Search results for "MUTATION"

showing 10 items of 2830 documents

Assessment of morphological CT imaging features for the prediction of risk stratification, mutations, and prognosis of gastrointestinal stromal tumors

2021

To investigate the correlation between CT imaging features and risk stratification of gastrointestinal stromal tumors (GISTs), prediction of mutation status, and prognosis. This retrospective dual-institution study included patients with pathologically proven GISTs meeting the following criteria: (i) preoperative contrast-enhanced CT performed between 2008 and 2019; (ii) no treatments before imaging; (iii) available pathological analysis. Tumor risk stratification was determined according to the National Institutes of Health (NIH) 2008 criteria. Two readers evaluated the CT features, including enhancement patterns and tumor characteristics in a blinded fashion. The differences in distributi…

Malemedicine.medical_specialtyMultivariate analysisGastrointestinal Stromal TumorsPopulationX-ray computedRisk Assessment030218 nuclear medicine & medical imaging03 medical and health sciences0302 clinical medicinemedicineHumansRadiology Nuclear Medicine and imagingProgression-free survivaleducationPathologicalTomographySurvival analysisGastrointestinal stromal tumors; Mutation; Progression-free survival; Survival analysis; Tomography X-ray computed; Aged; Female; Humans; Male; Middle Aged; Mutation; Prognosis; Retrospective Studies; Risk Assessment; Tomography X-Ray Computed; Gastrointestinal Stromal TumorsNeuroradiologyAgedRetrospective Studieseducation.field_of_studybusiness.industryProportional hazards modelTomography X-ray computedHazard ratioProgression-free survivalGeneral MedicineSurvival analysisMiddle AgedPrognosis030220 oncology & carcinogenesisMutationFemaleRadiologyGastrointestinal stromal tumors Mutation Progression-free survival Survival analysis Tomography X-ray computedbusiness
researchProduct

TET2 gene mutation is a frequent and adverse event in chronic myelomonocytic leukemia

2009

Background Acquired somatic deletions and loss-of-function mutations in one or several codons of the TET2 ( Ten-Eleven Translocation-2 ) gene were recently identified in hematopoietic cells from patients with myeloid malignancies, including myeloproliferative disorders and myelodys-plastic syndromes. The present study was designed to determine the prevalence of TET2 gene alterations in chronic myelomonocytic leukemias. Design and Methods Blood and bone marrow cells were collected from 88 patients with chronic phase chronic myelomonocytic leukemia and from 14 with acute transformation of a previously identified disease. Polymerase chain reaction analysis and direct sequencing were used to se…

Malemedicine.medical_specialtyMyeloidDNA Mutational AnalysisChronic myelomonocytic leukemiaSingle-nucleotide polymorphismKaplan-Meier EstimateGene mutationBiologymedicine.disease_causeDioxygenasesGene FrequencyMonocytosisInternal medicinehemic and lymphatic diseasesProto-Oncogene ProteinsmedicineHumansGenetic Predisposition to DiseaseLetters to the EditorAgedProportional Hazards ModelsAged 80 and overComparative Genomic HybridizationMutationHematologyLeukemia Myelomonocytic ChronicHematologyMiddle Agedmedicine.diseaseMyelodysplastic-Myeloproliferative DiseasesDNA-Binding ProteinsLeukemiamedicine.anatomical_structureImmunologyMutationFemaleOriginal Article
researchProduct

The parkin gene is not a major susceptibility locus for typical late-onset Parkinson's disease

2001

We investigated the parkin gene in 118 patients with typical Parkinson's disease (PD), i. e. in patients who had an onset of PD after the age of 45 years. The study group included 95 subjects with sporadic PD and 23 subjects from 18 families with autosomal recessive PD. No pathogenetic mutations in the parkin gene were detected either in familial or in sporadic patients. Our findings indicate that the parkin gene is not involved in the pathogenesis of classic late-onset PD.

Malemedicine.medical_specialtyNeurologyParkinson's diseaseUbiquitin-Protein LigasesDNA Mutational AnalysisMolecular Sequence DataLate onsetGenes RecessiveDermatologyDiseaseParkinPathogenesisLigasesParkinsonian DisordersmedicineHumansPoint MutationGenetic Predisposition to DiseaseGenetic TestingAge of OnsetAgedGeneticsbusiness.industryGeneral MedicineExonsParkin geneMiddle Agedmedicine.diseasenervous system diseasesPsychiatry and Mental healthSusceptibility locusChromosomes Human Pair 6FemaleNeurology (clinical)business
researchProduct

Murine tissue factor disulfide mutation causes a bleeding phenotype with sex specific organ pathology and lethality.

