Search results for "MUTATION"

showing 10 items of 2830 documents

Absence of germline CDKN2A mutation in Sicilian Patients with Familial Malignant Melanoma: could it be a population-specific genetic signature?

2015

Germline CDKN2A mutations have been described in 25% to 40% of melanoma families from several countries. Sicilian population is genetically different from the people of Europe and Northern Italy because of its historical background, therefore familial melanoma could be due to genes different from high-penetrance CDKN2A gene. Four hundred patients with cutaneous melanoma were observed in a 6-years period at the Plastic Surgery Unit of the University of Palermo. Forty-eight patients have met the criteria of the Italian Society of Human Genetics (SIGU) for the diagnosis of familial melanoma and were screened for CDKN2A and CDK4 mutations. Mutation testing revealed that none of the families car…

Male0301 basic medicineCancer ResearchMutation rateSettore MED/06 - Oncologia MedicaSettore MED/19 - Chirurgia Plasticap14ARFGermline0302 clinical medicineCDKN2ATumor Suppressor Protein p14ARFMedicineMelanomaSicilyfamilial melanomaGeneticseducation.field_of_studyMelanomaMiddle AgedGene Expression Regulation NeoplasticItalyOncologygermline mutation030220 oncology & carcinogenesisMolecular MedicineFemaleResearch PaperSignal TransductionAdultPopulation03 medical and health sciencesCDKN2Acutaneous melanomaGermline mutationp16INK4aHumansGenetic Predisposition to DiseaseeducationneoplasmsCyclin-Dependent Kinase Inhibitor p16Germ-Line MutationAgedPharmacologybusiness.industryGenetic heterogeneityp.R87W mutationmedicine.disease030104 developmental biologyMutationCutaneous melanomaCDKN2A; cutaneous melanoma; familial melanoma; germline mutation; p.R87W mutation; p14ARF; p16INK4a; Cancer Research; Oncology; Molecular Medicine; Pharmacologybusiness
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Variant recurrence in neurodevelopmental disorders: the use of publicly available genomic data identifies clinically relevant pathogenic missense var…

2019

Next-generation sequencing has revealed the major impact of de novo variants (DNVs) in developmental disorders (DD) such as intellectual disability, autism, and epilepsy. However, a substantial fraction of these predicted pathogenic DNVs remains challenging to distinguish from background DNVs, notably the missense variants acting via nonhaploinsufficient mechanisms on specific amino acid residues. We hypothesized that the detection of the same missense variation in at least two unrelated individuals presenting with a similar phenotype could be a powerful approach to reveal novel pathogenic variants. We looked for variations independently present in both our database of >1200 solo exomes and…

Male0301 basic medicineCandidate geneDevelopmental DisabilitiesMutation Missense030105 genetics & heredityBiology03 medical and health sciencesNeurodevelopmental disorderIntellectual DisabilityDatabases GeneticIntellectual disabilitymedicineHumansMissense mutationExomeGenetic Predisposition to DiseaseGenetic TestingAutistic DisorderGeneGenetics (clinical)Exome sequencingGeneticsComputational BiologyHigh-Throughput Nucleotide SequencingGenomicsSequence Analysis DNAmedicine.diseasePhenotype030104 developmental biologyNeurodevelopmental DisordersAutismFemaleTranscription FactorsGenetics in Medicine
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Novel Mutations in the NKX2.1 gene and the PAX8 gene in a Boy with Brain-Lung-Thyroid Syndrome

2017

Abstract Objective To elucidate the molecular mechanism which causes thyroid dysgenesis (TD) in a boy with brain-lung-thyroid syndrome. Design, patients, measurements We describe a patient with TD, respiratory disease and cerebral palsy who is heterozygous for mutations in two different genes, the PAX8 (p.E234K) and the NKX2.1 (p.A329GfsX108). In vitro studies were performed to functionally characterize these mutations. Congenital hypothyroidism (CH) was identified by neonatal screening associated with a hypoplastic thyroid gland. Postpartum he developed a brain-lung-thyroid syndrome with severe respiratory failure, symptomatic epilepsy and a considerable psychomotor retardation. The DNA-bi…

