Search results for "GENETICA"

showing 10 items of 906 documents

Histone acetylation deficits in lymphoblastoid cell lines from patients with Rubinstein-Taybi syndrome.

2012

Background: Rubinstein-Taybi syndrome (RSTS) is a congenital neurodevelopmental disorder defined by postnatal growth deficiency, characteristic skeletal abnormalities and mental retardation and caused by mutations in the genes encoding for the transcriptional co-activators with intrinsic lysine acetyltransferase (KAT) activity CBP and p300. Previous studies have shown that neuronal histone acetylation is reduced in mouse models of RSTS. Methods: The authors identified different mutations at the CREBBP locus and generated lymphoblastoid cell lines derived from nine patients with RSTS carrying distinct CREBBP mutations that illustrate different grades of the clinical severity in the spectrum …

AdultMaleAdolescentDNA Mutational AnalysisGene ExpressionHaploinsufficiencyHydroxamic AcidsHistone DeacetylasesHistonesNeurodevelopmental disorderSettore MED/38 - Pediatria Generale E SpecialisticaHistone H2AGeneticsmedicineHistone H2BHumansCREBBP geneChildGeneGenetics (clinical)Cell Line TransformedRubinstein-Taybi SyndromebiologyRubinstein–Taybi syndromeBase SequenceAcetylationmedicine.diseaseMolecular biologyCREB-Binding ProteinChromatinHistone Deacetylase InhibitorsHistoneSettore MED/03 - Genetica MedicaAcetylationChild PreschoolMutationbiology.proteinCancer researchLeukocytes MononuclearFemaleHaploinsufficiencyE1A-Associated p300 ProteinBiomarkersJournal of medical genetics
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Sister chromatid exchange in Waldenström's macroglobulinemia

1993

Results on sister chromatid exchange (SCE) frequency and interchromosomal distribution in bone marrow and peripheral blood cultures from patients with Waldenström's macroglobulinemia are reported. PHA-stimulated bone marrow cultures showed increased SCE frequencies in all 12 patients examined. The increase was particularly high in two cases (17.07 and 16.77 SCE/cell, respectively) and, in one of them, a very high SCE level was found in PHA-stimulated peripheral blood culture (40.81 SCE/cell). In LPS-stimulated cultures, increased SCE levels were observed in some patients. Comparison between SCE frequency in bone marrow cell cultures with either mitogen showed a significant increase in PHA-s…

AdultMaleCancer ResearchG chromosomeCellSister chromatid exchangeBiologyGeneticsmedicineHumansPooled dataMolecular BiologyAgedCell CycleMacroglobulinemiaWaldenstrom macroglobulinemiaMiddle AgedCell cyclemedicine.diseaseMolecular biologySettore BIO/18 - Geneticamedicine.anatomical_structureImmunologySister chromatid exchanges Waldenstrom's macroglobulinemiaFemaleBone marrowWaldenstrom MacroglobulinemiaSister Chromatid ExchangeCancer Genetics and Cytogenetics
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Cytochrome P450 2E1 variable number tandem repeat polymorphisms and health risks: A genotype-phenotype study in cancers associated with drinking and/…

2012

Cytochrome P450 2E1 (CYP2E1) is one of the main enzymes involved in the oxidation of ethanol and in the transformation of a number of potentially dangerous compounds. It has various polymorphic sites, one of which is a variable number tandem repeat (VNTR) polymorphism previously described in the 5'-flanking region. The aim of this study was to investigate the genotype-phenotype association between CYP2E1 VNTR polymorphisms and risky health habits in healthy subjects and to analyze the associations between these polymorphisms with drinking- and/or smoking-related cancers. We analyzed 166 healthy subjects by genotyping for the CYP2E1 VNTR polymorphism associated with drinking and/or smoking h…

AdultMaleCancer Researchmedicine.medical_specialtyCarcinoma HepatocellularAlcohol Drinkinghuman genetic variability genetic factors cytochrome P450 2E1 variable number tandem repeat polymorphisms predis-posing alleles health risks drinking- and/or smoking-related cancer.Minisatellite RepeatsBiologyBiochemistryGastroenterologyRestriction fragmentYoung AdultRisk-TakingRisk FactorsInternal medicineGenotypeOdds RatioGeneticsmedicineHumansGenetic Predisposition to DiseaseMolecular BiologyGenotypingGenetic Association StudiesGeneticsPolymorphism GeneticLiver NeoplasmsSmokingCytochrome P-450 CYP2E1Odds ratiomedicine.diseaseConfidence intervalPancreatic NeoplasmsVariable number tandem repeatSettore BIO/18 - GeneticaOncologyCase-Control StudiesHepatocellular carcinomabiology.proteinMolecular MedicineAdenocarcinomaFemalePolymorphism Restriction Fragment Length
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Chromosomal abnormalities in Waldenström's macroglobulinemia