2019

Tissue factor is highly expressed in sub-endothelial tissue. The extracellular allosteric disulfide bond Cys186-Cys209 of human tissue factor shows high evolutionary conservation and in vitro evidence suggests that it significantly contributes to tissue factor procoagulant activity. To investigate the role of this allosteric disulfide bond in vivo, we generated a C213G mutant tissue factor mouse by replacing Cys213 of the corresponding disulfide Cys190-Cys213 in murine tissue factor. A bleeding phenotype was prominent in homozygous C213G tissue factor mice. Pre-natal lethality of 1/3rd of homozygous offspring was observed between E9.5 and E14.5 associated with placental hemorrhages. After b…

Malemedicine.medical_specialtyOffspring610 Medicine & healthHemorrhage030204 cardiovascular system & hematologyBiologymedicine.disease_causeArticleThromboplastin11459 Center for Molecular Cardiology03 medical and health sciencesTissue factorArterial Thrombosis; Blood Coagulation and Fibrinolysis; Disorders of Coagulation and FibrinolysisMice0302 clinical medicineIn vivoPregnancyInternal medicinemedicineExtracellularAnimalsDisulfidesMutationHematologyPhenotypeIn vitroEndocrinologyPhenotype10036 Medical Clinic10076 Center for Integrative Human PhysiologyHemostasisMutation10209 Clinic for CardiologyFemale030215 immunologyHaematologica
researchProduct

Development of systemic lupus erythematosus in a patient with selective complete C1q deficiency

1997

A 7-year-old male with recurrent erythematous and desquamated skin lesions and respiratory infections was diagnosed as selective complete C1q deficiency following detailed studies of the complement system. His asymptomatic sister also had selective complete C1q deficiency. During a follow up period of 3 years, his skin lesions persisted, he suffered from recurrent bronchopneumonias and glomerulonephritis developed. Renal function deteriorated with the appearance of anti-DNA antibodies. Renal biopsy was consistent with systemic lupus erythematosus. The patient was treated with immunosuppressive drugs, but died of renal failure. It is postulated that in this patient defective clearance of ant…

Malemedicine.medical_specialtyPathologyBlood Protein DisordersRenal functionDiseaseAsymptomaticFatal OutcomemedicineHumansLupus Erythematosus SystemicPoint MutationRenal InsufficiencyChildLupus erythematosusmedicine.diagnostic_testbusiness.industryComplement C1qGlomerulonephritismedicine.diseaseDermatologyComplement systemPediatrics Perinatology and Child HealthRenal biopsymedicine.symptombusinessMalar rashEuropean Journal of Pediatrics
researchProduct

Boy with pseudohypoparathyroidism type 1a caused byGNASgene mutation (deltaN377), Crouzon-like craniosynostosis, and severe trauma-induced bleeding

2009

We report on a 6-month-old boy with craniosynostosis, pseudohypoparathyroidism type 1a (PHP1A), and a GNAS gene mutation. He had synostoses of the coronal, frontal, and sagittal sutures, brachyturricephaly, and hydrocephaly. He also had congenital hypothyroidism, round face, full cheeks, shortness of limbs, mild developmental delay, and muscular hypotonia. Because of progressive hydrocephaly, the synostosis was corrected surgically but circulatory decompensation led to disseminated intravascular coagulation and cerebral infarctions. Our patient died 8 days later. Postmortem molecular studies of GNAS, the gene for guanine nucleotide-binding protein, alpha-stimulating activity polypeptide (ge…

Malemedicine.medical_specialtyPathologyCraniosynostosisFatal OutcomeInternal medicineChromograninsCongenital HypothyroidismGTP-Binding Protein alpha Subunits GsGeneticsmedicineGNAS complex locusHumansGenetic Predisposition to DiseaseGenetics (clinical)PseudohypoparathyroidismDisseminated intravascular coagulationbiologyMuscular hypotoniabusiness.industryCraniofacial DysostosisInfantDysostosisSynostosismedicine.diseaseCongenital hypothyroidismEndocrinologyBrain InjuriesPseudohypoparathyroidismMutationbiology.proteinbusinessIntracranial HemorrhagesHydrocephalusAmerican Journal of Medical Genetics Part A
researchProduct

Factor V Leiden and prothrombin gene mutation in inflammatory bowel disease in a Mediterranean area.

2001

Abstract Background. Thromboembolism has been reported to be associated with inflammatory bowel disease. Aim. To evaluate the association of factor V Leiden and prothrombin gene mutation with inflammatory bowel disease in a population of patients with thromboembolic events and inflammatory bowel disease and in a control population of patients with inflammatory bowel disease without thromboembolic events. Patients and methods. A series of 18 patients with inflammatory bowel disease and a history of arterial or venous thrombosis and 45 patients with inflammatory bowel disease without thromboembolic events were evaluated for the presence of factor V Leiden and prothrombin gene mutation. Freque…

Malemedicine.medical_specialtyPathologyProthrombin gene mutationPopulationGene mutationGastroenterologyInflammatory bowel diseaseCrohn Diseasehemic and lymphatic diseasesInternal medicineThromboembolismFactor V LeidenmedicinePrevalenceHumansPoint Mutationeducationeducation.field_of_studyHepatologybusiness.industryMediterranean RegionGastroenterologyFactor VMiddle Agedmedicine.diseaseVenous thrombosisMediterranean areaColitis UlcerativeFemaleProthrombinFactor V Leiden mutationbusinessDigestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver
researchProduct

A premature infant with Costello syndrome due to a rare G13C HRAS mutation.

