Search results for "Fibromatosis"

showing 10 items of 56 documents

Differential diagnosis of myxoid soft tissue tumors. Experience in the Clinical University Hospital of Valencia.

2018

Abstract Soft tissue tumors with myxoid components are often a diagnostic challenge for the pathologist. We retrospectively reviewed 41 cases of soft tissue tumors with myxoid components diagnosed in our center over a five-year period. The most frequent diagnoses were myxofibrosarcoma and myxoid liposarcoma, followed by low-grade fibromyxoid sarcoma, low-grade fibromyxoid tumor and myxoid neurofibroma. Other diagnoses included were extraskeletal myxoid chondrosarcoma, myxoinflammatory fibroblastic sarcoma, low-grade myxoliposarcoma, myofibrosarcoma, fibromatosis, solitary fibrous tumor, non-ossifying variant of ossifying fibromyxoid tumor and ancient neurinoma with myxoid degeneration. Immu…

0301 basic medicineAdultSolitary fibrous tumorPathologymedicine.medical_specialtySoft Tissue NeoplasmsPathology and Forensic MedicineDiagnosis Differential03 medical and health sciences0302 clinical medicinemedicineHumansRetrospective StudiesMyxoid liposarcomabusiness.industryFibromatosisFibromyxoid TumorMyxofibrosarcomaSarcomaExtraskeletal Myxoid Chondrosarcomamedicine.diseaseHospitals030104 developmental biology030220 oncology & carcinogenesisSarcomaDifferential diagnosisbusinessRevista espanola de patologia : publicacion oficial de la Sociedad Espanola de Anatomia Patologica y de la Sociedad Espanola de Citologia
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Neurofibromatosis type 2 tumor suppressor protein is expressed in oligodendrocytes and regulates cell proliferation and process formation.

2017

The neurofibromatosis type 2 (NF2) tumor suppressor protein Merlin functions as a negative regulator of cell growth and actin dynamics in different cell types amongst which Schwann cells have been extensively studied. In contrast, the presence and the role of Merlin in oligodendrocytes, the myelin forming cells within the CNS, have not been elucidated. In this work, we demonstrate that Merlin immunoreactivity was broadly distributed in the white matter throughout the central nervous system. Following Merlin expression during development in the cerebellum, Merlin could be detected in the cerebellar white matter tract at early postnatal stages as shown by its co-localization with Olig2-positi…

0301 basic medicineCentral Nervous SystemCytoplasmlcsh:MedicineNervous SystemMyelinMiceCell MovementAnimal CellsCerebellumMedicine and Health SciencesNeurofibromatosis type 2lcsh:ScienceNeuronsStainingCerebral CortexNeurofibromin 2MultidisciplinarybiologyCell StainingBrainCell migrationCell biologyOligodendrogliamedicine.anatomical_structureGenetic DiseasesCell ProcessesAnatomyCellular TypesCellular Structures and OrganellesResearch ArticleCell typeNeurofibromatosis 2NeurogenesisNerve Tissue ProteinsTransfectionResearch and Analysis MethodsCell Line03 medical and health sciencesmedicineAnimalsImmunohistochemistry TechniquesCell ProliferationCell NucleusClinical GeneticsCell growthAutosomal Dominant Diseaseslcsh:RBiology and Life SciencesCell Biologymedicine.diseaseOligodendrocyteMyelin basic proteinMerlin (protein)Mice Inbred C57BLHistochemistry and Cytochemistry Techniques030104 developmental biologySpecimen Preparation and TreatmentAstrocytesNeurofibromatosis Type 2Cellular Neurosciencebiology.proteinImmunologic Techniqueslcsh:QSchwann CellsNeurosciencePLoS ONE
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Clinical and molecular characterization of 112 single-center patients with Neurofibromatosis type 1.

