Search results for "Abnormalities"

showing 10 items of 638 documents

Charcot-Marie-Tooth disease: Genetic and clinical spectrum in a Spanish clinical series

2013

Objectives: To determine the genetic distribution and the phenotypic correlation of an extensive series of patients with Charcot-Marie-Tooth disease in a geographically well-defined Mediterranean area. Methods: A thorough genetic screening, including most of the known genes involved in this disease, was performed and analyzed in this longitudinal descriptive study. Clinical data were analyzed and compared among the genetic subgroups. Results: Molecular diagnosis was accomplished in 365 of 438 patients (83.3%), with a higher success rate in demyelinating forms of the disease. The CMT1A duplication (PMP22 gene) was the most frequent genetic diagnosis (50.4%), followed by mutations in the GJB1…

Foot DeformitiesMalecongenital hereditary and neonatal diseases and abnormalitiesPathologymedicine.medical_specialtyDNA Mutational AnalysisNerve Tissue ProteinsDiseaseArticleConnexinsCentral nervous system diseaseDegenerative diseasestomatognathic systemCharcot-Marie-Tooth DiseaseGene duplicationHumansMedicineLongitudinal StudiesMuscle StrengthGeneRetrospective StudiesGeneticsSeries (stratigraphy)business.industryRetrospective cohort studymedicine.diseasePhenotypeMuscular Atrophystomatognathic diseasesSpainMutationSensation DisordersFemaleNeurology (clinical)businessMyelin ProteinsNeurology
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WT1 isoform expression pattern in acute myeloid leukemia.

2013

WT1 plays a dual role in leukemia development, probably due to an imbalance in the expression of the 4 main WT1 isoforms. We quantify their expression and evaluate them in a series of AML patients. Our data showed a predominant expression of isoform D in AML, although in a lower quantity than in normal CD34+ cells. We found a positive correlation between the total WT1 expression and A, B and C isoforms. The overexpression of WT1 in AML might be due to a relative increase in A, B and C isoforms, together with a relative decrease in isoform D expression.

Gene isoformAdultMalecongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchAdolescentCD34HL-60 CellsBiologyurologic and male genital diseasesPositive correlationCohort StudiesYoung AdultDual roleExpression patternhemic and lymphatic diseasesmedicineTumor Cells CulturedHumansProtein IsoformsWT1 ProteinsAgedAged 80 and overurogenital systemGene Expression Regulation LeukemicGene Expression ProfilingMyeloid leukemiaHematologyMiddle Agedmedicine.diseaseMolecular biologyfemale genital diseases and pregnancy complicationsLeukemiaLeukemia Myeloid AcuteOncologyCase-Control StudiesFemaleK562 CellsLeukemia research
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FISH of supernumerary marker chromosomes (SMCs) identifies six diagnostically relevant intervals on chromosome 22q and a novel type of bisatellited S…

2005

Supernumerary marker chromosomes (SMCs) are frequently found at pre- and postnatal cytogenetic diagnosis and require identification. A disproportionally large subset of SMCs is derived from the human chromosome 22 and confers tri- or tetrasomy for the cat eye chromosomal region (CECR, the proximal 2 Mb of chromosome 22q) and/or other segments of 22q. Using fluorescence in situ hybridization (FISH) and 15 different DNA probes, we studied nine unrelated patients with an SMC(22) that contained the CECR. Five patients showed the small (type I) cat eye syndrome (CES) chromosome and each one had the larger (type II) CES chromosome, small ring chromosome 22, der(22)t(11;22) extrachromosome, and a …

Genetic MarkersChromosomes Human Pair 22Marker chromosomeRing chromosomeAnal CanalTrisomyBiologyCraniofacial AbnormalitiesGeneticsmedicineHumansAbnormalities MultipleSmall supernumerary marker chromosomeIn Situ Hybridization FluorescenceGenetics (clinical)Chromosome AberrationsGeneticsmedicine.diagnostic_testSyndromemedicine.diseaseMolecular biologyCat eye syndromeColobomaChromosome 17 (human)Chromosome 21Chromosome 22Fluorescence in situ hybridizationEuropean Journal of Human Genetics
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An autosomal dominant retinitis pigmentosa family with close linkage to D7S480 on 7q.