2009

Costello syndrome is caused by mutations in the HRAS proto-oncogene whose clinical features in the first year of life include fetal and neonatal macrosomia with subsequent growth impairment due to severe feeding difficulties. We report on a premature male with Costello syndrome due to a rare G13C HRAS mutation and describe his clinical features and evolution during the first year of life. The diagnosis of Costello syndrome may be difficult at birth, especially in very preterm infants in whom feeding difficulties, reduced subcutaneous adipose tissue and failure to thrive are also part of their typical presentation.

Malemedicine.medical_specialtyPediatricsDevelopmental DisabilitiesProto-Oncogene MasprematureSettore MED/38 - Pediatria Generale E SpecialisticaCostello syndromePregnancyInternal medicineIntellectual DisabilityGeneticsmedicineHumansHRASGenetics (clinical)FetusPregnancybusiness.industryInfant NewbornNucleic acid amplification techniqueDNASyndromemedicine.diseaseEndocrinologyGenes rasSettore MED/03 - Genetica MedicaFailure to thriveMutation (genetic algorithm)MutationFemalePresentation (obstetrics)medicine.symptombusinessNucleic Acid Amplification TechniquesInfant PrematureAmerican journal of medical genetics. Part A
researchProduct

Cognitive correlates in amyotrophic lateral sclerosis: a population-based study in Italy.

2014

Background There is less data available regarding the characteristics of cognitive impairment in patients with amyotrophic lateral sclerosis (ALS) in a population-based series. Methodology Patients with ALS incident in Piemonte, Italy, between 2009 and 2011 underwent an extensive neuropsychological battery. Cognitive status was classified as follows: normal cognition, frontotemporal dementia (ALS-FTD), executive cognitive impairment (ALS-ECI), non-executive cognitive impairment (ALS-NECI), behavioural impairment (ALS-Bi), non-classifiable cognitive impairment. We also assessed 127 age-matched and gender-matched controls identified through patients’ general practitioners. Results Out of the …

Malemedicine.medical_specialtyPediatricsNeuromuscular diseasePopulationNeuropsychological TestsSuperoxide Dismutase-1Risk FactorsmedicineDementiaHumansEPIDEMIOLOGYAmyotrophic lateral sclerosisPsychiatryeducationCognitive reserveAgededucation.field_of_studyC9orf72 ProteinSuperoxide DismutaseDEMENTIAAmyotrophic Lateral SclerosisProteinsCognitionmedicine.diseaseSurvival AnalysisALS DEMENTIA EPIDEMIOLOGYDNA-Binding ProteinsPsychiatry and Mental healthItalyCase-Control StudiesMutationSurgeryFemaleSettore MED/26 - NeurologiaNeurology (clinical)ALSPsychologyCognition DisordersMotor neurone diseaseFrontotemporal dementia
researchProduct

Hyperekplexia caused by dominant-negative suppression of glyra1 function.

2007

Hyperekplexia (HE; startle disease; OMIM#149400) is a rare inheritable neurologic disorder characterized by an exaggerated response to sudden stimuli, muscular rigidity, and hyperreflexia, leading to chronic injuries due to unprotected falls. All symptoms are present at birth but gradually decline during the first year of life, although an exaggerated startle response remains during adulthood.1 Dysfunctional inhibitory neurotransmission by glycine (Gly) plays a central role in HE pathogenesis. All patients with HE carry mutations in genes encoding either for α1 (GLYRA1) or β (GLYRB) Gly receptor subunits, presynaptic Gly transporters (SLC6A5), or proteins involved in Gly receptor (GLYR) clu…

Malemedicine.medical_specialtySubunitReflex StartleNonsense mutationCompound heterozygosityGeneReceptors GlycineInternal medicinemedicineMissense mutationHumansGlycine ReceptorHyperekplexiaGlycine receptorNervous System DiseaseGeneticsStartle DiseaseNeuroscience (all)GephyrinbiologyInfantPenetrancePedigreeEndocrinologyHyperekplexiaNON PREVISTO DA NORME REDAZIONALI (“NEUROLOGY”)Codon NonsenseMutationbiology.proteinNeurology (clinical)medicine.symptomNervous System DiseasesCollybistinHuman
researchProduct