Search results for "chromosome"

showing 10 items of 1175 documents

X Chromosome Contribution to the Genetic Architecture of Primary Biliary Cholangitis

2021

Background & aims: Genome-wide association studies in primary biliary cholangitis (PBC) have failed to find X chromosome (chrX) variants associated with the disease. Here, we specifically explore the chrX contribution to PBC, a sexually dimorphic complex autoimmune disease. Methods: We performed a chrX-wide association study, including genotype data from 5 genome-wide association studies (from Italy, United Kingdom, Canada, China, and Japan; 5244 case patients and 11,875 control individuals). Results: Single-marker association analyses found approximately 100 loci displaying P < 5 × 10-4, with the most significant being a signal within the OTUD5 gene (rs3027490; P = 4.80 × 10-6; odds…

Canadian-US PBC Consortium0301 basic medicineMaleLinkage disequilibriumGenome-wide association studyDiseasePBCSettore MED/03 - GENETICA MEDICALinkage Disequilibrium0302 clinical medicineUK-PBC ConsortiumGenotypeMitochondrial Precursor Protein Import Complex ProteinsItalian PBC Genetics Study GroupOdds RatioX-Wide Association StudyJapan PBC-GWAS ConsortiumX chromosomeGeneticsLiver Cirrhosis BiliaryGastroenterologyForkhead Transcription FactorsDNA-Binding ProteinsShal Potassium Channels030211 gastroenterology & hepatologyFemaleAdultMonosaccharide Transport ProteinsSuperenhancerLocus (genetics)Single-nucleotide polymorphismBiologyProtein Serine-Threonine KinasesPolymorphism Single NucleotideArticleWhite People03 medical and health sciencesAsian PeopleProto-Oncogene ProteinsEndopeptidasesHumansCell LineageGenetic Predisposition to DiseaseMeta-analysiGenetic associationChromosomes Human XGastroenterology & HepatologyHepatology1103 Clinical SciencesMeta-analysis030104 developmental biologyGenetic Loci1114 Paediatrics and Reproductive MedicineMeta-analysis; Superenhancer; X-Wide Association Study1109 NeurosciencesCarrier ProteinsGenome-Wide Association Study
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MYCN gain and MYCN amplification in a stage 4S neuroblastoma.

2003

Abstract Stage 4S neuroblastoma is a disease associated with spontaneous regression and good survival. We present a patient whose evolution has shown the variety and complexity of this disease in infants. Biologic factors, such as ploidy, MYCN copy number, loss of 1p36, and other chromosomal gains and losses were determined. A complex pattern of genetic abnormalities, such as near-diploidy, MYCN gain (2–4 copies per haploid genome) and imbalance/deletion of 1p36 was seen in the diagnostic sample. An extensive disseminated disease after a latent period of 26 months was associated with a special genetic evolution, such as tetraploidy, MYCN amplification (2:100–500 copies), 1p36 deletion, and …

Cancer ResearchAdrenal Gland NeoplasmsGenes mycDiseaseBiologymedicine.disease_causeNeuroblastomaFatal OutcomeNeuroblastomaGene duplicationGeneticsmedicineHumansneoplasmsMolecular BiologyNeoplasm StagingGeneticsMutationTransition (genetics)Gene AmplificationInfantmedicine.diseaseAneuploidyPrimary tumorChromosomes Human Pair 1Stage 4S NeuroblastomaCancer researchDisease ProgressionFemalePloidyChromosome DeletionChromosomes Human Pair 17Cancer genetics and cytogenetics
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Arsenic-induced DNA hypomethylation affects chromosomal instability in mammalian cells

2004

Early genetic instability induced in dividing V79-Cl3 Chinese hamster cells by inorganic arsenic, as demonstrated in our previous investigation, was evidenced by aneuploidy and nuclear abnormalities, but not by chromosomal rearrangements. Here we report the results of cytogenetic and morphological analyses performed on the progeny of cells dividing at the end of sodium arsenite treatment after they had been expanded through 120 generations (ASO cells) and then cloned. The acquired genetic instability persisted and was increased by highly unstable chromosomal rearrangements, namely dicentric chromosomes and telomeric associations, which were not seen following acute exposure. A peculiar find…

