Search results for "Pair 1"

showing 10 items of 160 documents

Bipolar (neural and myoblastic) phenotype in cell lines derived from human germ cell tumours of testis.

1997

Non-seminomatous germ cell tumours of the testis (NSGCT) form a heterogeneous group of neoplasms. Cell lines derived from NSGCT may provide useful data concerning the biology of neoplasic precursor germ cells, differentiation of tumour stem cells and the relationship between various tissue components of these tumours. Four NSGCT were studied, two mixed tumours composed of teratocarcinoma, yolk sac and trophoblastic elements, and two malignant teratomas with a massive neuroectodermal component, equivalent to primary neuroectodermal tumours (PNET) of the testis. The explanted tumours gave rise to various cell populations, including epitheloid cells, flattened large cells, spindle cells and te…

AdultMalePathologymedicine.medical_specialtyNeurofilamentCellular differentiationBiologyHistogenesisPathology and Forensic MedicineCytokeratinTesticular NeoplasmsmedicineTumor Cells CulturedHumansIntermediate filamentMolecular BiologyChromosome AberrationsChromosomes Human Pair 12Glial fibrillary acidic proteinCell BiologyGeneral MedicineNeoplasms Germ Cell and EmbryonalImmunohistochemistryMicroscopy Electronmedicine.anatomical_structurePhenotypeKaryotypingbiology.proteinStem cellGerm cellBiomarkersVirchows Archiv : an international journal of pathology
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Atypical Pleomorphic Extraosseous Ewing Tumor/Peripheral Primitive Neuroectodermal Tumor with Unusual Phenotypic/Genotypic Profile

2002

A pleomorphic undifferentiated tumor primarily located in the retroperitoneum with a phenotype compatible with an extraosseous Ewing tumor/peripheral primitive neuroectodermal tumor (ET/pPNET) pattern and unusual molecular features is described. Immunohistochemically, HBA-71 (CD99/mic2) and several neural markers were intensively expressed together with scattered cells expressing carcinoembryonic antigen (CEA). Short-term culture showed biphasic neuroblastic and epithelioid cell populations, with the latter expressing germ cell markers (CEA, alpha-fetoprotein, and the beta-subunit of chorionic gonadotrophin). Conventional cytogenetics displayed several chromosomic rearrangements, especially…

AdultMalePathologymedicine.medical_specialtyOncogene Proteins FusionChromosomes Human Pair 22CD99Soft Tissue NeoplasmsChromosomal translocationSarcoma EwingBiologyTranslocation GeneticPathology and Forensic MedicineExonFatal OutcomeCarcinoembryonic antigenBiomarkers TumorTumor Cells CulturedmedicineHumansNeuroectodermal Tumors PrimitiveRetroperitoneal NeoplasmsMolecular BiologyGene Rearrangementmedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionPeripheral Primitive Neuroectodermal TumorChromosomes Human Pair 11Neoplasms Second PrimaryDNA NeoplasmCell BiologyGenes p53Chromosome Bandingmedicine.anatomical_structureKaryotypingMutationbiology.proteinEpithelioid cellGerm cellFluorescence in situ hybridizationDiagnostic Molecular Pathology
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Oculopharyngeal muscular dystrophy in a northern German family linked to chromosome 14q, and presenting carnitine deficiency

1997

We report the evaluation of oculopharyngeal muscular dystrophy (OPMD) in a large northern German family, which can be traced back six generations and is unrelated to French-Canadian families. The symptoms in this family start at about 50 years of age and include dysphagia, bilateral ptosis, and in some cases a slowly progressive atrophy and weakness of other extraocular, facial or limb girdle muscles. The muscle biopsies showed the pathognomonic ultrastructural finding of characteristic intranuclear filaments. Linkage analysis confirmed that this family is also linked to chromosome 14q markers. Haplotype analysis revealed that a unique haplotype segregates with the disease which is differen…

AdultMaleProbandPathologymedicine.medical_specialtyWeaknessGenetic LinkageBiopsyBiologyMuscular DystrophiesOculopharyngeal muscular dystrophySural NervePathognomonicGenetic linkageCarnitineGermanymedicineHumansCarnitineGenetics (clinical)AgedChromosomes Human Pair 14Family HealthGeneticsElectromyographyHaplotypeMiddle Agedmedicine.diseaseDysphagiaMitochondriaPedigreeMicroscopy ElectronPhenotypeNeurologyOculomotor MusclesPediatrics Perinatology and Child HealthPharyngeal MusclesFemaleNeurology (clinical)medicine.symptommedicine.drugNeuromuscular Disorders
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Association of microsatellite polymorphisms of the human 14q13.2 region with type 2 diabetes mellitus in Latvian and Finnish populations.