Male0301 basic medicineCandidate geneEndocrinology Diabetes and MetabolismThyroid Nuclear Factor 1030105 genetics & heredityBiologymedicine.disease_causeThyroid dysgenesisPAX8 Transcription Factor03 medical and health sciencesEndocrinologyChoreaCongenital HypothyroidismInternal MedicinemedicineHumansChildAthetosisGeneRespiratory Distress Syndrome NewbornMutationPsychomotor retardationGeneral Medicinemedicine.diseasePhenotypeCongenital hypothyroidismMutationCancer researchmedicine.symptomPAX8Experimental and Clinical Endocrinology & Diabetes
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WNT Signaling Perturbations Underlie the Genetic Heterogeneity of Robinow Syndrome

2018

International audience; Locus heterogeneity characterizes a variety of skeletal dysplasias often due to interacting or overlapping signaling pathways. Robinow syndrome is a skeletal disorder historically refractory to molecular diagnosis, potentially stemming from substantial genetic heterogeneity. All current known pathogenic variants reside in genes within the noncanonical Wnt signaling pathway including ROR2, WNT5A, and more recently, DVL1 and DVL3. However, ∼70% of autosomal-dominant Robinow syndrome cases remain molecularly unsolved. To investigate this missing heritability, we recruited 21 families with at least one family member clinically diagnosed with Robinow or Robinow-like pheno…

Male0301 basic medicineCandidate geneFrizzledGROWTH-PLATEDEP DOMAINlnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]PROTEINskeletal dysplasiaCraniofacial Abnormalities0302 clinical medicineLocus heterogeneityChromosome SegregationChild[ SDV.GEN.GH ] Life Sciences [q-bio]/Genetics/Human geneticsWnt Signaling PathwayGenetics (clinical)Genes DominantGeneticsWnt signaling pathwayMiddle AgedRobinow syndromeMENDELIAN-INHERITANCEPhenotypeChild PreschoolFemaleNEURAL-TUBE DEFECTSVERTEBRATE GASTRULATIONhuman embryonic developmentRare cancers Radboud Institute for Health Sciences [Radboudumc 9]AdultAdolescentCELL POLARITYLimb Deformities CongenitalMutation MissenseDwarfismBiologyArticledual molecular diagnosisDiagnosis DifferentialGenetic Heterogeneity03 medical and health sciencesFrizzledAll institutes and research themes of the Radboud University Medical CenterSkeletal disorderGeneticsmedicineHumansGenetic Association StudiesNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]Base SequenceGenetic heterogeneityMUTATIONSROR2medicine.diseaseDROSOPHILA TISSUE POLARITY030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsUrogenital AbnormalitiesAUTOSOMAL-DOMINANT030217 neurology & neurosurgery
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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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NBEA : developmental disease gene with early generalized epilepsy phenotypes

2018

Abstract: NBEA is a candidate gene for autism, and de novo variants have been reported in neurodevelopmental disease (NDD) cohorts. However, NBEA has not been rigorously evaluated as a disease gene, and associated phenotypes have not been delineated. We identified 24 de novo NBEA variants in patients with NDD, establishing NBEA as an NDD gene. Most patients had epilepsy with onset in the first few years of life, often characterized by generalized seizure types, including myoclonic and atonic seizures. Our data show a broader phenotypic spectrum than previously described, including a myoclonic-astatic epilepsy-like phenotype in a subset of patients. Ann Neurol 2018;84:796-803

Male0301 basic medicineCarrier Proteins/geneticsCandidate geneDiseaseNeurodevelopmental Disorders/geneticsEpilepsy0302 clinical medicineNerve Tissue Proteins/geneticsChildAtonic seizureGeneticsddc:618PhenotypePhenotypeNeurologyChild PreschoolEpilepsy GeneralizedFemaleNEUROBEACHINRare cancers Radboud Institute for Health Sciences [Radboudumc 9]AdolescentGenotypeGeneralized/geneticsNerve Tissue ProteinsBiologyPATIENTArticle03 medical and health sciencesAll institutes and research themes of the Radboud University Medical CentermedicineJournal ArticleHumansGeneralized epilepsyAUTISMPreschoolGeneSPECTRUMNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]EpilepsyDELETIONNBEA encodes neurobeachinmedicine.diseaseFRAMEWORK030104 developmental biology[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsNeurodevelopmental DisordersDE-NOVO MUTATIONSMutationAutismNeurology (clinical)Human medicineCarrier Proteins030217 neurology & neurosurgeryAnnals of neurology
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The Greeks in the West: genetic signatures of the Hellenic colonisation in southern Italy and Sicily