1992

We report the results of cytogenetic studies of direct bone marrow (BM) preparations and of short-term BM and peripheral blood (PB) cultures from 17 patients with Waldenström's macroglobulinemia. We noted clonal chromosome changes in 10 patients. Abnormalities affected chromosomes X, Y, 2, 4, 5, 15, 16, 18, 19, 20, 21, and 22; in particular, chromosomes 2, 4, and 5 were involved in structural changes: a homogeneously staining region [hsr(2)], a der(4)t(4;?)(q32;?), and a 5q+. The other chromosomes were involved in numerical abnormalities, such as pseudodiploidy (a 46,X,-X,+15 clone), loss of chromosome Y, and monosomy of chromosomes 16, 18, 19, 20, 21, and 22. Nonclonal chromosome rearrange…

AdultMaleCancer Researchmedicine.medical_specialtyMonosomyClone (cell biology)Chromosome rearrangements Waldenström's macroglobulinemiaBiologyGeneticsmedicineHumanseducationMolecular BiologyHomogeneously Staining RegionAgedGeneticsAged 80 and overChromosome Aberrationseducation.field_of_studyCytogeneticsMacroglobulinemiaWaldenstrom macroglobulinemiaChromosomeKaryotypeMiddle Agedmedicine.diseaseMolecular biologySettore BIO/18 - GeneticaChromosomes Human Pair 2FemaleWaldenstrom Macroglobulinemia
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Clinical relevance of postzygotic mosaicism in Cornelia de Lange syndrome and purifying selection of NIPBL variants in blood.

2021

Postzygotic mosaicism (PZM) in NIPBL is a strong source of causality for Cornelia de Lange syndrome (CdLS) that can have major clinical implications. Here, we further delineate the role of somatic mosaicism in CdLS by describing a series of 11 unreported patients with mosaic disease-causing variants in NIPBL and performing a retrospective cohort study from a Spanish CdLS diagnostic center. By reviewing the literature and combining our findings with previously published data, we demonstrate a negative selection against somatic deleterious NIPBL variants in blood. Furthermore, the analysis of all reported cases indicates an unusual high prevalence of mosaicism in CdLS, occurring in 13.1% of p…

AdultMaleCornelia de Lange SyndromeAdolescent Adult Cell Cycle Proteins Child Child Preschool Comparative Genomic Hybridization De Lange Syndrome Female Gene Deletion High-Throughput Nucleotide Sequencing Humans Male Middle Aged Mosaicism Mutation Missense Phenotype Retrospective Studies Spain Young AdultAdolescentSomatic cellScienceGenetic counselingMedizinMutation MissenseDiseasesCell Cycle ProteinsBiologyPaediatric researchGermlineArticle03 medical and health sciencesNegative selectionYoung AdultMedical researchDe Lange SyndromeGenetics researchmedicineMissense mutationHumansClinical significanceChild030304 developmental biologyRetrospective StudiesGenetics0303 health sciencesComparative Genomic HybridizationMultidisciplinaryMosaicismQ030305 genetics & heredityRHigh-Throughput Nucleotide SequencingNIPBLMiddle Agedmedicine.diseasePhenotypeSettore MED/03 - Genetica MedicaSpainChild PreschoolMedicineFemaleGene Deletion
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Further evidence of genetic heterogeneity in familial essential tremor.

2007

Familial essential tremor (FET) is a common hereditary movement disorder with phenotypic variability and genetic heterogeneity. To date, linkage analyses revealed three loci associated to essential tremor (ET) (ETM1 on 3q13, ETM2 on 2p22-25, and a locus on 6p23). We performed a genetic analysis of these candidate chromosomal regions in a fifth-generation Italian kindred with autosomal-dominant ET. Of the 22 clinically evaluated family members, nine were affected by ET. The genetic study indicates that the ET in this family is not associated to any of the known ET loci. These findings support evidence of further genetic heterogeneity for such disease. (C) 2007 Elsevier Ltd. All rights reserv…

AdultMaleGenetic LinkageLocus (genetics)DiseaseBiologyGenetic analysisGenetic HeterogeneityGenetic linkagemedicineHumansAge of OnsetAgedGeneticsEssential tremorGenetic heterogeneityMiddle Agedmedicine.diseasePhenotypePedigreeNeurologySettore MED/03 - Genetica MedicaDisease ProgressionEssential tremorFemaleSettore MED/26 - NeurologiaNeurology (clinical)Geriatrics and GerontologyAge of onsetLinkage analysiNeurological disease
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NDST1 missense mutations in autosomal recessive intellectual disability.

2014

NDST1 was recently proposed as a candidate gene for autosomal recessive intellectual disability in two families. It encodes a bifunctional GlcNAc N-deacetylase/N-sulfotransferase with important functions in heparan sulfate biosynthesis. In mice, Ndst1 is crucial for embryonic development and homozygous null mutations are perinatally lethal. We now report on two additional unrelated families with homozygous missense NDST1 mutations. All mutations described to date predict the substitution of conserved amino acids in the sulfotransferase domain, and mutation modeling predicts drastic alterations in the local protein conformation. Comparing the four families, we noticed significant overlap in …

