Search results for "mutation."

showing 10 items of 2808 documents

Atypical Pleomorphic Extraosseous Ewing Tumor/Peripheral Primitive Neuroectodermal Tumor with Unusual Phenotypic/Genotypic Profile

2002

A pleomorphic undifferentiated tumor primarily located in the retroperitoneum with a phenotype compatible with an extraosseous Ewing tumor/peripheral primitive neuroectodermal tumor (ET/pPNET) pattern and unusual molecular features is described. Immunohistochemically, HBA-71 (CD99/mic2) and several neural markers were intensively expressed together with scattered cells expressing carcinoembryonic antigen (CEA). Short-term culture showed biphasic neuroblastic and epithelioid cell populations, with the latter expressing germ cell markers (CEA, alpha-fetoprotein, and the beta-subunit of chorionic gonadotrophin). Conventional cytogenetics displayed several chromosomic rearrangements, especially…

AdultMalePathologymedicine.medical_specialtyOncogene Proteins FusionChromosomes Human Pair 22CD99Soft Tissue NeoplasmsChromosomal translocationSarcoma EwingBiologyTranslocation GeneticPathology and Forensic MedicineExonFatal OutcomeCarcinoembryonic antigenBiomarkers TumorTumor Cells CulturedmedicineHumansNeuroectodermal Tumors PrimitiveRetroperitoneal NeoplasmsMolecular BiologyGene Rearrangementmedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionPeripheral Primitive Neuroectodermal TumorChromosomes Human Pair 11Neoplasms Second PrimaryDNA NeoplasmCell BiologyGenes p53Chromosome Bandingmedicine.anatomical_structureKaryotypingMutationbiology.proteinEpithelioid cellGerm cellFluorescence in situ hybridizationDiagnostic Molecular Pathology
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Distinct neuropsychological profiles correspond to distribution of cortical thinning in inherited prion disease caused by insertional mutation

2012

Background The human prion diseases are a group of universally fatal neurodegenerative disorders associated with the auto-catalytic misfolding of the normal cell surface prion protein (PrP). Mutations causative of inherited human prion disease (IPD) include an insertion of six additional octapeptide repeats (6-OPRI) and a missense mutation (P102L) with large families segregating for each mutation residing in southern England. Here we report for the first time the neuropsychological and clinical assessments in these two groups. Method The cognitive profiles addressing all major domains were obtained for 26 patients (18 6-OPRI, 8 P102L) and the cortical thickness determined using 1.5T MRI in …

AdultMalePathologymedicine.medical_specialtyPrionsprion diseaseNeuroimagingDiseaseNeuropsychological Testsmedicine.disease_causePrion DiseasesExecutive FunctionYoung AdultHumansMedicineDementiaMissense mutationStrokeMemory DisordersMutationSettore M-PSI/02 - Psicobiologia E Psicologia Fisiologicabusiness.industryGenetic heterogeneityNeuropsychologyBrainMiddle Agedmedicine.diseaseMagnetic Resonance ImagingUnited KingdomMutagenesis InsertionalPsychiatry and Mental healthFemaleSurgeryNeurology (clinical)Cognition DisordersbusinessExecutive dysfunctionJournal of Neurology, Neurosurgery and Psychiatry
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Malignant paraganglioma caused by a novel germline mutation of the succinate dehydrogenase D-gene--a case report.