2015

Greek colonisation of South Italy and Sicily (Magna Graecia) was a defining event in European cultural history, although the demographic processes and genetic impacts involved have not been systematically investigated. Here, we combine high-resolution surveys of the variability at the uni-parentally inherited Y chromosome and mitochondrial DNA in selected samples of putative source and recipient populations with forward-in-time simulations of alternative demographic models to detect signatures of that impact. Using a subset of haplotypes chosen to represent historical sources, we recover a clear signature of Greek ancestry in East Sicily compatible with the settlement from Euboea during the…

Male0301 basic medicineDIVERSITYPopulation geneticsSicilyPhylogenyGenetics (clinical)POPULATIONGeneticseducation.field_of_studyGeographyGreecehuman population geneticEcologyY-CHROMOSOMEY-CHROMOSOME; POPULATION; ADMIXTURE; LINEAGES; MUTATIONS; DIVERSITY; MODELS; PAIR; TIME; WAVETIMEADMIXTUREFemaleGreeksPopulationMODELSSouth ItalySettore BIO/08 - ANTROPOLOGIABiologyArchaic periodArticleY-CHROMOSOME ; POPULATION ; LINEAGES ; ADMIXTURE ; MUTATIONS ; DIVERSITY ; EXPANSION ; ANCESTOR ; HISTORY ; MODELS03 medical and health sciencesPAIRDemography; Female; Geography; Greece; Haplotypes; Humans; Male; Mutation; Phylogeny; Sicily; Genetics Population; Genetics; Genetics (clinical)GeneticsHumansAncient Greeks population geneticseducationDemographygenetics (clinical); geneticsY chromosomeMUTATIONSHaplotypeLINEAGESpopulation geneticsColonisationGenetics Population030104 developmental biologyHaplotypesGreek ancestryMutationgenetic markersWAVE
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Mutation spectrum of NF1 gene in Italian patients with neurofibromatosis type 1 using Ion Torrent PGM™ platform

2017

Neurofibromatosis type 1 (NF1) is caused by mutations of the NF1 gene and is one of the most common human autosomal dominant disorders. The patient shows different signs on the skin and other organs from early childhood. The best known are six or more café au lait spots, axillary or inguinal freckling, increased risk of developing benign nerve sheath tumours and plexiform neurofibromas. Mutation detection is complex, due to the large gene size, the large variety of mutations and the presence of pseudogenes. Using Ion Torrent PGM™ Platform, 73 mutations were identified in 79 NF1 Italian patients, 51% of which turned out to be novel mutations. Pathogenic status of each variant was classifi…

Male0301 basic medicineDNA Mutational Analysismedicine.disease_causeChildGenetics (clinical)Sanger sequencingGeneticsMutationNeurofibromin 1biologyMosaicismCafe-au-Lait SpotsNeurofibromatosis type 1; Legius's syndrome; Next generation sequencingGeneral MedicineMiddle AgedItalyChild PreschoolsymbolsMedical geneticsFemalemedicine.symptomHumanAdultmedicine.medical_specialtyNeurofibromatosis 1AdolescentPseudogeneDNA Mutational Analysi03 medical and health sciencessymbols.namesakeGeneticNext generation sequencingCafé au lait spotSkin AbnormalitieGeneticsmedicineHumansCafe-au-Lait SpotNeurofibromatosisLegius's syndromeInfantSequence Analysis DNAIon semiconductor sequencingmedicine.diseaseNeurofibromin 1030104 developmental biologyMutationSkin Abnormalitiesbiology.proteinNeurofibromatosis type 1European Journal of Medical Genetics
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Sensitivity of pancreatic cancer cells to chemotherapeutic drugs, signal transduction inhibitors and nutraceuticals can be regulated by WT-TP53