AdultMaleModels MolecularCandidate geneAdolescentGenotypeProtein ConformationDNA Mutational AnalysisMutation MissenseGenes RecessiveBiologyBioinformaticsPolymorphism Single NucleotideAnimals Genetically ModifiedEpilepsyConsanguinityYoung AdultProtein structureIntellectual DisabilityIntellectual disabilityGeneticsmedicineMissense mutationAnimalsHumansChildGenetics (clinical)GeneticsGene knockdownMuscular hypotoniaBehavior AnimalComputational BiologyFaciesHigh-Throughput Nucleotide Sequencingmedicine.diseasePhenotypePedigreePhenotypeChild PreschoolGene Knockdown TechniquesDrosophilaFemaleSulfotransferasesGenome-Wide Association StudyAmerican journal of medical genetics. Part A
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Somatic loss of an EXT2 gene mutation during malignant progression in a patient with hereditary multiple osteochondromas

2015

Multiple osteochondromas (MO) is an autosomal-dominant skeletal disorder caused by mutations in the exostosin-1 ( EXT1 ) or exostosin-2 ( EXT2 ) genes. In this study, we report the analysis of the mutational status of the EXT2 gene in tumor samples derived from a patient affected by hereditary MO, documenting the somatic loss of the germline mutation in a giant chondrosarcoma and in a rapidly growing osteochondroma. The sequencing of all exons and exon–intron junctions of the EXT1 and EXT2 genes from blood DNA of the proband did not reveal any mutation in the EXT1 gene but did demonstrate the presence of the transition point mutation c.67C > T in the EXT2 gene, determining the introduction …

AdultMaleOsteochondromaCancer ResearchMultiple osteochondromaSettore MED/06 - Oncologia MedicaChondrosarcomaLoss of HeterozygositySettore BIO/11 - Biologia MolecolareBone NeoplasmsGene mutationBiologyN-Acetylglucosaminyltransferasesmedicine.disease_causeGermlineLoss of heterozygosityGermline mutationGeneticChondrosarcoma; Hereditary cancer; Hereditary multiple osteochondromas; Tumor suppressor gene; Molecular Biology; Genetics; Cancer ResearchSkeletal disorderGeneticsmedicineHumansTumor suppressor geneHereditary multiple osteochondromaMolecular BiologyGeneticsMutationChromosomes Human Pair 11DNA Neoplasmmedicine.diseaseHereditary cancerSettore MED/18 - Chirurgia GeneraleSettore MED/03 - Genetica MedicaMutationDisease ProgressionCancer Genetics
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The HLA locus and multiple sclerosis in Sicily

2005

The authors report the analysis of HLA-class II allelic heterogeneity in a well characterized multiple sclerosis (MS) Sicilian dataset. Family-based association analysis revealed evidence for excess transmission to affected individuals for alleles HLA-DRB1*1501, DRB1*04, and DQB1*0302. When analyzed as haplotypes, the authors observed excess transmission for the DRB1*0400-DQB1*0302 haplotype. Sicilian patients share the HLA-DRB1*1501 susceptibility allele with affecteds living in continental Italy, but also display the allelic heterogeneity that characterizes Mediterranean populations.

AdultMaleRiskmusculoskeletal diseasesMultiple SclerosisAdolescentGenes MHC Class IILocus (genetics)Human leukocyte antigenBiologySeverity of Illness IndexLinkage DisequilibriumCohort StudiesDisability EvaluationGene Frequencyimmune system diseasesMultiple Sclerosis/epidemiologyPrevalencemedicineHumansGenetic Predisposition to DiseaseAge of OnsetAlleleskin and connective tissue diseasesSicilyAllelesGenetic associationGeneticsHLA-D AntigensIncidenceMultiple sclerosisHaplotypeGene Poolmedicine.diseaselanguage.human_languageSettore BIO/18 - GeneticaHaplotypeslanguageFemaleAllelic heterogeneitySettore MED/26 - NeurologiaNeurology (clinical)Sicilian
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Expanding the phenotype associated to KMT2A variants: overlapping clinical signs between Wiedemann–Steiner and Rubinstein–Taybi syndromes

2020

Lysine-specific methyltransferase 2A (KMT2A) is responsible for methylation of histone H3 (K4H3me) and contributes to chromatin remodeling, acting as “writer” of the epigenetic machinery. Mutations in KMT2A were first reported in Wiedemann–Steiner syndrome (WDSTS). More recently, KMT2A variants have been described in probands with a specific clinical diagnosis comprised in the so-called chromatinopathies. Such conditions, including WDSTS, are a group of overlapping disorders caused by mutations in genes coding for the epigenetic machinery. Among them, Rubinstein–Taybi syndrome (RSTS) is mainly caused by heterozygous pathogenic variants in CREBBP or EP300. In this work, we used next generati…

AdultMaleRubinstein-Taybi SyndromeAdolescentHistone-Lysine N-MethyltransferaseWiedemann–SteinerArticlePhenotypeSettore MED/03 - Genetica MedicaSettore MED/38 - PEDIATRIA GENERALE E SPECIALISTICAKMT2A variantsMutationHumansFemaleEpigeneticsRubinstein–Taybi syndromesChildKMT2A Gene Wiedemann–Steiner syndrome Rubinstein–Taybi syndromeMyeloid-Lymphoid Leukemia Protein
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