2018

Abstract Background The aim of this retrospective study was to define clinical and molecular characteristics of a large sample of neurofibromatosis type 1 (NF1) patients, as well as to evaluate mutational spectrum and genotype-phenotype correlation. NF1 is a relatively common neurogenetic disorder (1:2500–1:3000 individuals). It is caused by mutations of the NF1 gene on chromosome 17ql1.2, with autosomal dominant pattern of inheritance and wide phenotypical variability. Café-au-lait spots (CALs), cutaneous and/or subcutaneous neurofibromas (CNFs/SCNFs), skinfold freckling, skeletal abnormalities, Lisch nodules of the iris and increased risk of learning and intellectual disabilities, as well…

0301 basic medicineGenotype-phenotype correlation; New mutation; NF1 gene; NF1 microdeletion syndrome; Adolescent; Adult; Age Factors; Child; Child Preschool; Cohort Studies; DNA Mutational Analysis; Female; Genes Neurofibromatosis 1; Genetic Association Studies; Genetic Predisposition to Disease; Humans; Italy; Male; Middle Aged; Neurofibromatosis 1; Prevalence; Prognosis; Retrospective Studies; Risk Assessment; Sex Factors; Young Adult; Mutation MissenseMaleGenotype-phenotype correlationDNA Mutational AnalysisDiseaseCohort Studies0302 clinical medicineDNA Mutational AnalysisGenotypePrevalenceMedicineYoung adultChildNew mutationlcsh:RJ1-570Age FactorsMiddle AgedPrognosisItalyNF1 geneChild PreschoolCohortFemaleNF1 microdeletion syndromeCohort studyAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosis 1AdolescentMutation MissenseRisk Assessment03 medical and health sciencesYoung AdultSex FactorsGenes Neurofibromatosis 1HumansGenetic Predisposition to DiseaseNeurofibromatosisPreschoolGenetic Association StudiesRetrospective Studiesbusiness.industryResearchRetrospective cohort studylcsh:Pediatricsmedicine.diseaseDermatology030104 developmental biologyGenesPediatrics Perinatology and Child HealthMutationMissensebusiness030217 neurology & neurosurgeryItalian journal of pediatrics
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A rare disease and education : Neurofibromatosis type 1 decreases educational attainment

2021

Rare heritable syndromes may affect educational attainment. Here, we study education in neurofibromatosis 1 (NF1) that is associated with multifaceted medical, social and cognitive consequences. Educational attainment in the Finnish population‐based cohort of 1408 individuals with verified NF1 was compared with matched controls using Cox proportional hazards model with delayed entry and competing risk for death. Moreover, models accounting for the effects of cancer at age 15–30 years, parental NF1 and developmental disorders were constructed. Overall, the attainment of secondary education was reduced in individuals with NF1 compared to controls (hazard ratio 0.83, 95%CI 0.74–0.92). History …

0301 basic medicineMale030105 genetics & heredityNeoplasmsneurofibromatosis 1ChildGenetics (clinical)FinlandLearning DisabilitiesHazard ratioCognitionVocational educationChild Preschooleducational attainmentCohortEducational StatusFemaleOriginal ArticleAdultopintomenestyscongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosis 1Adolescentrare diseaseneurofibromatoosiAffect (psychology)multiorgan syndromeschool performance03 medical and health sciencesRare DiseaseskoulutustasoGeneticsmedicineHumansEducation Graduateharvinaiset tauditNeurofibromatosisneoplasmsProportional Hazards ModelsVocational Educationperinnölliset tauditProportional hazards modelbusiness.industrySiblingsOriginal Articlesmedicine.diseaseEducational attainmenteye diseasesnervous system diseases030104 developmental biologybusinessDemographyFollow-Up Studies
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One NF1 Mutation may Conceal Another

2019

Neurofibromatosis type 1 (NF1) is an autosomal dominant disease with complete penetrance but high variable expressivity. NF1 is caused by loss-of-function mutations in the NF1 gene, a negative regulator of the RAS-MAPK pathway. The NF1 gene has one of the highest mutation rates in human disorders, which may explain the outbreak of independent de novo variants in the same family. Here, we report the co-occurrence of pathogenic variants in the NF1 and SPRED1 genes in six families with NF1 and Legius syndrome, using next-generation sequencing. In five of these families, we observed the co-occurrence of two independent NF1 variants. All NF1 variants were classified as pathogenic, according to t…

