Search results for " Pair 3"

showing 10 items of 21 documents

Aceruloplasminaemia: a family with a novel mutation and long-term therapy with deferasirox.

2014

Ceruloplasmin is a member of the multicopper oxidase family that plays a major role in the transport of iron in the body. Aceruloplasminaemia (ACP) is a rare disease and is clinically identified by iron overload in liver, pancreas, brain, and other organs, and by microcytic anaemia. So far, the iron chelator deferasirox was given for therapy only up to 6 months due to side effects. Here, we describe a novel mutation leading to ACP and report for the first time a long-term therapy, that is, 2 years with deferasirox. ACP was diagnosed in 3 siblings using clinical and biochemical characteristics, HFE and ceruloplasmin mutational analysis, liver biopsy, brain-, liver-, and heart-MRI. For iron d…

AdultBlood GlucoseMalemedicine.medical_specialtyEndocrinology Diabetes and MetabolismIronClinical BiochemistryCarbohydrate metabolismBiochemistryBenzoatesEndocrinologyInsulin resistanceHepcidinInternal medicineGermanyMedicineHumansChelating Agentsbiologymedicine.diagnostic_testbusiness.industryBiochemistry (medical)DeferasiroxCeruloplasminNeurodegenerative DiseasesGeneral MedicineTriazolesmedicine.diseaseIron Metabolism DisordersMagnetic Resonance ImagingPedigreeDeferasiroxEndocrinologymedicine.anatomical_structureTreatment OutcomeLiverLiver biopsyMutationbiology.proteinFemaleChromosomes Human Pair 3businessCeruloplasminPancreasmedicine.drugRare diseaseHormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme
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3q27.3 microdeletional syndrome: a recognisable clinical entity associating dysmorphic features, marfanoid habitus, intellectual disability and psych…

2013

Abstract: Background Since the advent of array-CGH, numerous new microdeletional syndromes have been delineated while others remain to be described. Although 3q29 subtelomeric deletion is a well-described syndrome, there is no report on 3q interstitial deletions. Methods We report for the first time seven patients with interstitial deletions at the 3q27.3q28 locus gathered through the Decipher database, and suggest this locus as a new microdeletional syndrome. Results The patients shared a recognisable facial dysmorphism and marfanoid habitus, associated with psychosis and mild to severe intellectual disability (ID). Most of the patients had no delay in gross psychomotor acquisition, but ha…

AdultMalePsychosisCandidate genePediatricsmedicine.medical_specialtyAdolescentLocus (genetics)ArachnodactylyYoung AdultIntellectual DisabilityIntellectual disabilityGeneticsMedicineHumansAbnormalities MultipleGenetics (clinical)GeneticsComparative Genomic Hybridizationbusiness.industryMood DisordersMarfanoidChromosome MappingFaciesInfantSyndromemedicine.diseasePhenotypeMood disordersChild PreschoolBone maturationFemaleHuman medicineChromosomes Human Pair 3Chromosome DeletionbusinessJournal of medical genetics
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A dominant gene for developmental dyslexia on chromosome 3.

2001

Developmental dyslexia is a neurofunctional disorder characterised by an unexpected difficulty in learning to read and write despite adequate intelligence, motivation, and education. Previous studies have suggested mostly quantitative susceptibility loci for dyslexia on chromosomes 1, 2, 6, and 15, but no genes have been identified yet. We studied a large pedigree, ascertained from 140 families considered, segregating pronounced dyslexia in an autosomal dominant fashion. Affected status and the subtype of dyslexia were determined by neuropsychological tests. A genome scan with 320 markers showed a novel dominant locus linked to dyslexia in the pericentromeric region of chromosome 3 with a m…

AdultMaleReading disabilityAdolescentLocus (genetics)Biologybehavioral disciplines and activitiesDyslexia03 medical and health sciences0302 clinical medicineGenetic linkageDCDC2Memorymental disordersGeneticsmedicineHumansChildGenetics (clinical)Finland030304 developmental biologyAgedGenes DominantGenetics0303 health sciencesAnalysis of VariancePsychological TestsRadiation Hybrid MappingReceptors Dopamine D2HaplotypeDyslexiaReceptors Dopamine D3Chromosome MappingOriginal ArticlesMiddle Agedmedicine.diseasePedigreeDevelopmental disorderChromosome 3HaplotypesReadingReceptors SerotoninFemaleChromosomes Human Pair 3Lod Score030217 neurology & neurosurgeryJournal of medical genetics
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Detection of a germline mutation and somatic homozygous loss of the von Hippel-Lindau tumor-suppressor gene in a family with a de novo mutation

