Search results for "Genomic instability"

showing 10 items of 45 documents

Deficiency of the Cockayne syndrome B (CSB) gene aggravates the genomic instability caused by endogenous oxidative DNA base damage in mice.

2007

The Cockayne syndrome B protein (CSB) has long been known to be involved in the repair of DNA modifications that block the RNA polymerase in transcribed DNA sequences (transcription-coupled repair). Recent evidence suggests that it also has a more general role in the repair of oxidative DNA base modifications such as 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxoG). In mammalian cells, 8-oxoG is a substrate of the repair glycosylase OGG1. Mice without this enzyme accumulate 8-oxoG in the genome and have elevated spontaneous mutation rates. To elucidate the role of CSB in the prevention of mutations by oxidative DNA base damage, we have generated mice that are deficient in Csb or Ogg1 or both ge…

Genome instabilityMaleCancer ResearchDNA repairDNA damageMice Inbred StrainsMice TransgenicBiologymedicine.disease_causeCockayne syndromeGenomic InstabilityDNA GlycosylasesMiceBacterial ProteinsGeneticsmedicineLac RepressorsAnimalsPoint MutationPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneSequence DeletionGeneticsMice KnockoutMutationPoint mutationmedicine.diseaseMolecular biologyRepressor ProteinsMutagenesis InsertionalOxidative StressDNA Repair EnzymesLiverDNA glycosylaseMutationFemaleDNA DamageOncogene
researchProduct

Genomic instability in an interspecific hybrid of the genus Saccharomyces: a matter of adaptability

2020

Ancient events of polyploidy have been linked to huge evolutionary leaps in the tree of life, while increasing evidence shows that newly established polyploids have adaptive advantages in certain stress conditions compared to their relatives with a lower ploidy. The genus Saccharomyces is a good model for studying such events, as it contains an ancient whole-genome duplication event and many sequenced Saccharomyces cerevisiae are, evolutionary speaking, newly formed polyploids. Many polyploids have unstable genomes and go through large genome erosions; however, it is still unknown what mechanisms govern this reduction. Here, we sequenced and studied the natural S. cerevisiae × Saccharomyces…

Genome instabilityNuclear geneDNA Copy Number VariationsPopulationGene DosageHybridsWineGenome instabilityadaptationSaccharomyces cerevisiaeBiologyGenomeGenomic InstabilityPolyploidy03 medical and health sciencesSaccharomycesCopy-number variationAdaptationeducation030304 developmental biologyhybridsresequencing0303 health scienceseducation.field_of_study030306 microbiologyChimeraGeneral MedicineGenomicsSequence Analysis DNAbiology.organism_classificationgenome instabilityEvolutionary biologyEpistasisPloidyMicrobial evolution and epidemiology: Mechanisms of evolutionSaccharomyces kudriavzeviiGenome FungalSaccharomyces kudriavzeviiResequencingResearch ArticleMicrobial Genomics
researchProduct

Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

2015

Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed …

Genome instabilityRedox signalingRNA UntranslatedEpigenetic regulation of neurogenesisDNA RepairHuR mRNA-binding protein in the 3′-untranslated regionClinical BiochemistryHDAC histone deacetylaseReview ArticleAP-1 activator protein 1BiochemistryApe-1 apurinic/apyrimidinic endonuclease 1GPx-1 glutathione peroxidase-1Epigenesis GeneticHistonesTrx thioredoxinPHD prolylhydroxylaseBER base excision repairlcsh:QH301-705.5HO-1 heme oxygenase-1EpigenomicsGeneticsRegulation of gene expressionNox member of the NADPH oxidase familylcsh:R5-920JmjC Jumonji C domain-containing histone demethylasesHIF-1α hypoxia inducible factor-1α5-hmC 5-hydroxymethylcytosineddc:Cell biologyMMP matrix metalloproteinaseGrx glutaredoxinGAPDH glyceraldehyde-3-phosphate dehydrogenaseNrf2 nuclear factor erythroid related factor 2DNA methylationEpigeneticslcsh:Medicine (General)Oxidation-ReductionSignal Transduction5-mC 5-methylcytosineDNA repairDNA damageNF-κB nuclear factor-κBBiologyGenomic InstabilityRNS reactive nitrogen speciesROS reactive oxygen speciesNER nucleotide excision repairSOD superoxide dismutaseOxyR transcription factor (hydrogen peroxide-inducible genes activator)HumansEpigeneticsOrganic ChemistryPETN pentaerithrityl tetranitrateGene regulationOxidative StressDNMT DNA methyltransferaseGene Expression Regulationlcsh:Biology (General)AREs AU-rich elementsHAT histone acetyltransferaseKeap1 kelch-like ECH-associated protein 1BiomarkersCOPD chronic obstructive pulmonary disorderDNA DamageRedox Biology
researchProduct

