Search results for "MUTATION"

showing 10 items of 2830 documents

Clinical characteristics of patients with familial amyotrophic lateral sclerosis carrying the pathogenic GGGGCC hexanucleotide repeat expansion of C9…

2012

A large hexanucleotide (GGGGCC) repeat expansion in the first intron of C9ORF72, a gene located on chromosome 9p21, has been recently reported to be responsible for 40% of familial amyotrophic lateral sclerosis cases of European ancestry. The aim of the current article was to describe the phenotype of amyotrophic lateral sclerosis cases carrying the expansion by providing a detailed clinical description of affected cases from representative multi-generational kindreds, and by analysing the age of onset, gender ratio and survival in a large cohort of patients with familial amyotrophic lateral sclerosis. We collected DNA and analysed phenotype data for 141 index Italian familial amyotrophic l…

MaleParentsPathologyphenotype-genotype correlationCohort Studies0302 clinical medicineC9orf72amyotrophic lateral sclerosigeneticsAmyotrophic lateral sclerosisAge of Onsetamyotrophic lateral sclerosis; familial als; C9Orf72; phenotype-genotype correlation0303 health sciencesSex CharacteristicsDNA Repeat ExpansionAdult Age of Onset Aged Amyotrophic Lateral Sclerosis; genetics/pathology Cohort Studies DNA Repeat Expansion DNA; genetics Female Humans Italy Male Middle Aged Mutation; genetics Parents Pedigree Phenotype Proteins; genetics Sex Characteristics Survival AnalysisMiddle Aged3. Good healthPedigreeSettore MED/26 - NEUROLOGIAPhenotypeItalyC9Orf72Settore MED/26 - NeurologiaFemaleFrontotemporal dementiaAdultmedicine.medical_specialtySOD1BiologyTARDBP03 medical and health sciencesInternal medicinemedicineHumans030304 developmental biologyAgedamyotrophic lateral sclerosis familial ALS C9ORF72 gene phenotype–genotype correlationC9orf72 ProteinAmyotrophic Lateral Sclerosisgenetics/pathologyProteinsOriginal ArticlesDNAmedicine.diseaseSurvival AnalysisC9orf72 ProteinSettore BIO/18 - Geneticaamyotrophic lateral sclerosis; familial ALS C9ORF72 gene; phenotype-genotype correlation;MutationNeurology (clinical)Age of onsetTrinucleotide repeat expansionfamilial al030217 neurology & neurosurgery
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Identification of the novel D297fsX318 PINK1 mutation and phenotype variation in a family with early-onset Parkinson's disease

2008

Herein we first describe a novel homozygous single nucleotide deletion in PINK1 exon 4 (889delG) which results in a loss of kinase domain on the PINK1 protein (D297fsX318). This mutation was identified in two brothers with early-onset Parkinson disease (EOPD) from a Sicilian consanguineous family. Of note, while one of the two patients developed mental deterioration and psychiatric problems, the other showed no cognitive decline. The present study supports the view that PINK1 is a pathogenic gene in some Italian families with EOPD and contributes to define the PINK1-associated phenotype. Herein we first describe a novel homozygous single nucleotide deletion in PINK1 exon 4 (889delG) which r…

MaleParkinson's diseaseGenotypeParkinson's diseaseMolecular Sequence DataPINK1DiseaseBiologyAntiparkinson AgentsLevodopaExonmedicineHumansAmino Acid SequenceAge of OnsetCognitive declineGeneAgedGeneticsGenotype–phenotype correlationPINK1Parkinson DiseaseExonsFamilial formmedicine.diseasePhenotypePedigreeSettore BIO/18 - GeneticaPhenotypeNeurologyMutationMutation (genetic algorithm)Settore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyCognition DisordersProtein KinasesGene DeletionParkinsonism & Related Disorders
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A multi-centre clinico-genetic analysis of the VPS35 gene in Parkinson disease indicates reduced penetrance for disease-associated variants

