) in terms of control of clinical and laboratory manifestations. Methods. Patients with TRAPS treated with colchicine monotherapy were retrospectively enrolled; demographic, clinical and therapeutic data were collected and statistically analysed after having clustered patients according to different times at disease onset, penetrance of mutations, dosage of colchicine, and different disease manifestations. Results. 24 patients (14 males; 15 with pediatric disease onset) treated with colchicine monotherapy were enrolled. Colchicine resulted in …

Male0301 basic medicineEye DiseasesTRAPSColchicineAIDA NetworkGene mutationGastroenterologyReceptors Tumor Necrosis Factorchemistry.chemical_compoundSettore MED/38 - Pediatria Generale E Specialistica0302 clinical medicineReceptorsPathologyRB1-214ColchicineAge of OnsetYoung adultChildAmyloidosisAmyloidosisSyndromeMiddle AgedColchicine tumor necrosis factor TRAPSInflamacióPenetrancePhenotypeChild PreschoolFemaleJoint DiseasesResearch ArticleAdultRiskmedicine.medical_specialtyAdolescentFeverArticle SubjectImmunologyAdolescent; Adult; Age of Onset; Amyloidosis; Child; Child Preschool; Colchicine; Exanthema; Eye Diseases; Female; Fever; Humans; Joint Diseases; Male; Middle Aged; Mutation; Myalgia; Phenotype; Receptors Tumor Necrosis Factor; Retrospective Studies; Risk; Syndrome; Young AdultLower riskYoung Adult03 medical and health sciencesInternal medicinemedicineHumansPreschoolRetrospective StudiesInflammation030203 arthritis & rheumatologybusiness.industryTRAPSRetrospective cohort studyMyalgiaCell BiologyExanthemamedicine.disease030104 developmental biologychemistryMutationAge of onsetColchicineTumor Necrosis FactorbusinessMediators of Inflammation
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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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