Cancer ResearchAneuploidyAntineoplastic Agentsgenomic instability arsenicChinese hamsterArsenicDicentric chromosomechemistry.chemical_compoundChromosome instabilityChromosomal InstabilityCricetinaemedicineAnimalsChromosome AberrationsbiologyChromosomeGeneral MedicineDNA Methylationmedicine.diseasebiology.organism_classificationMolecular biologySettore BIO/18 - GeneticachemistryDNA methylationCytogenetic AnalysisCarcinogensDNADNA hypomethylation
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A new pericentric inv(8) in acute nonlymphocytic leukemia.

1993

Abstract Chromosome studies were carried out on unstimulated bone marrow cells from a patient with a diagnosis of acute nonlymphocytic leukemia (FAB M6 ANLL). Cytogenetic analysis revealed a mosaic chromosome pattern 46,XX46,XX,inv(8)(p21q24). This pericentric inversion has not been previously described in ANLL. Because, fragile sites, zinc finger gene loci, and the MYC protooncogene have been localized to band 8q24, a putative role for these sites and genes could be considered.

Cancer ResearchBiologychromosome Acute nonlymphocytic leukemia cytogeneticshemic and lymphatic diseasesGeneticsmedicineHumansMolecular BiologyGeneChromosomal inversionZinc fingerGeneticsChromosomal fragile siteChromosomeMiddle Agedmedicine.diseaseMolecular biologySettore BIO/18 - GeneticaLeukemiaLeukemia Myeloid Acutemedicine.anatomical_structureKaryotypingChromosome InversionFemaleBone marrowChromosomes Human Pair 8Cancer genetics and cytogenetics
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Functional impact and evolution of a novel human polymorphic inversion that disrupts a gene and creates a fusion transcript

2015

Despite many years of study into inversions, very little is known about their functional consequences, especially in humans. A common hypothesis is that the selective value of inversions stems in part from their effects on nearby genes, although evidence of this in natural populations is almost nonexistent. Here we present a global analysis of a new 415-kb polymorphic inversion that is among the longest ones found in humans and is the first with clear position effects. This inversion is located in chromosome 19 and has been generated by non-homologous end joining between blocks of transposable elements with low identity. PCR genotyping in 541 individuals from eight different human populatio…

Cancer ResearchDNA End-Joining Repairlcsh:QH426-470GenotypeChromosome inversionPopulationChromosome BreakpointsBiologyChromosome breakpointsGenoma humàPolymorphism Single NucleotideEvolution MolecularChromosome Breakpoints03 medical and health sciences0302 clinical medicinePolymorphism Single nucleotideChromosome 19DNA end-joining repairGeneticsTranscription factorsHumansAlleleeducationMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and Systematics030304 developmental biologyChromosomal inversionGeneticsGene expression regulation0303 health scienceseducation.field_of_studyGenètica de poblacionsHaplotypelcsh:GeneticsDNA transposable elementsGenetics PopulationGene Expression RegulationFusion transcriptChromosome InversionDNA Transposable ElementsChromosomes Human Pair 19030217 neurology & neurosurgeryResearch ArticleTranscription Factors
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Pattern of secondary genomic changes in pancreatic tumors ofTgfα/Trp53+/−transgenic mice

2003

Trp53+/− mice overexpressing Tgfα in a pancreas-specific manner represent a well-established animal model for pancreatic cancer. In this study we analyzed 38 pancreatic adenocarcinomas of these mice for secondary genomic changes by comparative genomic hybridization (CGH), loss of heterozygosity (LOH) analysis, real-time PCR, and methylation-specific analysis. CGH screening of the tumors revealed a recurrent pattern of genomic changes. In more than 50% of the tumors, chromosome 11 was affected. The gain of the proximal part spans about 16 cM, including the genes for Egfr, Rel, and Stk10. The distal part of chromosome 11, which contains the Trp53 locus, was deleted. LOH analysis proved that a…