2008

Background Paragangliomas of the head and neck are rare, mostly benign tumors. Approximately 10% to 15% of paragangliomas are caused by mutations in the succinate dehydrogenase (SDH) genes B, C, or D. These are often multifocal as part of paraganglioma syndromes and hormone secreting, and malignant particularly associated with mutations in SDHB. Methods and Results A 29-year-old man was seen with recurrent paraganglioma. The patient's father reportedly suffered from bilateral carotid body tumors. Imaging studies showed metastases in both lungs and the liver. There was no increased hormone production by the tumor. Sequence analysis of the SDH genes revealed a novel C to T nonsense mutation i…

AdultMalePathologymedicine.medical_specialtySDHBNonsense mutationmedicine.disease_causeRisk AssessmentSkull Base NeoplasmsPheochromocytomaParagangliomaTreatment RefusalGermline mutationParagangliomamedicineMalignant ParagangliomaHumansGenetic Predisposition to DiseaseGerm-Line MutationNeoplasm StagingMutationbusiness.industryBiopsy Needlemedicine.diseaseImmunohistochemistryPedigreeSuccinate DehydrogenaseOtorhinolaryngologyPositron-Emission TomographySDHDbusinessHeadneck
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Cutaneous Lymphadenoma Is a Distinct Trichoblastoma-like Lymphoepithelial Tumor With Diffuse Androgen Receptor Immunoreactivity, Notch1 Ligand in Ree…

2021

The term "cutaneous lymphadenoma" was coined in this journal for an unusual lymphoepithelial cutaneous adnexal neoplasm, possibly with immature pilosebaceous differentiation. Some authors further proposed that cutaneous lymphadenoma was an adamantinoid trichoblastoma. However, although a hair follicle differentiation is widely accepted, the fact that this is a lymphoepithelial tumor is not appropriately explained by the trichoblastoma hypothesis. Our goal was to further clarify the phenotypic and genotypic features of cutaneous lymphadenoma in a series of 11 cases. Histologically, a lobular architecture surrounded by a dense fibrous stroma was present in all cases. The lobules were composed…

AdultMalePathologymedicine.medical_specialtySkin NeoplasmsCD30EGFRDNA Mutational Analysisadamantinoid trichoblastomaGene mutationBiologyStem cell markerT-Lymphocytes RegulatoryPathology and Forensic MedicineLymphocytes Tumor-Infiltratingandrogen receptormedicineBiomarkers TumorHumansReceptor Notch1Reed-Sternberg CellsAgedNotch1Jagged-1cutaneous lymphadenomaHigh-Throughput Nucleotide SequencingEpithelial CellsOriginal ArticlesMiddle Agedmedicine.diseaseHair follicleAdenolymphomaImmunohistochemistryAndrogen receptorErbB ReceptorsTrichoblastomamedicine.anatomical_structureReceptors AndrogenMutationIntraepithelial lymphocyteSurgeryFemaleAnatomyHair FollicleImmunostainingThe American journal of surgical pathology
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Evaluation of prognostic factors and their capacity to predict biological behavior in gastrointestinal stromal tumors.

2011

Gastrointestinal stromal tumors (GISTs) are c-KIT-signaling-driven mesenchymal tumors of the human digestive tract, many of which have c-KIT or PDGFRα activating mutations. The authors studied the immunohistochemical markers, c-KIT and PDGFRα mutations, in GISTs and their association with the clinicopathological and clinical follow-up in 145 GISTs. Tumors were located mainly in the stomach, the median tumor size being 7.5 cm. The mitotic index was ≤5 mitoses per 50 high-power fields in 61% of cases, 96% expressed CD117, and c-KIT or PDGFRα mutations were detected in 68% of cases. The median follow-up of the series was 52 months (range = 1 to 244.9 months). Tumor size, cell morphology, mito…

AdultMalePathologymedicine.medical_specialtyStromal cellMitotic indexReceptor Platelet-Derived Growth Factor alphaGastrointestinal Stromal Tumorsmedicine.disease_causeCell morphologyDisease-Free SurvivalPathology and Forensic MedicineYoung AdultPredictive Value of TestsStomach NeoplasmsIntestinal NeoplasmsmedicineBiomarkers TumorMitotic IndexHumansAgedAged 80 and overMutationbiologyCD117StomachMesenchymal stem cellMiddle AgedPrognosisProto-Oncogene Proteins c-kitmedicine.anatomical_structureKi-67 AntigenMutationbiology.proteinImmunohistochemistrySurgeryFemaleAnatomyInternational journal of surgical pathology
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Mutations in myosin heavy chain 11 cause a syndrome associating thoracic aortic aneurysm/aortic dissection and patent ductus arteriosus

