Search results for "Xq28"

showing 6 items of 6 documents

Xq28 duplication includingMECP2in six unreported affected females: what can we learn for diagnosis and genetic counselling?

2017

Duplication of the Xq28 region, involving MECP2 (dupMECP2), has been primarily described in males with severe developmental delay, spasticity, epilepsy, stereotyped movements and recurrent infections. Carrier mothers are usually asymptomatic with an extremely skewed X chromosome inactivation (XCI) pattern. We report a series of six novel symptomatic females carrying a de novo interstitial dupMECP2, and review the 14 symptomatic females reported to date, with the aim to further delineate their phenotype and give clues for genetic counselling. One patient was adopted and among the other 19 patients, seven (37%) had inherited their duplication from their mother, including three mildly (XCI: 70…

0301 basic medicineGeneticsPediatricsmedicine.medical_specialtyGenetic counselingMECP2 duplication syndrome030105 genetics & heredityBiologymedicine.diseaseX-inactivation3. Good healthXq2803 medical and health sciencesEpilepsy0302 clinical medicineGene duplicationGeneticsmedicineAsymptomatic carrierSkewed X-inactivation030217 neurology & neurosurgeryGenetics (clinical)Clinical Genetics
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Large national series of patients with Xq28 duplication involving MECP2: Delineation of brain MRI abnormalities in 30 affected patients.

2016

International audience; Xq28 duplications encompassing MECP2 have been described in male patients with a severe neurodevelopmental disorder associated with hypotonia and spasticity, severe learning disability, stereotyped movements, and recurrent pulmonary infections. We report on standardized brain magnetic resonance imaging (MRI) data of 30 affected patients carrying an Xq28 duplication involving MECP2 of various sizes (228 kb to 11.7 Mb). The aim of this study was to seek recurrent malformations and attempt to determine whether variations in imaging features could be explained by differences in the size of the duplications. We showed that 93% of patients had brain MRI abnormalities such …

0301 basic medicineMalePathologyMethyl-CpG-Binding Protein 2[SDV]Life Sciences [q-bio]030105 genetics & heredityCorpus callosumLateral ventricles0302 clinical medicineGene DuplicationIKBKGFLNAChildGenetics (clinical)GeneticsBrain Diseasesmedicine.diagnostic_testMiddle AgedPrognosisMagnetic Resonance ImagingHypotonia3. Good healthPedigree[SDV] Life Sciences [q-bio]medicine.anatomical_structurePhenotypeXq28 duplicationChild PreschoolFemalemedicine.symptomAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentGenotypeBiologygenotype-phenotype correlationWhite matter03 medical and health sciencesYoung AdultGeneticsmedicineHumansGenetic Association StudiesChromosomes Human X[ SDV ] Life Sciences [q-bio]Infant NewbornInfantMagnetic resonance imagingHyperintensitynervous system diseasesMental Retardation X-LinkedMECP2 gene030217 neurology & neurosurgeryAmerican journal of medical genetics. Part A
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Four unrelated patients with lubs X-linked mental retardation syndrome and different Xq28 duplications

2010

The Lubs X-linked mental retardation syndrome (MRXSL) is caused by small interstitial duplications at distal Xq28 including the MECP2 gene. Here we report on four novel male patients with MRXSL and different Xq28 duplications delineated by microarray-based chromosome analysis. All mothers were healthy carriers of the duplications. Consistent with an earlier report [Bauters et al. (2008); Genome Res 18: 847-858], the distal breakpoints of all four Xq28 duplications were located in regions containing low-copy repeats (LCRs; J, K, and L groups), which may facilitate chromosome breakage and reunion events. The proximal breakpoint regions did not contain known LCRs. Interestingly, we identified …