1996

von Hippel-Lindau (VHL) disease is a pleiotropic disorder featuring a variety of malignant and benign tumors of the eye, central nervous system, kidney, and adrenal gland. Recently the VHL gene has been identified in the chromosomal region 3p25-26. Prognosis and successful management of VHL patients and their descendants depend on unambiguous diagnosis. Due to recurrent hemangioblastomas, a29-year-old patient without familial history of VHL disease was diagnosed to be at risk for the disease. Histopathological examination of a small renal mass identified a clear cell tumor with a G1 grading. Genetic characterization of the germline and of the renal tumor was performed. Polymerase chain reac…

AdultMalemedicine.medical_specialtyvon Hippel-Lindau DiseaseTumor suppressor geneDNA Mutational AnalysisMolecular Sequence Dataurologic and male genital diseasesPolymerase Chain ReactionGermlineGermline mutationVon Hippel–Lindau tumor suppressorGeneticsmedicineHumansGenes Tumor SuppressorSpinal Cord NeoplasmsVon Hippel–Lindau diseaseGerm-Line MutationPolymorphism Single-Stranded ConformationalGenetics (clinical)Sequence Deletionbiologymedicine.diagnostic_testHomozygoteCytogeneticsExonsmedicine.diseaseKidney Neoplasmsfemale genital diseases and pregnancy complicationsHemangioblastomaPedigreeKaryotypingChromosomal regionbiology.proteinCancer researchFemaleChromosomes Human Pair 3Chromosome DeletionFluorescence in situ hybridizationHuman Genetics
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Segmental duplication associated with evolutionary instability of human chromosome 3p25.1

2005

Fluorescence in situ hybridization (FISH) of human bacterial artificial chromosome (BAC) clones to orangutan metaphase spreads localized a breakpoint between human chromosome 3p25.1 and orangutan chromosome 2 to a <30-kb interval. The inversion occurred in a relatively gene-rich region with seven genes within 500 kb. The underlying breakpoint is closely juxtaposed to validated genes, however no functional gene has been disrupted by the evolutionary rearrangement. An approximately 21-kb DNA segment at the 3p25.1 breakpoint region has been duplicated intrachromosomally and interchromosomally to multiple regions in the orangutan and human genomes, providing additional evidence for the role …

BiologyEvolution MolecularChromosomal InstabilityGene DuplicationYeastsChromosome regionsGeneticsmedicineAnimalsHumansMolecular BiologyIn Situ Hybridization FluorescencePhylogenyGenetics (clinical)Segmental duplicationGeneticsBacterial artificial chromosomeGorilla gorillamedicine.diagnostic_testChromosome MappingKaryotypeChromosome 17 (human)KaryotypingChromosomes Human Pair 3Chromosome 21Chromosome 22Fluorescence in situ hybridizationCytogenetic and Genome Research
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The BCL6 gene in B-cell lymphomas with 3q27 translocations is expressed mainly from the rearranged allele irrespective of the partner gene

2003

The BCL6 gene, which functions as a transcription repressor, is the target of multiple chromosomal translocations in non-Hodgkin's lymphomas (NHL). These translocations occur in the nontranslated region of the BCL6 gene, juxtaposing regulatory sequences of the diverse partner genes to the open reading frame of the BCL6 gene and thus are thought to deregulate BCL6 gene expression. The levels of expression of the BCL6 gene and protein have been demonstrated to predict the clinical outcome of diffuse large B-cell lymphomas. By contrast, the prognostic significance of BCL6 gene translocations is unclear. In this study we have sought an explanation for this apparent discrepancy. We examined tumo…

Cancer ResearchLymphoma B-CellBiologyTranslocation Geneticimmune system diseasesProto-Oncogene Proteinshemic and lymphatic diseasesGene expressionTumor Cells CulturedHumansRNA MessengerAllelePromoter Regions GeneticGeneAllelesGene RearrangementGeneticsRegulation of gene expressionPromoterHematologyGene rearrangementBCL6Neoplasm ProteinsDNA-Binding ProteinsGene Expression Regulation NeoplasticRepressor ProteinsOncologyRegulatory sequenceMutationProto-Oncogene Proteins c-bcl-6Cancer researchChromosomes Human Pair 3Transcription FactorsLeukemia
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Genomic Abnormalities Acquired in the Blastic Transformation of Splenic Marginal Zone B-cell Lymphoma

2003

Among 20 cases of typical splenic marginal zone lymphoma (SMZL), two cases had blastic transformation. The genetic mechanisms underlying the morphologic transformation were investigated by comparing genetic changes in initial and blastic phases. A complex karyotype including trisomy of 3q and genomic gain of 17q22-q24 was seen in both cases at diagnosis. However, the extra copy of 3q was lost during the transformation process in both tumors. Additionally, the Karpas 1718 cell line, which was derived from a patient with transformed SMZL and carried a trisomy of 3q, also evidenced the spontaneous loss of the extra 3q during the culturing process. Other acquired abnormalities observed exclusiv…

Cancer ResearchPathologymedicine.medical_specialtyLymphoma B-CellTrisomyChromosomal translocationBiologyComplex KaryotypeTumor Cells CulturedmedicineChromosomes HumanHumansSplenic marginal zone lymphomaChromosome AberrationsLymphoma Non-HodgkinSplenic NeoplasmsHematologymedicine.diseaseTransformation (genetics)OncologyKaryotypingDisease ProgressionB-Cell Non-Hodgkin LymphomaChromosomes Human Pair 3Chromosome DeletionAbnormalityBlast CrisisTrisomyChromosomes Human Pair 17Comparative genomic hybridizationLeukemia & Lymphoma
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Investigations for fine mapping of amplifications in chromosome 3q26.3-28 frequently occurring in squamous cell carcinomas of the head and neck.