2007

A polymorphic microsatellite in intron 6 of the human proteasome core particle PSMA6 gene (HSMS006), and four other microsatellites localized upstream on human chromosome 14q13.2 (HSMS801, HSMS702, HSMS701, HSMS602), were genotyped in 104 type 2 diabetic patients and 129 age-matched control subjects from Latvia and replicated in 91 type 2 diabetic patients and 88 age-matched healthy control subjects from the Botnia Study in Finland. In type 2 diabetic patients from both populations the HSMS006 (TG)22 allele was two times more frequent compared to the control group. In the Latvian population the (CAA)8 allele of the HSMS602 marker was less frequent in the diabetic group, as was the (AC)24 al…

AdultMaleProteasome Endopeptidase ComplexPopulationPSMA6Type 2 diabetesBiologyGene FrequencyPolymorphism (computer science)Multienzyme ComplexesGeneticsmedicineHumansAlleleeducationAllele frequencyGenetics (clinical)AllelesFinlandAgedGeneticsChromosomes Human Pair 14education.field_of_studyPolymorphism GeneticType 2 Diabetes MellitusMiddle Agedmedicine.diseaseLatviaDiabetes Mellitus Type 2Case-Control StudiesMicrosatelliteFemaleMicrosatellite RepeatsAnnals of human genetics
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Variations in genes regulating neuronal migration predict reduced prefrontal cognition in schizophrenia and bipolar subjects from mediterranean Spain…

2005

Both neural development and prefrontal cortex function are known to be abnormal in schizophrenia and bipolar disorder. In order to test the hypothesis that these features may be related with genes that regulate neuronal migration, we analyzed two genomic regions: the lissencephaly critical region (chromosome 17p) encompassing the LIS1 gene and which is involved in human lissencephaly; and the genes related to the platelet-activating-factor, functionally related to LIS1, in 52 schizophrenic patients, 36 bipolar I patients and 65 normal control subjects. In addition, all patients and the 25 control subjects completed a neuropsychological battery. Thirteen (14.8%) patients showed genetic varia…

AdultMalePsychosisBipolar DisorderAdolescentLissencephalyNeuropsychological TestsCognitionCell MovementPredictive Value of TestsmedicineHumansBipolar disorderPlatelet Activating FactorPrefrontal cortexMolecular BiologyNeuronsAnalysis of VarianceReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceMiddle Agedmedicine.diseaseLogistic ModelsSpainSchizophreniaEndophenotype1-Alkyl-2-acetylglycerophosphocholine EsteraseSchizophreniaFemaleAnalysis of variancePsychologyMicrotubule-Associated ProteinsNeuroscienceNeural developmentChromosomes Human Pair 17Neuroscience
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Risk gene variants for nicotine dependence in the CHRNA5-CHRNA3-CHRNB4 cluster are associated with cognitive performance

2010

Recent studies strongly support an association of the nicotinic acetylcholine receptor gene cluster CHRNA5-CHRNA3-CHRNB4 with nicotine dependence (ND). However, the precise genotype-phenotype relationship is still unknown. Clinical and epidemiological data on smoking behavior raise the possibility that the relevant gene variants may indirectly contribute to the development of ND by affecting cognitive performance in some smokers who consume nicotine for reasons of "cognition enhancement." Here, we tested seven single nucleotide polymorphisms (SNPs) rs684513, rs637137, rs16969968, rs578776, rs1051730, rs3743078, rs3813567 from the CHRNA5-CHRNA3-CHRNB4 gene cluster for association with ND, me…

AdultMaleRiskGenotypeGene ExpressionNerve Tissue ProteinsSingle-nucleotide polymorphismReceptors NicotinicBiologyBioinformaticsPolymorphism Single NucleotideNicotineCellular and Molecular NeuroscienceCognitionGene clustermedicineHumansGenetic Predisposition to DiseaseRNA MessengerRisk factorAlleleGenetic Association StudiesGenetics (clinical)AgedGeneticsChromosomes Human Pair 15Gene Expression ProfilingCHRNA5HaplotypeWechsler ScalesGenetic VariationCognitionTobacco Use DisorderMiddle AgedPsychiatry and Mental healthMultigene Familybiology.proteinFemalemedicine.drugAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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Sleep disturbances in Angelman syndrome: a questionnaire study.

2003

Only few studies are available on sleep disorders in Angelman syndrome (AS), a neurodevelopmental disorder with several behavior disturbances. The aim of this study was to determine the prevalence of sleep disorders in a relatively large group of AS subjects, compared to that of age-matched controls. Forty-nine consecutive parents of patients with AS (26 males and 23 females aged 2.3-26.2 years) were interviewed and filled out a comprehensive sleep questionnaire. Based on their genetic etiology, four groups were defined: deletion of chromosome 15q11-13 (25 subjects); methylation imprinting mutation (six subjects), UBE3A mutations (seven subjects) and paternal uniparental disomy (five subjec…

AdultMaleSleep Wake DisordersPediatricsmedicine.medical_specialtyAdolescentUbiquitin-Protein LigasesComorbidityNeurodevelopmental disorderDevelopmental NeuroscienceReference ValuesAngelman syndromeSurveys and QuestionnairesmedicineUBE3APrevalenceHumansWakefulnessPsychiatryChildangelman syndrome; questionnaire study; sleep disordersSleep disorderChromosomes Human Pair 15questionnaire studySleep terrorAge FactorsGeneral MedicineSomnambulismDNA MethylationUniparental Disomymedicine.diseaseSleep in non-human animalsItalyChild PreschoolPediatrics Perinatology and Child HealthMutationsleep disordersFemaleNeurology (clinical)Sleep onsetAngelman SyndromePsychologySleepBraindevelopment
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Epimutation at human chromosome 14q32.2 in a boy with a upd(14)mat-like clinical phenotype.