AdultMaleHeterozygoteBotulinum ToxinsAdolescentMethyl-CpG-Binding Protein 2MECP2 duplication syndromeMothersBiologyMECP2Gene duplicationGeneticsmedicineHumansChildGenetics (clinical)X chromosomeMuscle contractureChromosome AberrationsGeneticsChromosomes Human XBreakpointInfantmedicine.diseasePedigreeXq28Child PreschoolMental Retardation X-LinkedFemaleChromosome breakageAmerican Journal of Medical Genetics Part A
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123 MOLECULAR GENETIC ANALYSIS IN HUNTER DISEASE

1991

Clinical and biochemical studies have revealed a great phenotypic variability in mucopolysaccharidosis type II (Hunter disease), probably due to different mutations in the IDS gene that has been localized in Xq28. Using a cDNA probe containing almost the entire coding region of the human IDS gene, we performed a molecular analysis on 7 patients with Hunter disease. In one patient, a complete deletion of the IDS coding sequences was found. Another patient had structural alterations of the IDS gene including a partial deletion. In 5 patients, however, after restriction digestion of the DNA by PstI and TaqI and Southern hybridization with the IDS cDNA, the audiographic patterns obtained were s…

GeneticsTaqIPoint mutationBiologyMolecular biologyXq28chemistry.chemical_compoundchemistryComplementary DNAPediatrics Perinatology and Child HealthCoding regionMucopolysaccharidosis type IIGeneSouthern blotPediatric Research
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Interstitial deletion of chromosome 2p15-16.1: Report of two patients and critical review of current genotype–phenotype correlation

2011

Abstract We report two individuals with developmental delay and dysmorphic features, in whom array-based comparative genomic hybridization (array CGH) led to the identification of a 2p15p16.1 de novo deletion. In the first patient (Patient 1) a familial deletion of 6q12, inherited from her father, was also detected. In the second patient (Patient 2) in addition to the 2p15p16.1 microdeletion a de novo deletion in Xq28 was detected. Both individuals shared dysmorphic features and developmental delay with the six reported patients with a 2p15p16.1 microdeletion described in medical literature. Conclusion: in the first patient a 642 kb 2p16.1 deletion (from 60.604 to 61.246 Mb), and a 930 kb 6…

MaleGenotypeDevelopmental delayDevelopmental DisabilitiesBioinformaticsContiguous gene syndromeGenotype phenotypeCorrelationGeneticsHumansChromosomal delectionMedicineAbnormalities MultipleClinical phenotypeGenetic Association StudiesIn Situ Hybridization FluorescenceSex Chromosome AberrationsGenetics (clinical)Sequence DeletionGeneticsChromosomes Human XComparative Genomic Hybridizationbusiness.industryInfantChromosomeSyndromeGeneral MedicineMicrodeletion syndromemedicine.diseaseXq28PhenotypeChild PreschoolChromosomes Human Pair 2FemaleChromosome DeletionbusinessComparative genomic hybridizationEuropean Journal of Medical Genetics
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Deletion of the Hunter gene and both DXS466 and DXS304 in a patient with mucopolysaccharidosis type II.

1992

Hunter syndrome is an X-linked mucopoly-saccharidosis due to deficiency of the lysosomal enzyme iduronate-2-sulfatase (IDS). A cDNA clone containing the entire coding region of the human IDS gene, mapped in Xq28, has been used as molecular probe to study a patient with Hunter syndrome. A submicroscopic deletion has been detected that spans the IDS gene as well as DXS466 and DXS304, 2 loci mapped probably not more than 900 kb from the IDS locus. A detailed clinical description of the patient is provided and his phenotype is compared to that of other patients with IDS deletion described recently. By following the segregation of a restriction fragment length polymorphism at the IDS locus in th…

MaleX ChromosomeLocus (genetics)Iduronate SulfataseBiologyGene mappingmedicineHumansMucopolysaccharidosis type IIChildGenetics (clinical)X chromosomeMucopolysaccharidosis IIGeneticsIduronate-2-sulfataseChromosome MappingHunter syndromeDNAmedicine.diseaseXq28PedigreeBlotting SouthernFemaleRestriction fragment length polymorphismChromosome DeletionPolymorphism Restriction Fragment LengthAmerican journal of medical genetics
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