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is a highly metastatic malignancy. Approximately 85% of pancreatic cancers are classified as PDACs. The survival of PDAC patients is very poor and only 5–10% of patients survive 5 years after diagnosis. Mutations at the KRAS and TP53 gene are frequently observed in PDAC patients. The PANC-28 cell line lacks wild-type (WT) TP53. In the following study, we have investigated the effects of restoration of WT TP53 activity on the sensitivity of PANC-28 pancreatic cancer cells to various drugs which are used to treat PDAC patients as well as other cancer patients. In addition, we have examined the effects of signal transduction inhibitors which tar…

Male0301 basic medicineDrugCancer ResearchmiRsendocrine system diseasesmedia_common.quotation_subjectSignal transduction inhibitorsTargeted therapeuticAntineoplastic AgentsMalignancymedicine.disease_causeProto-Oncogene Proteins p21(ras)03 medical and health sciences0302 clinical medicineChloroquinePancreatic cancerGeneticsmedicineHumansTP53Molecular BiologyneoplasmsSignal transduction inhibitorTargeted therapeuticsCell Proliferationmedia_commontarget therapeuticsCell growthbusiness.industryCancermedicine.diseasedigestive system diseasesMetforminPancreatic Neoplasms030104 developmental biology030220 oncology & carcinogenesisDietary SupplementsMutationCancer researchmiRs.Molecular MedicineFemaleKRASTumor Suppressor Protein p53businessSignal Transductionmedicine.drugDrug sensitivity
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Corticotroph aggressive pituitary tumours and carcinomas frequently harbour ATRX mutations

2021

Abstract Context Aggressive pituitary tumors (APTs) are characterized by unusually rapid growth and lack of response to standard treatment. About 1% to 2% develop metastases being classified as pituitary carcinomas (PCs). For unknown reasons, the corticotroph tumors are overrepresented among APTs and PCs. Mutations in the alpha thalassemia/mental retardation syndrome X-linked (ATRX) gene, regulating chromatin remodeling and telomere maintenance, have been implicated in the development of several cancer types, including neuroendocrine tumors. Objective To study ATRX protein expression and mutational status of the ATRX gene in APTs and PCs. Design We investigated ATRX protein expression by us…

Male0301 basic medicineEndocrinology Diabetes and MetabolismClinical Biochemistrypituitary adenomapituitary carcinomaBiochemistryPATHWAYCohort Studies0302 clinical medicineEndocrinologyGene FrequencyTELOMERESCorticotrophsClinical Laboratory MedicineGenomicsMiddle AgedCushing’s diseaseEUROPEAN-SOCIETY3. Good healthEuropeKlinisk laboratoriemedicinACTH-Secreting Pituitary Adenoma030220 oncology & carcinogenesisDAXX/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingCushing's diseaseFemaleATRX (alpha thalassemia/mental retardation syndrome X-linked); aggressive PitNETs; pituitary carcinoma; pituitary adenoma; Cushings diseaseAcademicSubjects/MED00250EXPRESSIONAdenomaAdultX-linked Nuclear Proteinmedicine.medical_specialtyGENESAdolescentATRX (alpha thalassemia/mental retardation syndrome X-linked)3122 CancersNonsense mutationContext (language use)CLASSIFICATIONYoung Adult03 medical and health sciencesDeath-associated protein 6SDG 3 - Good Health and Well-beingPituitary adenomaInternal medicineADENOMASmedicineHumansGenetic Predisposition to DiseaseNeoplasm InvasivenessPituitary NeoplasmsClinical Research ArticlesATRXAgedCancer och onkologiaggressive PitNETsbusiness.industryCarcinomaBiochemistry (medical)Pituitary tumorsCancerAMPLIFICATIONNeuroendocrinologymedicine.disease030104 developmental biologyEndocrinologyPituitary3121 General medicine internal medicine and other clinical medicineCancer and OncologyMutationPituitary carcinomaCancer researchbusinessATRX (alpha thalassemia/mental retardation syndrome X-linked); Cushing’s disease; aggressive PitNETs; pituitary adenoma; pituitary carcinoma
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