0301 basic medicineMutation ratemedicine.medical_specialtySPRED1congenital hereditary and neonatal diseases and abnormalities<i>SPRED1</i>lcsh:QH426-470[SDV]Life Sciences [q-bio]030105 genetics & heredityBiologyneurofibromatosis type 103 medical and health sciencesGeneticsmedicineNeurofibromatosisneoplasmsGenetics (clinical)Legius syndromeGeneticsMolecular pathologyAutosomal dominant traitmedicine.diseasePenetrance<i>NF1</i>eye diseases3. Good healthnervous system diseases[SDV] Life Sciences [q-bio]Legius syndromelcsh:Genetics030104 developmental biologyNF1Medical geneticsSPRED1 Genede novo variantGenes
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Recent Advances in Desmoid Tumor Therapy

2020

The desmoid tumor is a locally aggressive proliferative disease within the family of soft-tissue sarcomas. Despite its relatively good prognosis, the clinical management of desmoid tumors requires constant multidisciplinary evaluation due to its highly variable clinical behavior. Recently, active surveillance has being regarded as the appropriate strategy at diagnosis, as indolent persistence or spontaneous regressions are not uncommon. Here, we review the most recent advances in desmoid tumor therapy, including low-dose chemotherapy and treatment with tyrosine kinase inhibitors. We also explore the recent improvements in our knowledge of the molecular biology of this disease, which are lea…

0301 basic medicineOncologyCancer Researchmedicine.medical_specialtymedicine.medical_treatmentProliferative diseasedesmoid tumorDiseaseReviewchemotherapylcsh:RC254-282aggressive fibromatosis03 medical and health sciences0302 clinical medicineInternal medicinedesmoid tumor; aggressive fibromatosis; active surveillance; chemotherapy; tyrosine kinase inhibitorstyrosine kinase inhibitorsmedicineChemotherapybusiness.industryactive surveillanceTumor therapyaggressive fibromatosimedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensClinical trialbody regions030104 developmental biologyOncology030220 oncology & carcinogenesisAggressive fibromatosisGood prognosisbusinessCancers
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NF1 microdeletion syndrome: case report of two new patients

2019

Abstract Background 17q11.2 microdeletions, which include the neurofibromatosis type 1 (NF1) gene region, are responsible for the NF1 microdeletion syndrome, observed in 4.2% of all NF1 patients. Large deletions of the NF1 gene and its flanking regions are associated with a more severe NF1 phenotype than the NF1 general population. Case presentation We hereby describe the clinical and molecular features of two girls (aged 2 and 4 years, respectively), with non-mosaic atypical deletions. Patient 1 showed fifteen café-au-lait spots and axillary freckling, as well as a Lisch nodule in the left eye, strabismus, high-arched palate, malocclusion, severe kyphoscoliosis, bilateral calcaneovalgus fo…

0301 basic medicinePathologymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesGenotype-phenotype correlationNeurofibromatosesLisch noduleContiguous gene syndromePopulationCase ReportContiguous gene syndromeChromosomesCraniofacial Abnormalities03 medical and health sciences0302 clinical medicineAtypical deletionIntellectual DisabilitymedicineHumansMultiplex ligation-dependent probe amplificationNeurofibromatosiseducationChildPreschoolNeurofibromatoseseducation.field_of_studybusiness.industryLearning DisabilitiesPair 17lcsh:RJ1-570Axillary frecklinglcsh:Pediatricsmedicine.diseaseeye diseasesMLPA030104 developmental biologyNF1 geneChild PreschoolFemalemedicine.symptomChromosome DeletionbusinessAtypical deletion; Contiguous gene syndrome; Genotype-phenotype correlation; MLPA; NF1 gene; Child Preschool; Chromosome Deletion; Chromosomes Human Pair 17; Craniofacial Abnormalities; Female; Humans; Intellectual Disability; Learning Disabilities; Neurofibromatoses030217 neurology & neurosurgeryChromosomes Human Pair 17Comparative genomic hybridizationHumanItalian Journal of Pediatrics
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Decayed, missing, and restored teeth in patients with Neurofibromatosis Type 1.