2009

Recently, three reports described deletions and epimutations affecting the imprinted region at chromosome 14q32.2 in individuals with a phenotype typical for maternal uniparental disomy of chromosome 14 [upd(14)mat]. In this study, we describe another patient with upd(14)mat-like phenotype including low birth weight, neonatal feeding problems, muscular hypotonia, motor and developmental delay, small hands and feet, and truncal obesity. Conventional cytogenetic analyses, fluorescence in situ hybridization subtelomere screening, multiplex ligation-dependent probe amplification analysis of common microdeletion and microduplication syndromes, and methylation analysis of SNRPN all gave normal re…

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesMolecular Sequence DataMothersBiologyMethylationPolymorphism Single NucleotideEpigenesis GeneticGenomic ImprintingIntergenic regionGeneticsmedicineHumansAbnormalities MultipleEpigeneticsChildGenetics (clinical)GeneticsChromosomes Human Pair 14Muscular hypotoniamedicine.diagnostic_testBase SequenceChromosomeUniparental DisomySubtelomerePhenotypeDifferentially methylated regionsPhenotypeMutationFemaleFluorescence in situ hybridizationClinical genetics
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Two independent chromosomal rearrangements, a very small (550 kb) duplication of the 7q subtelomeric region and an atypical 17q11.2 <i>(NF1)&lt…

2006

Most patients with neurofibromatosis (NF1) are endowed with heterozygous mutations in the <i>NF1</i> gene. Approximately 5% show an interstitial deletion of chromosome 17q11.2 (including <i>NF1</i>) and in most cases also a more severe phenotype. Here we report on a 7-year-old girl with classical NF1 signs, and in addition mild overgrowth (97th percentile), relatively low OFC (10th–25th percentile), facial dysmorphy, hoarse voice, and developmental delay. FISH analysis revealed a 17q11.2 microdeletion as well as an unbalanced 7p;13q translocation leading to trisomy of the 7q36.3 subtelomeric region. The patient’s mother and grandmother who were phenotypically normal …

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesNeurofibromatosesmedia_common.quotation_subjectBiologyCytogeneticsGene DuplicationGene duplicationGeneticsmedicineHumansGirlNeurofibromatosisneoplasmsMolecular BiologyGeneIn Situ Hybridization FluorescenceGenetics (clinical)Oligonucleotide Array Sequence AnalysisNeurofibromatosesmedia_commonGeneticsInfantChromosomeTelomereSubtelomeremedicine.diseaseeye diseasesnervous system diseasesChild PreschoolFemaleChromosome DeletionChromosomes Human Pair 7Chromosomes Human Pair 17Cytogenetic and Genome Research
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Intragenic KANSL1 mutations and chromosome 17q21.31 deletions: broadening the clinical spectrum and genotype-phenotype correlations in a large cohort…

2015

Background The 17q21.31 deletion syndrome phenotype can be caused by either chromosome deletions or point mutations in the KANSL1 gene. To date, about 60 subjects with chromosome deletion and 4 subjects with point mutation in KANSL1 have been reported. Prevalence of chromosome deletions compared with point mutations, genotype–phenotype correlations and phenotypic variability have yet to be fully clarified. Methods We report genotype–phenotype correlations in 27 novel subjects with 17q21.31 deletion and in 5 subjects with KANSL1 point mutation , 3 of whom were not previously reported. Results The prevalence of chromosome deletion and KANSL1 mutation was 83% and 17%, respectively. All patient…

AdultMalemedicine.medical_specialtyAdolescentgenotype-phenotype correlationsKoolen De Vries syndromeKANSL1 mutationHaploinsufficiencyBiologySettore MED/03 - GENETICA MEDICASeverity of Illness IndexCraniofacial AbnormalitiesYoung AdultSeizuresMolecular geneticsGeneticsmedicineHumansAbnormalities MultipleLanguage Development DisordersChildGenetics (clinical)Genetic Association StudiesGeneticsOptic nerve hypoplasiaFetal Growth RetardationPoint mutationMacrocephalyInfantNuclear ProteinsSyndromeclinical heterogeneitySmith–Magenis syndromemedicine.diseaseChild PreschoolSpeech delayFemalemedicine.symptomChromosome DeletionSmith-Magenis SyndromeHaploinsufficiencyChromosomes Human Pair 1717q21.31 deletion
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