1995

Retinitis pigmentosa is the most prevalent inherited disorder of the retina. It can be autosomal dominant (adRP), autosomal recessive (arRP) or X-linked (XLRP). A form of adRP mapping to chromosome 7q was reported in a large Spanish pedigree. We have typed DNA from the members of another Spanish family for polymorphic markers from the known candidate genes. Positive lod scores were obtained only for the markers located on 7q31-35, giving a maximum lod score of 2.98 (3.01 by multipoint analysis) at theta = 0.00 for D7S480. A brief clinical evaluation is given.

Genetic MarkersMaleCandidate genecongenital hereditary and neonatal diseases and abnormalitiesgenetic structuresBiologyAutosomal dominant retinitis pigmentosaGene mappingRetinitis pigmentosaGeneticsmedicineHumansGeneGenetics (clinical)Genes DominantLinkage (software)GeneticsChromosome Mappingmedicine.diseaseHuman geneticseye diseasesPedigreeGenetic markerFemaleLod ScoreChromosomes Human Pair 7Retinitis PigmentosaHuman genetics
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Comparative architectural aspects of regions of conserved synteny on human chromosome 11p15.3 and mouse chromosome 7 (including genes WEE1 and LMO1)

2001

Human chromosome 11p15.3 is associated with chromosome aberrations in the Beckwith Wiedemann Syndrome and implicated in the pathogenesis of different tumor types including lung cancer and leukemias. To date, only single tumor-relevant genes with linkage to this region (e.g. LMO1) have been found suggesting that this region may harbor additional potential disease associated genes. Although this genomic area has been studied for years, the exact order of genes/chromosome markers between D11S572 and the WEE1 gene locus remained unclear. Using the FISH technique and PAC clones of the flanking markers we determined the order of the genomic markers. Based on these clones we established a PAC cont…

Genetic Markerscongenital hereditary and neonatal diseases and abnormalitiesBeckwith–Wiedemann syndromeCell Cycle ProteinsBiologyChromosomesEvolution MolecularContig MappingMiceChromosome regionsGene OrderMetalloproteinsGeneticsmedicineAnimalsHumansCloning MolecularMolecular BiologyGeneConserved SequenceIn Situ Hybridization FluorescenceGenetics (clinical)Repetitive Sequences Nucleic AcidSyntenyOncogene ProteinsGeneticsChromosome 7 (human)Base CompositionChromosomes Human Pair 11Nuclear ProteinsChromosomeSequence Analysis DNALIM Domain ProteinsProtein-Tyrosine Kinasesmedicine.diseaseAT Rich SequenceGC Rich SequenceDNA-Binding ProteinsChromosome 3CpG IslandsChromosome 21Transcription FactorsCytogenetic and Genome Research
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De novo t(12;17)(p13.3;q21.3) translocation with a breakpoint near the 5' end of the HOXB gene cluster in a patient with developmental delay and skel…

2007

A boy with severe mental retardation, funnel chest, bell-shaped thorax, and hexadactyly of both feet was found to have a balanced de novo t(12;17)(p13.3;q21.3) translocation. FISH with BAC clones and long-range PCR products assessed in the human genome sequence localized the breakpoint on chromosome 17q21.3 to a 21-kb segment that lies <30 kb upstream of the HOXB gene cluster and immediately adjacent to the 3′ end of the TTLL6 gene. The breakpoint on chromosome 12 occurred within telomeric hexamer repeats and, therefore, is not likely to affect gene function directly. We propose that juxtaposition of the HOXB cluster to a repetitive DNA domain and/or separation from required cis-regulatory …

GeneticsMaleChromosomes Human Pair 12Developmental DisabilitiesBreakpointGenes HomeoboxChromosomeChromosome MappingChromosomal translocationChromosome BreakageBiologyTranslocation GeneticMusculoskeletal AbnormalitiesPosition effectChild PreschoolGene clusterGeneticsHumansHuman genomeGeneGenetics (clinical)Chromosome 12Chromosomes Human Pair 17European journal of human genetics : EJHG
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Genetics of the Charcot-Marie-Tooth disease in the Spanish Gypsy population: the hereditary motor and sensory neuropathy-Russe in depth

