Search results for "uniparental disomy"

showing 5 items of 15 documents

The genetic tumor background is an important determinant for heterogeneous MYCN ‐amplified neuroblastoma

2016

Amplification of MYCN is the signature genetic aberration of 20–25% of neuroblastoma and a stratifying marker associated with aggressive tumor behavior. The detection of heterogeneous MYCN amplification (hetMNA) poses a diagnostic dilemma due to the uncertainty of its relevance to tumor behavior. Here, we aimed to shed light on the genomic background which permits hetMNA in neuroblastoma and tied the occurrence to other stratifying markers and disease outcome. We performed SNP analysis using Affymetrix Cytoscan HD arrays on 63 samples including constitutional DNA, tumor, bone marrow and relapse samples of 26 patients with confirmed hetMNA by MYCN‐FISH. Tumors of patients ≤18m were mostly an…

Male0301 basic medicineCancer ResearchPathologymedicine.medical_specialtyTumor Markers and Signaturesuniparental disomyAdolescentMYCN amplificationAneuploidyBiologyPolymorphism Single NucleotideN-Myc Proto-Oncogene ProteinBenign tumorGenetic HeterogeneityNeuroblastoma03 medical and health sciences0302 clinical medicineNeuroblastomamedicineHumansChildIn Situ Hybridization FluorescenceChromosome AberrationsOncogene ProteinsN-Myc Proto-Oncogene ProteinGenetic heterogeneityGene AmplificationInfantNuclear ProteinsAneuploidymedicine.diseaseUniparental disomy030104 developmental biologyOncologyChild Preschool030220 oncology & carcinogenesisintratumoral heterogeneityCancer researchFemaleChromosome DeletionTrisomySNP arrayInternational Journal of Cancer
researchProduct

SNPs array karyotyping reveals a novel recurrent 20p13 amplification in primary myelofibrosis.

2011

The molecular pathogenesis of primary mielofibrosis (PMF) is still largely unknown. Recently, single-nucleotide polymorphism arrays (SNP-A) allowed for genome-wide profiling of copy-number alterations and acquired uniparental disomy (aUPD) at high-resolution. In this study we analyzed 20 PMF patients using the Genome-Wide Human SNP Array 6.0 in order to identify novel recurrent genomic abnormalities. We observed a complex karyotype in all cases, detecting all the previously reported lesions (del(5q), del(20q), del(13q), +8, aUPD at 9p24 and abnormalities on chromosome 1). In addition, we identified several novel cryptic lesions. In particular, we found a recurrent alteration involving cytob…

MaleMicroarraysMIELOFIBROSISChromosomes Human Pair 20Loss of Heterozygositylcsh:MedicineLoss of heterozygosityCohort StudiesHematologic Cancers and Related DisordersGene duplicationTaq Polymeraselcsh:ScienceOligonucleotide Array Sequence AnalysisMultidisciplinaryMYELOFIBROSIS; SNPKaryotypeGenomicsHematologyUniparental disomyMedicineFemaleImmunohistochemical AnalysisSNP arrayResearch ArticleTest Evaluationmedicine.medical_specialtyDNA Copy Number VariationsImmunologySNPLocus (genetics)Single-nucleotide polymorphismReceptors Cell SurfaceBiologyPolymorphism Single NucleotideDiagnostic MedicinemedicineGeneticsHumansBiologyAgedEvolutionary BiologyMyeloproliferative DisordersPopulation Biologylcsh:RCytogeneticsGene AmplificationComputational BiologyDNAUniparental Disomymedicine.diseaseMolecular biologyMYELOFIBROSISPrimary MyelofibrosisKaryotypingGenetic PolymorphismImmunologic TechniquesClinical Immunologylcsh:QPopulation GeneticsPLoS ONE
researchProduct

Novel deletion of the E3A ubiquitin protein ligase gene detected by multiplex ligation-dependent probe amplification in a patient with Angelman syndr…

2010

Angelman syndrome (AS) is a severe neurobehavioural disorder caused by failure of expression of the maternal copy of the imprinted domain located on 15q11-q13. There are different mechanisms leading to AS: maternal microdeletion, uniparental disomy, defects in a putative imprinting centre, mutations of the E3 ubiquitin protein ligase (UBE3A) gene. However, some of suspected cases of AS are still scored negative to all the latter mutations. Recently, it has been shown that a proportion of negative cases bear large deletions overlapping one or more exons of the UBE3A gene. These deletions are difficult to detect by conventional gene-scanning methods due to the masking effect by the non-delete…

Malecongenital hereditary and neonatal diseases and abnormalitiesClinical Biochemistrygene dosageBiochemistryGene dosageExonSettore BIO/13 - Biologia ApplicataAngelman syndromemedicineUBE3AHumansMultiplexGenetic TestingMultiplex ligation-dependent probe amplificationChildMolecular BiologyGeneticsbiologyubiquitin-protein ligasesgenetic association studiemedicine.diseaseMolecular biologyUniparental disomyUbiquitin ligaseAngelman syndromebiology.proteinMolecular MedicineOriginal ArticleFemaleGene Deletion
researchProduct

Assessment of Clonal Evolution in 42 AML with NPM1 Mutations by Molecular Characterization of Paired Diagnosis and Relapse Samples

2011

Abstract Abstract 237 Mutations in the nucleophosmin 1 (NPM1) gene represent one of the most frequent gene mutations in acute myeloid leukemia (AML), in particular in cytogenetically normal (CN)-AML. NPM1 mutations (NPM1mut) are considered as an early genetic event in the pathogenesis of AML. To address the role of clonal evolution from diagnosis to relapse in NPM1mut AML, we applied high-resolution genome-wide single nucleotide polymorphism (SNP) array analysis using the Affymetrix 6.0 platform to detect copy number alterations (CNAs) and uniparental disomies (UPDs) in paired samples from 42 patients. In addition, we determined NPM1 and FLT3 [internal tandem duplication (ITD) and tyrosine …

Oncologymedicine.medical_specialtyPathologyNPM1ImmunologyCell BiologyHematologyBiologyGene mutationmedicine.diseaseBiochemistrySomatic evolution in cancerUniparental disomyETV6Internal medicinemedicineCopy-number variationSNP arrayChromosome 13Blood
researchProduct

Genome-wide parent-of-origin DNA methylation analysis reveals the intricacies of human imprinting and suggests a germline methylation-independent mec…

2014

Genomic imprinting is a form of epigenetic regulation that results in the expression of either the maternally or paternally inherited allele of a subset of genes (Ramowitz and Bartolomei 2011). This imprinted expression of transcripts is crucial for normal mammalian development. In humans, loss-of-imprinting of specific loci results in a number of diseases exemplified by the reciprocal growth phenotypes of the Beckwith-Wiedemann and Silver-Russell syndromes, and the behavioral disorders Angelman and Prader-Willi syndromes (Kagami et al. 2008; Buiting 2010; Choufani et al. 2010; Eggermann 2010; Kelsey 2010; Mackay and Temple 2010). In addition, aberrant imprinting also contributes to multige…

PlacentaADNGene ExpressionBiologyMethylationGenomic ImprintingPregnancyGerm cellsGeneticsmedicineHumansEpigeneticsRNA-Directed DNA MethylationAllelesEmbryonic Stem CellsGenetics (clinical)GeneticsGenome HumanResearchDNAGenomicsDNA Methylationmedicine.diseaseUniparental disomyCèl·lules germinalsGenòmicaGerm CellsDifferentially methylated regionsDNA methylationIllumina Methylation AssayCpG IslandsFemaleMetilacióGenomic imprintingReprogrammingGenome Research
researchProduct