Cancer ResearchLocus (genetics)Biologymedicine.diseaseMolecular biologyLoss of heterozygosityChromosome 15Chromosome 4CDKN2APancreatic cancerDNA methylationGeneticsmedicineComparative genomic hybridizationGenes, Chromosomes and Cancer
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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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Deletion of the PER3 Gene on Chromosome 1p36 in Recurrent ER-Positive Breast Cancer

2010

El pdf del artículo es la versión de autor.-- et al.

Cancer ResearchMicroarrayGene DosageGene ExpressionEstrogen receptorBreast NeoplasmsGene dosageMiceBreast cancerOriginal ReportsAnimalsHumansMedicineGenetic Predisposition to DiseaseCopy-number variationskin and connective tissue diseasesSequence Deletionbusiness.industryCancerPeriod Circadian ProteinsPrognosismedicine.diseaseSurvival AnalysisDisease Models AnimalReceptors EstrogenOncologyChromosomes Human Pair 1Cancer researchFemaleBreast diseaseNeoplasm Recurrence LocalbusinessTamoxifenmedicine.drugJournal of Clinical Oncology
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Complex rearrangement of chromosomes 6 and 11 as the sole anomaly in atypical teratoid/rhabdoid tumors of the central nervous system.

2000

Atypical teratoid/rhabdoid tumor of the central nervous system is a rare childhood tumor with a distinct histologic appearance and an aggressive clinical course. Few tumors have been analyzed cytogenetically. The only consistent chromosomal abnormality identified in some of these tumors has been monosomy or deletions of chromosome 22; in others, a normal chromosome 22 was present. The authors report an atypical teratoid/rhabdoid neoplasm of the central nervous system with a novel complex rearrangement affecting chromosomes 6 and 11 as the sole anomaly. The involvement of region 11p15 could be important in the pathogenesis of this entity.

Cancer ResearchMonosomymedicine.medical_specialtyPathologyCentral nervous systemBiologyTranslocation GeneticCentral nervous system diseaseCentral Nervous System NeoplasmsGeneticsmedicineHumansRing ChromosomesChildMolecular BiologyIn Situ Hybridization FluorescenceRhabdoid TumorGeneticsChromosome Aberrationsmedicine.diagnostic_testChromosomes Human Pair 11CytogeneticsTeratomaGene rearrangementmedicine.diseaseTeratoid tumormedicine.anatomical_structureKaryotypingChromosomes Human Pair 6FemaleChromosome 22Fluorescence in situ hybridizationCancer genetics and cytogenetics
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Abstract 2435: Amplification of CDK4 and MDM2 is associated with atypical clinical features in high risk neuroblastoma patients

2016

Abstract MYCN-amplification and 11q-deletion are important, although incomplete, markers of high-risk neuroblastoma. Thus, characterization of additional genomic alterations that can be used as prognostic and/or predictive markers is of clinical importance in order to provide best treatment possible. By using SNP-microarrays we identified a small group of neuroblastomas with high grade amplification of one or multiple loci on 12q, commonly involving the potential oncogenic target genes CKD4 (12q13-14) and/or MDM2 (12q15). The CDK4 and MDM2 regions were co-amplified in 13/16 samples, two tumors had CDK4-amplification in absence of MDM2-amplification while one tumor had MDM2-amplification wit…

Cancer ResearchMutationDNA repairmedicine.medical_treatmentCancerBiologymedicine.diseasemedicine.disease_causeTargeted therapyOncologyNeuroblastomaCancer researchmedicinebiology.proteinMdm2neoplasmsExome sequencingChromosome 12Cancer Research
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