Search results for "030105 genetics & heredity"

showing 10 items of 119 documents

Specific mosaicKRASmutations affecting codon 146 cause oculoectodermal syndrome and encephalocraniocutaneous lipomatosis

2016

Oculoectodermal syndrome (OES) and encephalocraniocutaneous lipomatosis (ECCL) are rare disorders that share many common features, such as epibulbar dermoids, aplasia cutis congenita, pigmentary changes following Blaschko lines, bony tumor-like lesions, and others. About 20 cases with OES and more than 50 patients with ECCL have been reported. Both diseases were proposed to represent mosaic disorders, but only very recently whole-genome sequencing has led to the identification of somatic KRAS mutations, p.Leu19Phe and p.Gly13Asp, in affected tissue from two individuals with OES. Here we report the results of molecular genetic studies in three patients with OES and one with ECCL. In all four…

0301 basic medicineGeneticsSanger sequencingLipomatosis030105 genetics & heredityRASopathyBiologymedicine.diseasemedicine.disease_causeAplasia cutis congenita3. Good health03 medical and health sciencessymbols.namesake030104 developmental biologyGermline mutationGenotypeEncephalocraniocutaneous LipomatosisGeneticsmedicinesymbolsKRASmedicine.symptomGenetics (clinical)Clinical Genetics
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Autosomal recessive mutations inTHOC6cause intellectual disability: syndrome delineation requiring forward and reverse phenotyping

2016

THOC6 is a part of the THO complex, which is involved in coordinating mRNA processing with export. The THO complex interacts with additional components to form the larger TREX complex (transcription export complex). Previously, a homozygous missense mutation in THOC6 in the Hutterite population was reported in association with syndromic intellectual disability. Using exome sequencing, we identified three unrelated patients with bi-allelic mutations in THOC6 associated with intellectual disability and additional clinical features. Two of the patients were compound heterozygous for a stop and a missense mutation, and the third was homozygous for a missense mutation; the missense mutations wer…

0301 basic medicineGeneticseducation.field_of_studyMicrocephalybusiness.industryPopulationTranscription export complex030105 genetics & heredityCompound heterozygositymedicine.disease03 medical and health sciences030104 developmental biologyIntellectual disabilityGeneticsMedicineMissense mutationbusinesseducationExomeGenetics (clinical)Exome sequencingClinical Genetics
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Homozygous FIBP nonsense variant responsible of syndromic overgrowth, with overgrowth, macrocephaly, retinal coloboma and learning disabilities

2016

The acidic fibroblast growth factor (FGF) intracellular binding protein (FIBP) interacts directly with the fibroblast growth factor FGF1. Although FIBP is known to be implicated in the FGF signaling pathway, its precise function remains unclear. Gain-of-function variants in several FGF receptors (FGFRs) are implicated in a wide spectrum of growth disorders from achondroplasia to overgrowth syndromes. In a unique case from a consanguineous union presenting with overgrowth, macrocephaly, retinal coloboma, large thumbs, severe varicose veins and learning disabilities, exome sequencing identified a homozygous nonsense FIBP variant. The patient's fibroblasts exhibit FIBP cDNA degradation and an …

0301 basic medicineGeneticsmedia_common.quotation_subjectNonsenseMacrocephaly030105 genetics & heredityFGF1BiologyFibroblast growth factormedicine.diseasePhenotype03 medical and health sciences030104 developmental biologyFibroblast growth factor receptorGeneticsmedicinemedicine.symptomAchondroplasiaGenetics (clinical)Exome sequencingmedia_commonClinical Genetics
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Genetic counselling difficulties and ethical implications of incidental findings from array-CGH: a 7-year national survey

2016

Microarray-based comparative genomic hybridization (aCGH) is commonly used in diagnosing patients with intellectual disability (ID) with or without congenital malformation. Because aCGH interrogates with the whole genome, there is a risk of being confronted with incidental findings (IF). In order to anticipate the ethical issues of IF with the generalization of new genome-wide analysis technologies, we questioned French clinicians and cytogeneticists about the situations they have faced regarding IF from aCGH. Sixty-five IF were reported. Forty corresponded to autosomal dominant diseases with incomplete penetrance, 7 to autosomal dominant diseases with complete penetrance, 14 to X-linked di…

