Search results for "Speech delay"

showing 5 items of 15 documents

Variable phenotype in 17q12 microdeletions: Clinical and molecular characterization of a new case

2014

Microdeletions of 17q12 including the hepatocyte nuclear factor 1 beta (HNF1B) gene, as well as point mutations of this gene, are associated with the Renal Cysts and Diabetes syndrome (RCAD, OMIM 137920) and genitourinary alterations. Also, microdeletions encompassing HNF1B were identified as a cause of Mayer-Rokitansky-Kuster-Hauser Syndrome (MRKH, OMIM 277000) in females and, recently, were associated with intellectual disability, autistic features, cerebral anomaly and facial dysmorphisms. In this report, we describe a boy with a deletion in 17q12 region detected by SNP array, encompassing the HNF1B gene, that showed dysmorphic features, intellectual disability (ID), serious speech delay…

MaleLIM-Homeodomain ProteinsSingle-nucleotide polymorphismHaploinsufficiencyBiologyBioinformaticsPolymorphism Single NucleotideIntellectual DisabilityIntellectual disabilityGeneticsmedicineHumansAbnormalities MultipleLanguage Development DisordersAutistic DisorderChildHNF1B 17q12 SNP array Renal Cysts and Diabetes syndrome Intellectual disabilityHepatocyte Nuclear Factor 1-betaGeneticsHaplotypeForkhead Transcription FactorsGeneral Medicinemedicine.diseaseHNF1BPenetrancePhenotypeHaplotypesSpeech delayFemalemedicine.symptomChromosome DeletionHaploinsufficiencySNP arrayAcetyl-CoA CarboxylaseChromosomes Human Pair 17Transcription Factors
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Disruption of the ASTN2 / TRIM32 locus at 9q33.1 is a risk factor in males for Autism Spectrum Disorders, ADHD and other neurodevelopmental phenotypes

2014

Rare copy number variants (CNVs) disrupting ASTN2 or both ASTN2 and TRIM32 have been reported at 9q33.1 by genome-wide studies in a few individuals with neurodevelopmental disorders (NDDs). The vertebrate-specific astrotactins, ASTN2 and its paralog ASTN1, have key roles in glial-guided neuronal migration during brain development. To determine the prevalence of astrotactin mutations and delineate their associated phenotypic spectrum, we screened ASTN2/TRIM32 and ASTN1 (1q25.2) for exonic CNVs in clinical microarray data from 89 985 individuals across 10 sites, including 64 114 NDD subjects. In this clinical dataset, we identified 46 deletions and 12 duplications affecting ASTN2. Deletions o…

MaleReceptors Cell Surface/geneticsAutismChild Development Disorders Pervasive/geneticsGene ExpressionGenome-wide association studyMedical and Health SciencesTripartite Motif ProteinsRisk FactorsReceptors2.1 Biological and endogenous factorsProtein IsoformsNerve Tissue Proteins/geneticsCopy-number variationAetiologyChildGenetics (clinical)Sequence DeletionPediatricGenetics & HeredityGeneticseducation.field_of_studySingle NucleotideArticlesGeneral MedicineExonsBiological SciencesMental HealthPhenotypeAutism spectrum disorderOrgan SpecificityCerebellar cortexChild PreschoolCell SurfaceSpeech delayFemalemedicine.symptomTranscription Initiation SiteAttention Deficit Disorder with Hyperactivity/geneticsChromosomes Human Pair 9HumanPair 9AdultPediatric Research InitiativeChild Development DisordersAdolescentDNA Copy Number VariationsIntellectual and Developmental Disabilities (IDD)Ubiquitin-Protein LigasesPopulationTranscription Factors/geneticsNerve Tissue ProteinsReceptors Cell SurfaceBiologyPolymorphism Single NucleotideChromosomesYoung AdultClinical ResearchProtein Isoforms/geneticsBehavioral and Social ScienceGeneticsmedicineAttention deficit hyperactivity disorderHumansGenetic Predisposition to DiseasePolymorphismPreschooleducationMolecular BiologyGenetic Association StudiesPervasiveGlycoproteinsHuman GenomeNeurosciencesInfant NewbornGlycoproteins/geneticsInfantNewbornmedicine.diseaseBrain DisordersAttention Deficit Disorder with HyperactivityChild Development Disorders PervasiveCase-Control StudiesAutismTranscription Factors
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12p13.33 microdeletion including ELKS/ERC1, a new locus associated with childhood apraxia of speech.

