Search results for "1 microdeletion"

showing 4 items of 4 documents

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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Search for a gene responsible for Floating-Harbor syndrome on chromosome 12q15q21.1.

2012

International audience; Floating-Harbor syndrome (FHS) is characterized by characteristic facial dysmorphism, short stature with delayed bone age, and expressive language delay. To date, the gene(s) responsible for FHS is (are) unknown and the diagnosis is only made on the basis of the clinical phenotype. The majority of cases appeared to be sporadic but rare cases following autosomal dominant inheritance have been reported. We identified a 4.7 Mb de novo 12q15-q21.1 microdeletion in a patient with FHS and intellectual deficiency. Pangenomic 244K array-CGH performed in a series of 12 patients with FHS failed to identify overlapping deletions. We hypothesized that FHS is caused by haploinsuf…

AdultHeart Septal Defects VentricularMaleCandidate geneFloating Harbor syndrome[SDV.GEN] Life Sciences [q-bio]/GeneticsHaploinsufficiencyBiologyBioinformaticsShort statureCraniofacial Abnormalities03 medical and health sciences12q15q21.1 microdeletion[SDV.BDD] Life Sciences [q-bio]/Development BiologyGeneticsmedicineHumansAbnormalities MultipleGenetic Predisposition to Disease[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyChild[SDV.BDD]Life Sciences [q-bio]/Development BiologyGenetics (clinical)Growth Disorders030304 developmental biologySequence DeletionPhenocopyGenetics0303 health sciencesComparative Genomic Hybridization[SDV.GEN]Life Sciences [q-bio]/GeneticsChromosomes Human Pair 12Genetic heterogeneity030305 genetics & heredityChromosomeHigh-Throughput Nucleotide Sequencinghigh-throughput sequencingmedicine.disease3. Good healthPhenotypeFloating–Harbor syndromeChild PreschoolMutation (genetic algorithm)Femalemedicine.symptomHaploinsufficiency[ SDV.GEN ] Life Sciences [q-bio]/Genetics
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EPHA7 haploinsufficiency is associated with a neurodevelopmental disorder

2021

International audience; Ephrin receptor and their ligands, the ephrins, are widely expressed in the developing brain. They are implicated in several developmental processes that are crucial for brain development. Deletions in genes encoding for members of the Eph/ephrin receptor family were reported in several neurodevelopmental disorders. The ephrin receptor A7 gene (EPHA7) encodes a member of ephrin receptor subfamily of the protein-tyrosine kinase family. EPHA7 plays a role in corticogenesis processes, determines brain size and shape, and is involved in development of the central nervous system. One patient only was reported so far with a de novo deletion encompassing EPHA7 in 6q16.1. We…

MaleMicrocephaly[SDV]Life Sciences [q-bio]6q161 microdeletionInheritance PatternsEPHA7HaploinsufficiencyBiologyspeech and language developmentNeurodevelopmental disorderExome SequencingGeneticsmedicineEphrinHumansGenetic Predisposition to DiseasemicrocephalyGenetics (clinical)Genetic Association StudiesIn Situ Hybridization FluorescenceGeneticsComparative Genomic Hybridization6q16.1 microdeletionErythropoietin-producing hepatocellular (Eph) receptorReceptor EphA7medicine.diseasePenetrancePhenotypeneurodevelopmental disorderPedigree[SDV] Life Sciences [q-bio]PhenotypeNeurodevelopmental Disordersintellectual disabilityEPHA7MutationChromosomes Human Pair 6FemaleHaploinsufficiencyClinical Genetics
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2p15-p16.1 microdeletions encompassing and proximal to BCL11A are associated with elevated HbF in addition to neurologic impairment.

2015

Elevated fetal hemoglobin (HbF) ameliorates the clinical severity of hemoglobinopathies such as β-thalassemia and sickle cell anemia. Currently, the only curative approach for individuals under chronic transfusion/chelation support therapy is allogeneic stem cell transplantation. However, recent analyses of heritable variations in HbF levels have provided a new therapeutic target for HbF reactivation: the transcriptional repressor BCL11A. Erythroid-specific BCL11A abrogation is now actively being sought as a therapeutic avenue, but the specific impact of such disruption in humans remains to be determined. Although single nucleotide polymorphisms in BCL11A erythroid regulatory elements have …

Malecongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyAdolescentImmunologyBiologyBiochemistrySettore MED/38 - Pediatria Generale E SpecialisticaRed Cells Iron and ErythropoiesisInternal medicinehemic and lymphatic diseasesFetal hemoglobinmedicineGene silencingHumansChildNervous System DiseaseFetal HemoglobinNuclear ProteinHematologyNuclear ProteinsCell BiologyHematologymedicine.diseasePhenotypeSickle cell anemiaUp-RegulationTransplantationRepressor ProteinsSettore MED/03 - Genetica MedicaChromosomes Human Pair 22p15-p16.1 microdeletions BCL11A HbF neurologicImmunologyFemaleStem cellChromosome DeletionNervous System DiseasesCarrier ProteinHaploinsufficiencyCarrier ProteinsHumanBlood
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