0301 basic medicineGeneticsmedicine.medical_specialtyeducation.field_of_studyEthical issuesbusiness.industryGenetic counselingPopulationRetrospective cohort study030105 genetics & hereditymedicine.diseasePenetrance3. Good health03 medical and health sciencesGeneralization (learning)Family medicineIntellectual disabilityGeneticsMedicinebusinesseducationGenetics (clinical)Comparative genomic hybridizationClinical Genetics
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Novel deletion in 11p15.5 imprinting center region 1 in a patient with Beckwith-Wiedemann syndrome provides insight into distal enhancer regulation a…

2016

Background Beckwith–Wiedemann syndrome (BWS) is an early-onset overgrowth disorder with a high risk for embryonal tumors. It is mainly caused by dysregulation of imprinted genes on chromosome 11p15.5; however, the driving forces in the development of tumors are not fully understood. Procedure We report on a female patient presenting with macrosomia, macroglossia, organomegaly and extensive bilateral nephroblastomatosis. Adjuvant chemotherapy was initiated; however, the patient developed hepatoblastoma and Wilms tumor at 5 and 12 months of age, respectively. Subsequent radiofrequency ablation of the liver tumor and partial nephrectomy followed by consolidation therapy achieved complete remis…

0301 basic medicineHepatoblastomaPathologymedicine.medical_specialtyBeckwith-Wiedemann SyndromeBeckwith–Wiedemann syndrome030105 genetics & hereditymedicine.disease_cause03 medical and health sciencesGenomic ImprintingInsulin-Like Growth Factor IIMacroglossiaMedicineHumansImprinting (psychology)NephroblastomatosisSequence Deletionbusiness.industryChromosomes Human Pair 11Infant NewbornWilms' tumorHematologyDNA Methylationmedicine.diseasePrognosis030104 developmental biologyCell Transformation NeoplasticPhenotypeOncologyPediatrics Perinatology and Child HealthCancer researchFemalemedicine.symptombusinessGenomic imprintingCarcinogenesisPediatric bloodcancer
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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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Identification of a new locus and validation of previously reported loci showing differential methylation associated with smoking. The REGICOR study.

2015

Smoking increases the risk of many diseases and could act through changes in DNA methylation patterns. The aims of this study were to determine the association between smoking and DNA methylation throughout the genome at cytosine-phosphate-guanine (CpG) site level and genomic regions. A discovery cross-sectional epigenome-wide association study nested in the follow-up of the REGICOR cohort was designed and included 645 individuals. Blood DNA methylation was assessed using the Illumina HumanMethylation450 BeadChip. Smoking status was self-reported using a standardized questionnaire. We identified 66 differentially methylated CpG sites associated with smoking, located in 38 genes. In most of …

0301 basic medicineMaleCancer ResearchLocus (genetics)Genome-wide association study030105 genetics & heredityBiologyBioinformaticsEpigenesis GeneticEpigènesiCohort StudiesThrombospondin 103 medical and health sciencesTabaquismeHumansEpigeneticsMolecular BiologyAgedGeneticsRegulation of gene expressionGene Expression ProfilingSmokingMethylationDNA MethylationMiddle AgedGene expression profiling030104 developmental biologyCross-Sectional StudiesCpG siteGene Expression RegulationDNA methylationCpG IslandsFemaleCarrier ProteinsCorrigendumResearch PaperGenome-Wide Association StudyEpigenetics
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Exome sequencing in congenital ataxia identifies two new candidate genes and highlights a pathophysiological link between some congenital ataxias and…

2019

To investigate the genetic basis of congenital ataxias (CAs), a unique group of cerebellar ataxias with a nonprogressive course, in 20 patients from consanguineous families, and to identify new CA genes. Singleton -exome sequencing on these 20 well-clinically characterized CA patients. We first checked for rare homozygous pathogenic variants, then, for variants from a list of genes known to be associated with CA or very early-onset ataxia, regardless of their mode of inheritance. Our replication cohort of 180 CA patients was used to validate the new CA genes. We identified a causal gene in 16/20 families: six known CA genes (7 patients); four genes previously implicated in another neurologi…