2012

Abstract: Background Two recent studies identified a mutation (p.Asp620Asn) in the vacuolar protein sorting 35 gene as a cause for an autosomal dominant form of Parkinson disease. Although additional missense variants were described, their pathogenic role yet remains inconclusive. Methods and results We performed the largest multi-center study to ascertain the frequency and pathogenicity of the reported vacuolar protein sorting 35 gene variants in more than 15,000 individuals worldwide. p.Asp620Asn was detected in 5 familial and 2 sporadic PD cases and not in healthy controls, p.Leu774Met in 6 cases and 1 control, p.Gly51Ser in 3 cases and 2 controls. Overall analyses did not reveal any sig…

MaleParkinson's diseasePopulationVesicular Transport ProteinsLocus (genetics)DiseaseBiologyVPS35 protein humanBioinformaticsgenetics [Vesicular Transport Proteins]genetics [Parkinson Disease]Risk Factorsmedicinemetabolism [Vesicular Transport Proteins]GeneticsMissense mutationVPS35 GeneHumansGenetic epidemiologyGenetic Predisposition to Diseaseddc:6101506Genome-wideeducationGenetics (clinical)Genetic Association StudiesGeneticsVacuolar protein sortingeducation.field_of_studyGenotype-Phenotype CorrelationsParkinson DiseaseComplex traitsmedicine.diseasePenetranceddc:MutationFemaleHuman medicineParkinson-s diseaseJournal of Medical Genetics
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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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Prognostic significance of K-Ras mutation rate in metastatic colorectal cancer patients

2015

// Bruno Vincenzi 1 , Chiara Cremolini 2 , Andrea Sartore-Bianchi 3 , Antonio Russo 4 , Francesco Mannavola 5 , Giuseppe Perrone 6 , Francesco Pantano 1 , Fotios Loupakis 2 , Daniele Rossini 2 , Elena Ongaro 7 , Erica Bonazzina 3 , Emanuela Dell’Aquila 1 , Marco Imperatori 1 , Alice Zoccoli 1 , Giuseppe Bronte 4 , Giovanna De Maglio 7 , Gabriella Fontanini 8 , Clara Natoli 9 , Alfredo Falcone 2 , Daniele Santini 1 , Andrea Onetti-Muda 6 , Salvatore Siena 3 , Giuseppe Tonini 1 and Giuseppe Aprile 7 1 Department of Medical Oncology, Campus Bio-Medico University of Rome, Rome, Italy 2 Azienda Ospedaliero-Universitaria Pisana, Istituto Toscano Tumori, Pisa, Italy 3 Niguarda Cancer Center, Osped…

MalePathologyColorectal cancerSettore MED/06 - Oncologia MedicaColorectal NeoplasmRetrospective StudieAntineoplastic Combined Chemotherapy ProtocolsTumor Cells Culturededucation.field_of_studyUnivariate analysisBevacizumab; Colorectal cancer; K-Ras; Mutation rate; Prognosis; OncologyLiver NeoplasmsMiddle AgedPrognosisBevacizumabSurvival RateOncologyLiver NeoplasmCohortFemaleK-Ras; mutation rate; colorectal cancer; bevacizumab; prognosisColorectal NeoplasmsK-RasResearch Papermedicine.drugHumanmedicine.medical_specialtyBevacizumabPrognosiMutation ratePopulationBevacizumab; Colorectal cancer; K-Ras; Mutation rate; Prognosis; Antineoplastic Combined Chemotherapy Protocols; Colorectal Neoplasms; Female; Follow-Up Studies; Humans; Liver Neoplasms; Male; Middle Aged; Mutation; Neoplasm Staging; Prognosis; Proto-Oncogene Proteins p21(ras); Real-Time Polymerase Chain Reaction; Retrospective Studies; Survival Rate; Tumor Cells Cultured; OncologyReal-Time Polymerase Chain ReactionFollow-Up StudieProto-Oncogene Proteins p21(ras)Internal medicinemedicineHumanseducationSurvival rateRetrospective StudiesNeoplasm StagingAntineoplastic Combined Chemotherapy Protocolbusiness.industryCancerRetrospective cohort studymedicine.diseaseColorectal cancerK-RaMutationbusinessFollow-Up Studies
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Expanding the clinical spectrum of hereditary fibrosing poikiloderma with tendon contractures, myopathy and pulmonary fibrosis due to FAM111B mutatio…