2017

Background NF1 is a relatively frequently occurring autosomal dominant inherited disease. There are conflicting reports about oral health status in NF1. The aim of this study was to analyze the dental status of patients with neurofibromatosis type 1 (NF1). Material and methods Radiographs of 179 patients with NF1 were analyzed for decayed, missing, and filled teeth (DMFT) in a cross-sectional, retrospective study. The results were compared to age- and sex-matched controls of individuals not affected by NF1. The NF1 group was differentiated for facial tumor type and localization. Results Missing teeth were more frequently registered in the NF1 group. On the other hand, decayed teeth were mor…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesRadiographyDentistry030105 genetics & heredityOral health03 medical and health sciences0302 clinical medicinestomatognathic systemMedicineIn patientNeurofibromatosisGeneral DentistryneoplasmsReference groupbusiness.industryDMFT IndexResearchRetrospective cohort study:CIENCIAS MÉDICAS [UNESCO]medicine.diseasenervous system diseasesstomatognathic diseasesUNESCO::CIENCIAS MÉDICASOdontostomatology for the Disabled or Special PatientsInherited diseasebusiness030217 neurology & neurosurgeryJournal of clinical and experimental dentistry
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Update on the role of molecular factors and fibroblasts in the pathogenesis of Dupuytren’s disease

2016

The mechanism by which the fibroblast is able to trigger palmar fibromatosis is still not yet fully understood. It would appear certain that the “abnormal” fibroblasts continuously synthesise profibrotic cytokines which are able to determine the activation to myofibroblasts, to stimulate them to the further proliferation and synthesis of other cytokines, to modify the cells’ differentiation and ultrastructural characteristics, as well as the production of matrix and other proteins. Several fibroblast growth factors have been suggested to be responsible of an abnormal cell activation with an aberrantly elevated collagen synthesis and extracellular deposition in Dupuytren’s disease, as TGF-Be…

0301 basic medicinemedicine.medical_specialtySettore MED/19 - Chirurgia PlasticaReviewMatrix metalloproteinaseFibroblast growth factorBiochemistryPathogenesis03 medical and health sciences0302 clinical medicineInternal medicinemedicineExtracellularFibroblastMolecular BiologyCytokines Fibroblast Dupuytren’s disease030222 orthopedicsbiologyCell Biology030104 developmental biologyEndocrinologymedicine.anatomical_structurebiology.proteinCancer researchMyofibroblastPlatelet-derived growth factor receptorPalmar Fibromatosis
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Unilateral laryngeal and hypoglossal paralysis (Tapia's syndrome) in a patient with an inflammatory pseudotumor of the neck

2012

Tapia’s syndrome (TS) is a rare condition thought tobe causedby njury to the extracranial course of both recurrent laryngeal branch f the vagal nerve and hypoglossal nerve. First described in 1904, t occurs with unilateral paralysis of the vocal cord and tongue, ith normal function of the soft palate. Commonly reported causes re direct trauma, neurofibromatosis of X and XII nerves, carotid rtery dissection involving the ascending pharyngeal artery, and isplacement of endotracheal tube during general anesthesia [1].

AdultHypoglossal Nerve DiseasesGranuloma Plasma CellTongueTonguemedicine.arterymedicineParalysisHumansNeurofibromatosisNeurologic ExaminationSoft palateElectromyographybusiness.industryNeck tumors cranial nervesAscending pharyngeal arterySyndromeGeneral MedicineAnatomymedicine.diseaseMagnetic Resonance ImagingDissectionmedicine.anatomical_structureInflammatory pseudotumorFemaleSurgeryNeurology (clinical)Atrophymedicine.symptomTomography X-Ray ComputedbusinessVocal Cord ParalysisHypoglossal nerveNeckClinical Neurology and Neurosurgery
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