2002

<i>Objective:</i> Overrepresentations of chromosomal material on the long arm of chromosome 3 frequently occur in squamous cell carcinoma of the head and neck. This experimental study was conducted for further fine mapping of these overrepresentations by interphase fluorescence in situ hybridization (FISH) of tumor cells in cell lines. <i>Methods:</i> Seven cell lines derived from squamous cell carcinomas of the head and neck were investigated by comparative genomic hybridization to analyze unbalanced chromosomal aberrations. Overrepresentations of chromosomal material on the telomeric part of the long arm of chromsome 3 were further analyzed by interphase FISH using…

Chromosome AberrationsCancer Researchmedicine.diagnostic_testCellGene AmplificationChromosomeChromosome MappingGeneral MedicineBiologyMolecular biologymedicine.anatomical_structureOncologyChromosome 3Cell cultureHead and Neck NeoplasmsmedicineCarcinoma Squamous CellTumor Cells CulturedHumansBasal cellChromosomes Human Pair 3Head and neckIn Situ Hybridization FluorescenceComparative genomic hybridizationFluorescence in situ hybridizationOncology
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MICRODISSECTION AND DOP-PCR-BASED REVERSE CHROMOSOME PAINTING AS A FAST AND RELIABLE STRATEGY IN THE ANALYSIS OF VARIOUS STRUCTURAL CHROMOSOME ABNORM…

1996

Reverse chromosome painting has become a powerful tool in clinical genetics for the characterization of cytogenetically unclassifiable aberrations. In this report, the application of a sensitive and rapid procedure for the complete and precise identification of four different de novo structural chromosome abnormalities is presented. These chromosome rearrangements include a marker derived from chromosome 3(cen-q11), an interstitial deletion of chromosome 13 [del(13)(q14q22)], an unbalanced translocation [46,XY, -4, +der(4)t(4;8)(p 15.2;p21.1)] leading to Wolf-Hirschhorn syndrome, and a partial inverted duplication in conjunction with a partial deletion of chromosome 5p [46,XX, -5, +der(5)(:…

Cri-du-Chat SyndromeDerivative chromosomeMarker chromosomeChromosomal translocationBiologyPolymerase Chain ReactionTranslocation GeneticChromosome (genetic algorithm)PregnancyPrenatal DiagnosismedicineHumansWolf–Hirschhorn syndromeIn Situ Hybridization FluorescenceGenetics (clinical)Chromosomal inversionChromosome 13Chromosome AberrationsGeneticsChromosomes Human Pair 13DissectionInfant NewbornObstetrics and Gynecologymedicine.diseaseMolecular biologyGenetic TechniquesChromosome 3FemaleChromosomes Human Pair 3Chromosomes Human Pair 4Gene DeletionChromosomes Human Pair 8Prenatal Diagnosis
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Isolation and differential expression of two isoforms of the ROBO2/Robo2 axon guidance receptor gene in humans and mice.

2006

AbstractExpression of Robo receptor molecules is important for axon guidance across the midline of the mammalian central nervous system. Here we describe novel isoform a of human ROBO2, which is initially strongly expressed in the fetal human brain but thereafter only weakly expressed in adult brain and a few other tissues. The known isoform b of ROBO2 shows a more or less ubiquitous expression pattern, suggesting diverse functional roles. The genomic structure and distinct expression patterns of Robo2a and Robo2b have been conserved in the mouse, but in contrast to human ROBO2a mouse Robo2a is also abundant in adult brain. Exons 1 and 2 of human ROBO2a lie in an inherently unstable DNA seg…

Fetal brain developmentGene isoformSegmental duplicationMolecular Sequence DataBreak in syntenyBiologyLoss of heterozygosity03 medical and health sciencesMice0302 clinical medicineChromosome 3p12.3GeneticsAnimalsHumansProtein IsoformsAmino Acid SequenceReceptors ImmunologicGene030304 developmental biologySegmental duplicationSyntenyEvolutionary breakpointGenetics0303 health sciencesAxon guidanceChromosomeBrainGene Expression Regulation DevelopmentalROBO2ExonsChromosomes MammalianHuman genomeAxon guidanceChromosomes Human Pair 3030217 neurology & neurosurgeryGenomics
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