0301 basic medicineMaleCandidate geneAtaxiaAdolescentCerebellar AtaxiaGenotype[SDV]Life Sciences [q-bio]Consanguinity030105 genetics & heredityBiologyPathophysiologyCohort Studies03 medical and health sciencesGenetic HeterogeneityYoung AdultmedicineSTXBP1HumansExomeGenetic Predisposition to DiseaseChildGenetics (clinical)Exome sequencingGeneticsEarly infantile epileptic encephalopathies[SDV.GEN]Life Sciences [q-bio]/GeneticsBRAT1Genetic heterogeneityPhenotype3. Good health030104 developmental biologyPhenotype[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolMutationCerebellar atrophyCongenital ataxiaAtaxiaFemaleFrancemedicine.symptomSpasms Infantileexome sequencing
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12q14.3 microdeletion involving HMGA2 gene cause a Silver-Russell syndrome-like phenotype: a case report and review of the literature

2020

Abstract Background Silver-Russell Syndrome (SRS) is a genetic disorder characterized by intrauterine and postnatal growth restriction and normal head circumference with consequent relative macrocephaly. Addictional findings are protruding forehead in early life, body asymmetry (of upper and lower limbs) and substantial feeding difficulties. Although several genetic mechanisms that cause the syndrome are known, more than 40% of patients with a SRS-like phenotype remain without an etiological diagnosis. In the last few years, different clinical reports have suggested that mutations or deletions of the HMGA2 gene can be responsible for a SRS-like phenotype in patients with negative results of…

0301 basic medicineMaleCase Report030105 genetics & heredityBioinformaticsHMGA2 gene03 medical and health sciencesHMGA2parasitic diseasesmedicineHumansGeneChromosome 12biologybusiness.industrySilver–Russell syndromeNetchine-Harbison clinical scoring systemHMGA2 Proteinlcsh:RJ1-570Genetic disorderlcsh:PediatricsFailure to thrivemedicine.diseasePhenotypeSilver-Russell Syndrome030104 developmental biologyPhenotypeSettore MED/03 - Genetica MedicaChild PreschoolFailure to thriveEtiologybiology.proteinmedicine.symptombusinessGene DeletionItalian Journal of Pediatrics
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Standardising clinical outcomes measures for adult clinical trials in Fabry disease: A global Delphi consensus.

2021

International audience; Background: Recent years have witnessed a considerable increase in clinical trials of new investigational agents for Fabry disease (FD). Several trials investigating different agents are currently in progress; however, lack of standardisation results in challenges to interpretation and comparison. To facilitate the standardisation of investigational programs, we have developed a common framework for future clinical trials in FD.Methods and findings: A broad consensus regarding clinical outcomes and ways to measure them was obtained via the Delphi methodology. 35 FD clinical experts from 4 continents, representing 3389 FD patients, participated in 3 rounds of Delphi p…

0301 basic medicineMaleDelphi TechniqueEndocrinology Diabetes and Metabolism[SDV]Life Sciences [q-bio]Delphi methodDisease030105 genetics & heredityKidneyBiochemistry0302 clinical medicineEndocrinologyClinical outcomesClinical Trials as TopicGlobosidesTrihexosylceramidesMiddle Aged3. Good healthClinical trialIsoenzymesTreatment OutcomeInclusion and exclusion criteriaSecondary Outcome MeasureFemaleAdultmedicine.medical_specialtyConsensusLysosomal storage disorders03 medical and health sciencesQuality of life (healthcare)Inherited metabolic disordersGeneticsmedicineHumansEnzyme Replacement TherapyIntensive care medicineMolecular BiologyFabry diseaseSphingolipidsbusiness.industryClinical study designmedicine.diseaseFabry diseaseClinical trialDelphi consensusalpha-GalactosidaseQuality of LifeFabry DiseaseGlycolipidsbusiness030217 neurology & neurosurgeryMolecular genetics and metabolism
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