2012

Four private mutations responsible for three forms demyelinating of Charcot-Marie-Tooth (CMT) or hereditary motor and sensory neuropathy (HMSN) have been associated with the Gypsy population: the NDRG1 p.R148X in CMT type 4D (CMT4D/HMSN-Lom); p.C737_P738delinsX and p.R1109X mutations in the SH3TC2 gene (CMT4C); and a G>C change in a novel alternative untranslated exon in the HK1 gene causative of CMT4G (CMT4G/HMSN-Russe). Here we address the findings of a genetic study of 29 Gypsy Spanish families with autosomal recessive demyelinating CMT. The most frequent form is CMT4C (57.14%), followed by HMSN-Russe (25%) and HMSN-Lom (17.86%). The relevant frequency of HMSN-Russe has allowed us to inv…

GeneticsProbandcongenital hereditary and neonatal diseases and abnormalitiesWeaknesseducation.field_of_studyHaplotypePopulationBiologymedicine.diseaseTooth diseaseDistal sensory lossGeneticsmedicinemedicine.symptomeducationHereditary motor and sensory neuropathyFounder mutationGenetics (clinical)Clinical Genetics
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Mitochondrial DNA variations in patients with Type 2 (non-insulin dependent) diabetes mellitus and a Welsh control population

1999

The LDL-receptor gene point mutation FH-Genoa/Palermo is the most frequent mutation responsible for Familial Hypercholesterolemia in Sicily. The mutation does not introduce or abolish any useful restriction site. We establish a GeneComb-based strategy to identify this mutation in a population of Sicilian unrelated clinically diagnosed FH probands. The method was very sensitive and specific; 12 out of 90 (13.3%) unrelated FH probands were found to carry the FH-Genoa/Palermo mutation. According to these results, the FH-Genoa/Palermo is the more frequent LDL-receptor gene mutation among the Sicilian FH patients. Moreover FH-Genoa/Palermo is the mutation cluster to date more represented in Sout…

GeneticsProbandcongenital hereditary and neonatal diseases and abnormalitieseducation.field_of_studyPoint mutationPopulationnutritional and metabolic diseasesFamilial hypercholesterolemiaGene mutationBiologymedicine.diseaseRestriction siteLDL receptorMutation (genetic algorithm)Geneticsmedicineskin and connective tissue diseaseseducationGenetics (clinical)Human Mutation
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Cytogenetic response induced by interferon alpha in the myeloproliferative disorder with eosinophilia, T cell lymphoma and the chromosomal translocat…

1998

Cytogenetic response induced by interferon alpha in the myeloproliferative disorder with eosinophilia, T cell lymphoma and the chromosomal translocation t(8;13)(p11;q12)

Geneticscongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchAlpha interferonChromosomal translocationHematologyBiologymedicine.diseaseCytogenetic ResponseLymphomaOncologyhemic and lymphatic diseasesCancer researchmedicineEosinophiliaT-cell lymphomamedicine.symptomLeukemia
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Imprint switching on human chromosome 15 may involve alternative transcripts of the SNRPN gene

1996

Imprinting on human chromosome 15 is regulated by an imprinting centre, which has been mapped to a 100–kb region including exon 1 of SNRPN. From this region we have identified novel transcripts, which represent alternative transcripts of the SNRPN gene. The novel exons lack protein coding potential and are expressed from the paternal chromosome only. We have also identified intragenic deletions and a point mutation in patients who have Angelman or Prader–Willi syndrome due to a parental imprint switch failure. This suggests that imprint switching on human chromosome 15 may involve alternative SNRPN transcripts.

Geneticscongenital hereditary and neonatal diseases and abnormalitiesChromosome 15ExonAlternative splicingHappy puppet syndromeGeneticsBiologyImprinting (psychology)Genomic imprintingGeneSNRPN GeneNature Genetics
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