2012

Speech sound disorders are heterogeneous conditions, and sporadic and familial cases have been described. However, monogenic inheritance explains only a small proportion of such disorders, in particular in cases with childhood apraxia of speech (CAS). Deletions of <5 Mb involving the 12p13.33 locus is one of the least commonly deleted subtelomeric regions. Only four patients have been reported with such a deletion diagnosed with fluorescence in situ hybridisation telomere analysis or array CGH. To further delineate this rare microdeletional syndrome, a French collaboration together with a search in the Decipher database allowed us to gather nine new patients with a 12p13.33 subtelomeric or …

MaleSpeech productionApraxiasLocus (genetics)Nerve Tissue ProteinsBiologyArticlePregnancyGeneticsmedicineHumansSpeechFamilyGenetic Predisposition to DiseaseLanguage Development DisordersChildGeneGenetics (clinical)In Situ Hybridization FluorescenceAdaptor Proteins Signal TransducingGeneticsChromosomes Human Pair 12medicine.diseaseSubtelomereSpeech TherapistPhenotypeChild PreschoolChildhood apraxia of speechSpeech delayFemaleFrancemedicine.symptomChromosome DeletionEuropean journal of human genetics : EJHG
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Rubinstein–Taybi syndrome 2 with cerebellar abnormality and neural tube defect

2019

Rubinstein-Taybi syndrome (RSTS) is a rare dominant disorder with intellectual disability, postnatal growth deficiency, and multiple congenital anomalies. Approximately 50-70% of the patients have a mutation in the CREBBP gene (RSTS1) and 5-10% display an EP300 gene mutation (RSTS2). Craniospinal abnormalities such as microcranium, scoliosis, and lordosis are frequent findings in RSTS1, but malformations of the brain or spinal cord are seen only occasionally. Here, we report on a 3-year-old boy with facial abnormalities of RSTS, broad thumbs and halluces, developmental delay, autistic features, cerebellar underdevelopment, and a neural tube defect. Molecular diagnostic of the CREBBP and EP3…

Malespeech delayHeterozygoteCerebellumGenotypecerebellar abnormalityScoliosisGene mutationPathology and Forensic MedicineCerebellummedicinetethered cordHumansmicrocephalyGenetic TestingNeural Tube DefectsFrameshift MutationEP300Genetic Association StudiesGenetics (clinical)Sequence DeletionRubinstein-Taybi Syndromeautistic behaviorRubinstein–Taybi syndromeNeural tube defectGenome Humanbusiness.industryNeural tubeHigh-Throughput Nucleotide Sequencingstereotypic movementsvesicoureteral refluxOriginal Articleslumbosacral myeloceleExonsGeneral MedicineAnatomymedicine.diseaseSpinal cordCREB-Binding Proteinmedicine.anatomical_structuresyringohydromyeliaChild PreschoolMutationPediatrics Perinatology and Child Healthbroad thumbs and hallucesAnatomybusinessE1A-Associated p300 ProteinClinical Dysmorphology
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A girl with an atypical form of ataxia telangiectasia and an additional de novo 3.14Mb microduplication in region 19q12

2011

A 9-year-old girl born to healthy parents showed manifestations suggestive of ataxia telangiectasia (AT), such as short stature, sudden short bouts of horizontal and rotary nystagmus, a weak and dysarthric voice, rolling gait, unstable posture, and atactic movements. She did not show several cardinal features typical of AT such as frequent, severe infections of the respiratory tract. In contrast, she showed symptoms not generally related to AT, including microcephaly, profound motor and mental retardation, small hands and feet, severely and progressively reduced muscle tone with slackly protruding abdomen and undue drooling, excess fat on her upper arms, and severe oligoarthritis. A cranial…

medicine.medical_specialtyMicrocephalyPathologyCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsProtein Serine-Threonine KinasesBiologyShort statureAtaxia Telangiectasia Mutated ProteinsAtaxia TelangiectasiaInternal medicineChromosome DuplicationGene duplicationGeneticsmedicineHumansLymphocytesChildSalivaCerebellar hypoplasiaMetaphaseGenetics (clinical)Mental DisordersTumor Suppressor ProteinsGeneral Medicinemedicine.diseaseDNA-Binding ProteinsEndocrinologyChromosome InversionAtaxia-telangiectasiaChromosomal regionSpeech delayMicrocephalyFemalemedicine.symptomApoptosis Regulatory ProteinsChromosomes Human Pair 19DNA DamageEuropean Journal of Medical Genetics
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