2015

Background Hereditary Fibrosing Poikiloderma (HFP) with tendon contractures, myopathy and pulmonary fibrosis (POIKTMP [MIM 615704]) is a very recently described entity of syndromic inherited poikiloderma. Previously by using whole exome sequencing in five families, we identified the causative gene, FAM111B (NM_198947.3), the function of which is still unknown. Our objective in this study was to better define the specific features of POIKTMP through a larger series of patients. Methods Clinical and molecular data of two families and eight independent sporadic cases, including six new cases, were collected. Results Key features consist of: (i) early-onset poikiloderma, hypotrichosis and hypoh…

MalePathologyMyopathyPulmonary FibrosisMedicine/Public HealthCell Cycle ProteinsGrowthHypotrichosisContracturesTendons030207 dermatology & venereal diseases0302 clinical medicineFibrosisPulmonary fibrosisSerineGenetics(clinical)Pharmacology (medical)TrypsinExomeChildGenetics (clinical)FAM111BSkinMedicine(all)0303 health sciencesMicroscopyMuscle WeaknessMusclesSkin Diseases GeneticGeneral MedicineMiddle AgedMagnetic Resonance ImagingMuscle atrophy3. Good healthMuscular AtrophyTissuesLiverChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtyContractureAdolescentMolecular Sequence DataPoikiloderma03 medical and health sciencesPoikilodermaMuscular DiseasesmedicineHumansAdiposisAmino Acid SequenceCysteineExocrine pancreatic insufficiencyMyopathyMuscle Skeletal030304 developmental biologyMuscle contractureHypohidrosisSclerosisbusiness.industryResearchInfantProteinsmedicine.diseaseFibrosisGenesMutationSkin AbnormalitiesHypotrichosisExocrine Pancreatic Insufficiencybusiness
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BRAF-V600E expression in precursor versus differentiated dendritic cells defines clinically distinct LCH risk groups.

2014

BRAF-V600E expression is identified in hematopoietic progenitor and precursor myeloid dendritic cells in patients with high-risk LCH, and enforced expression of BRAF-V600E in CD11c+ cells recapitulates a high-risk LCH-like phenotype in mice.

MalePathologyendocrine system diseasesCellular differentiationCD34Antigens CD34Mice0302 clinical medicineLangerhans cell histiocytosisBone MarrowRisk FactorsImmunology and Allergyskin and connective tissue diseasesChild0303 health sciencesCell Differentiation3. Good healthHistiocytosismedicine.anatomical_structurePhenotypeTreatment Outcome030220 oncology & carcinogenesisChild PreschoolAntigens Surface2723 Immunology and AllergyFemaleProto-Oncogene Proteins B-rafmedicine.medical_specialtyImmunologyCD11c610 Medicine & healthBiologyArticle03 medical and health sciencesGermline mutationmedicineAnimalsHumansCell LineageGenetic Predisposition to DiseaseLectins C-TypeProgenitor cellneoplasms030304 developmental biology2403 ImmunologyHistocompatibility Antigens Class II302InfantCorrectionDendritic Cellsmedicine.diseaseHematopoietic Stem Cellsdigestive system diseasesCD11c Antigenenzymes and coenzymes (carbohydrates)Histiocytosis Langerhans-CellMannose-Binding Lectins10032 Clinic for Oncology and HematologyMutationBone marrowThe Journal of experimental medicine
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A European family with histidine 58 transthyretin mutation in familial amyloid polyneuropathy

1997

1. IntroductionMore than 50 mutations of the transthyretin (TTR) [1]molecule resulting in different clinical forms of amyloidosisincluding familial amyloid polyneuropathy (FAP) havebeen reported to date. Within this FAP spectrum severaltransthyretin mutations are more frequent, others are rare.One mutation, the codon 58 histidine for leucine has pre-viously been recorded only in American subjects (Mary-land/German type), originally reported in a large kinship[2,3] and in another family from Ohio [4]. In the originaldescription of the Maryland/German type of amyloidosis[2], it was stated that the early immigrants in this pedigreewere from the Rhine river area, "nearly all of them from thelef…