2006

We have recently described two kindreds presenting thoracic aortic aneurysm and/or aortic dissection ( TAAD) and patent ductus arteriosus (PDA)(1,2) and mapped the disease locus to 16p12.2-p13.13 (ref. 3). We now demonstrate that the disease is caused by mutations in the MYH11 gene affecting the C-terminal coiled-coil region of the smooth muscle myosin heavy chain, a specific contractile protein of smooth muscle cells (SMC). All individuals bearing the heterozygous mutations, even if asymptomatic, showed marked aortic stiffness. Examination of pathological aortas showed large areas of medial degeneration with very low SMC content. Abnormal immunological recognition of SM-MHC and the colocal…

AdultMalePathologymedicine.medical_specialty[SDV]Life Sciences [q-bio]Molecular Sequence DataANEURYSM/DISSECTION030204 cardiovascular system & hematologyBiologyThoracic aortic aneurysmProtein Structure SecondaryDISEASEFamilial thoracic aortic aneurysmCOILED-COILS03 medical and health sciencesAortic aneurysm0302 clinical medicineDuctus arteriosusGeneticsmedicineMYH11LOCUSHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAmino Acid SequenceDuctus Arteriosus Patent[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyAortic dissection0303 health sciencesAortic Aneurysm ThoracicBase SequenceMyosin Heavy ChainsSMC proteinHEAVY-CHAIN ISOFORMSAnatomymedicine.diseasePedigreeAortic Dissectionmedicine.anatomical_structureMutationbiology.proteincardiovascular systemFemaleACTA2SMOOTH-MUSCLE MYOSIN
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The Disease-Specific Phenotype in Cardiomyocytes Derived from Induced Pluripotent Stem Cells of Two Long QT Syndrome Type 3 Patients

2013

Long QT syndromes (LQTS) are heritable diseases characterized by prolongation of the QT interval on an electrocardiogram, which often leads to syncope and sudden cardiac death. Here we report the generation of induced pluripotent stems (iPS) cells from two patients with LQTS type 3 carrying a different point mutation in a sodium channel Nav1.5 (p.V240M and p.R535Q) and functional characterization of cardiomyocytes (CM) derived from them. The iPS cells exhibited all characteristic properties of pluripotent stem cells, maintained the disease-specific mutation and readily differentiated to CM. The duration of action potentials at 50% and 90% repolarization was longer in LQTS-3 CM as compared t…

AdultMalePluripotent Stem Cellsmedicine.medical_specialtyLong QT syndromeCellular differentiationlcsh:MedicineAction PotentialsNAV1.5 Voltage-Gated Sodium ChannelQT intervalMembrane PotentialsNAV1.5 Voltage-Gated Sodium ChannelInternal medicinemedicineRepolarizationHumansPoint MutationMyocytes CardiacInduced pluripotent stem celllcsh:ScienceCells CulturedMultidisciplinarybusiness.industryPoint mutationSodium channellcsh:RCell Differentiationmedicine.diseaseLong QT SyndromeEndocrinologylcsh:QFemalebusinessResearch ArticlePLoS ONE
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Detection of HIV type 1 non-B subtypes in Sicily, Italy.