MalePathologymedicine.medical_specialtyAtaxiaAmyloid Neuropathiesmedicine.disease_causeAtrophyLeucineGermanymedicineHumansPoint MutationPrealbuminHistidineCodonGenetics (clinical)Genes DominantMutationDysesthesiabiologybusiness.industryPoint mutationAmyloidosisMiddle Agedmedicine.diseaseUnited StatesTransthyretinNeurologyPediatrics Perinatology and Child Healthbiology.proteinNeurology (clinical)medicine.symptomRestriction fragment length polymorphismbusinessNeuromuscular Disorders
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SIL1 mutations and clinical spectrum in patients with Marinesco-Sjogren syndrome.

2013

Marinesco-Sjogren syndrome is a rare autosomal recessive multisystem disorder featuring cerebellar ataxia, early-onset cataracts, chronic myopathy, variable intellectual disability and delayed motor development. More recently, mutations in the SIL1 gene, which encodes an endoplasmic reticulum resident co-chaperone, were identified as the main cause of Marinesco-Sjogren syndrome. Here we describe the results of SIL1 mutation analysis in 62 patients presenting with early-onset ataxia, cataracts and myopathy or combinations of at least two of these. We obtained a mutation detection rate of 60% (15/25) among patients with the characteristic Marinesco-Sjogren syndrome triad (ataxia, cataracts, m…

MalePathologymedicine.medical_specialtyAtaxiaultrastructure [Muscle Skeletal]SIL1 protein humanAdolescentMarinesco–Sjögren syndromeDNA Mutational Analysisgenetics [Mutation]Bioinformaticsmedicine.disease_causepathology [Muscle Skeletal]physiopathology [Spinocerebellar Degenerations]Cataractspathology [Brain]Intellectual disabilitymedicineGuanine Nucleotide Exchange FactorsHumansddc:610MyopathyMuscle SkeletalCells CulturedRetrospective StudiesSpinocerebellar DegenerationsFamily HealthMutationB-LymphocytesCerebellar ataxiabusiness.industryBrainmedicine.diseasegenetics [Guanine Nucleotide Exchange Factors]Magnetic Resonance Imaging10124 Institute of Molecular Life Sciencesgenetics [Spinocerebellar Degenerations]2728 Neurology (clinical)pathology [Spinocerebellar Degenerations]Mutationultrastructure [Brain]570 Life sciences; biologyAllelic heterogeneityFemaleNeurology (clinical)Neurosciences & Neurologymedicine.symptombusinessBrain : a journal of neurology
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Portal Vein Thrombosis in a Preterm Newborn with Mutation of the MTHFR and PAI-1 Genes and Sepsis by Candida parapsilosis

2016

Objective This report discusses the role of both congenital and acquired risk factors in the pathogenesis of portal vein thrombosis (PVT). Study Design We describe the clinical management and treatment of PVT in a preterm newborn with a homozygous mutation of the methylenetetrahydrofolate reductase (MTHFR) and plasminogen activator inhibitor-1 (PAI-1) genes and sepsis by Candida parapsilosis. Results Although literature data suggest a minor role of genetic factors in thrombophilia in the case of only one mutation, we hypothesize that combined thrombophilic genetic defects may have a cumulative effect and significantly increase the thrombotic risk. Conclusion It could be appropriate to incl…

MalePathologymedicine.medical_specialtyCandida parapsilosis030204 cardiovascular system & hematologyBioinformaticsCandida parapsilosisThrombophiliaSepsisPathogenesis03 medical and health sciences0302 clinical medicineSepsis030225 pediatricsPlasminogen Activator Inhibitor 1medicineHumansMethylenetetrahydrofolate Reductase (NADPH2)Venous ThrombosisPolymorphism GeneticbiologyPortal Veinbusiness.industryCandidiasisInfant NewbornAnticoagulantsFactor VObstetrics and Gynecologyportal thrombosis fungal infection gene polymorphismmedicine.diseasebiology.organism_classificationPortal vein thrombosisSurgical Procedures OperativeMethylenetetrahydrofolate reductaseMutationPediatrics Perinatology and Child Healthbiology.proteinGene polymorphismbusinessPlasminogen activatorAmerican Journal of Perinatology
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