2004

To evaluate the presence of HIV-1 non-B subtypes in Sicily, we sequenced and genotyped HIV-1 PR and RT regions of the pol gene using plasma from 169 HIV-1-infected adult patients. All samples were obtained from a study of antiretroviral-associated resistance mutations resulting in virological failure during highly active antiretroviral therapy (HAART). Eight (4.7%) patients had the non-B HIV-1 subtype including some circulating recombinant forms (CRFs). All of these individuals acquired the infection by heterosexual transmission. The detection of HIV-1 non-B strains was significantly associated with younger age of HIV-1 acquisition. Our findings indicate, for the first time, the presence of…

AdultMalePol genesYounger ageImmunologyMolecular Sequence DataHuman immunodeficiency virus (HIV)HIV Infectionsmedicine.disease_causeVirusVirologyAntiretroviral Therapy Highly ActiveDrug Resistance ViralmedicineHumansIn patientTreatment FailurebiologyAdult patientsvirus diseasesMiddle Agedbiology.organism_classificationAntiretroviral therapyVirologyGenes polInfectious DiseasesItalyLentivirusImmunologyMutationHIV-1RNA ViralFemaleAIDS research and human retroviruses
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Oxidative stress and antioxidant response in fibroblasts from Werner and Atypical Werner Syndromes

2014

Werner Syndrome (WS, ICD-10 E34.8, ORPHA902) and Atypical Werner Syndrome (AWS, ICD-10 E34.8, ORPHA79474) are very rare inherited syndromes characterized by premature aging. While approximately 90% of WS individuals have any of a range of mutations in theWRN gene, there exists a clinical subgroup in which the mutation occurs in the LMNA/C gene in heterozygosity. Although both syndromes exhibit an age-related pleiotropic phenotype, AWS manifests the onset of the disease during childhood, while major symptoms in WS appear between the ages of 20 and 30. To study the molecular mechanisms of progeroid diseases provides a useful insight into the normal aging process. Main changes found were the d…

AdultMalePremature agingAgingWerner Syndrome HelicaseAdolescentBiologymedicine.disease_causeAntioxidantsCell LineWerner Syndrome HelicaseLMNAProgeriaSuperoxide Dismutase-1antioxidant enzymesmedicineoxidative stressHumansRNA MessengerAtypical Werner syndromeChildeducationCell ProliferationWerner syndromeeducation.field_of_studyProgeriaAtypical Werner SyndromeRecQ Helicasespremature agingSuperoxide DismutaseAging PrematurethioredoxinglutaredoxinCell BiologyFibroblastsLamin Type Amedicine.diseaseGlutathioneMolecular biologyExodeoxyribonucleasesCase-Control StudiesMutationDNA damageFemaleWerner SyndromeThioredoxinOxidative stressResearch PaperAging
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Whole-exome sequencing identifies the first French MODY 6 family with a new mutation in the NEUROD1 gene

2020

Abstract Aim The aim of the present study was to identify the affected gene in a French family with maturity-onset diabetes of the young (MODY) using whole-exome sequencing (WES). Methods WES was performed in one patient with MODY, and candidate variants were confirmed in members of the immediate family by Sanger sequencing. Results In the proband, a new heterozygous missense mutation (c.340A>C) was identified in the NEUROD1 gene by WES analysis and confirmed by Sanger sequencing. Additional Sanger sequencing of the proband's sister and mother revealed the same heterozygous mutation. The proband and his sister displayed typical clinical characteristics of MODY, while their mother had the sa…

AdultMaleProbandHeterozygoteEndocrinology Diabetes and Metabolism[SDV]Life Sciences [q-bio]Mutation MissenseMothers030209 endocrinology & metabolism030204 cardiovascular system & hematologyBiology03 medical and health sciencessymbols.namesake0302 clinical medicineEndocrinologyDiabetic NeuropathiesExome SequencingBasic Helix-Loop-Helix Transcription FactorsInternal MedicinemedicineHumansHypoglycemic AgentsInsulinMissense mutationDiabetic NephropathiesAge of OnsetGeneExome sequencingAgedSanger sequencingGeneticsDiabetic RetinopathySiblingsGeneral Medicinemedicine.disease[SDV] Life Sciences [q-bio]Diabetes Mellitus Type 2Mutation (genetic algorithm)symbolsFemaleFranceMODY 6NEUROD1 Gene
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