Molecular and physiological consequences of faulty eukaryotic ribonucleotide excision repair

2019

Abstract The duplication of the eukaryotic genome is an intricate process that has to be tightly safe‐guarded. One of the most frequently occurring errors during DNA synthesis is the mis‐insertion of a ribonucleotide instead of a deoxyribonucleotide. Ribonucleotide excision repair (RER) is initiated by RNase H2 and results in error‐free removal of such mis‐incorporated ribonucleotides. If left unrepaired, DNA‐embedded ribonucleotides result in a variety of alterations within chromosomal DNA, which ultimately lead to genome instability. Here, we review how genomic ribonucleotides lead to chromosomal aberrations and discuss how the tight regulation of RER timing may be important for preventin…

Genome instabilityRibonucleotideDNA RepairDNA repairDNA damageRibonucleotide excision repairRibonuclease HContext (language use)ReviewBiologyGenomic InstabilityGeneral Biochemistry Genetics and Molecular Biology570 Life sciences03 medical and health scienceschemistry.chemical_compound0302 clinical medicineAnimalsHumansMolecular Biology030304 developmental biology0303 health sciencesGeneral Immunology and MicrobiologyGeneral NeuroscienceRNA–DNA hybridDNA Replication Repair & RecombinationEukaryotaDNAtopoisomerase 1ChromatinChromatinCell biologychemistryribonucleotide excision repairGenetic FitnessRNase H2030217 neurology & neurosurgeryDNA570 BiowissenschaftenThe EMBO Journal
researchProduct

Checkpoint adaptation in recombination-deficient cells drives aneuploidy and resistance to genotoxic agents.

2020

Abstract Human cancers frequently harbour mutations in DNA repair genes, rendering the use of DNA damaging agents as an effective therapeutic intervention. As therapy-resistant cells often arise, it is important to better understand the molecular pathways that drive resistance in order to facilitate the eventual targeting of such processes. We employ recombination-defective diploid yeast as a model to demonstrate that, in response to genotoxic challenges, nearly all cells eventually undergo checkpoint adaptation, resulting in the generation of aneuploid cells with whole chromosome losses that have acquired resistance to the initial genotoxic challenge. We demonstrate that adaptation inhibit…

Genome instabilitySaccharomyces cerevisiae ProteinsDNA RepairDNA repairAneuploidySaccharomyces cerevisiaeBiologyBiochemistryGenomic Instabilitychemistry.chemical_compoundGene Knockout TechniquesDrug Resistance FungalmedicineCytotoxicityMolecular BiologyRecombination GeneticSirolimusCell BiologyCell Cycle Checkpointsmedicine.diseaseAneuploidyPhenotypeDiploidyCell biologyRad52 DNA Repair and Recombination ProteinchemistryAdaptationPloidyDNADNA repair
researchProduct

Long-Lasting Genomic Instability Following Arsenite Exposure inMammalian Cells: The Role of Reactive Oxygen Species

2011

Previously, we reported that the progeny of mammalian cells, which has been exposed to sodium arsenite for two cell cycles, exhibited chromosomal instability and concurrent DNA hypomethylation, when they were subsequently investigated after two months of subculturing (about 120 cell generations) in arsenite-free medium. In this work, we continued our investigations of the long-lasting arsenite-induced genomic instability by analyzing additional endpoints at several time points during the cell expanded growth. In addition to the progressive increase of aneuploid cells, we also noted micronucleated and multinucleated cells that continued to accumulate up to the 50th cell generation, as well a…

Genome instabilitySodium arseniteEpidemiologyArsenitesHealth Toxicology and MutagenesisPopulationCellarsenite; genomic instability; reactive oxygen speciesCHO CellsBiologyGenomic Instabilitychemistry.chemical_compoundMultinucleateCricetulusChromosome instabilityCricetinaemedicineAnimalseducationGenetics (clinical)Arseniteeducation.field_of_studyCell cycleDNA MethylationFlow CytometryMolecular biologyarseniteSettore BIO/18 - Geneticamedicine.anatomical_structurechemistryEnvironmental PollutantsReactive Oxygen Species
researchProduct

Patterns of genomic instability in gastric cancer: clinical implications and perspectives

2007

In gastric cancer (GC) the loss of genomic stability represents a key molecular step that occurs early in the carcinogenesis process and creates a permissive environment for the accumulation of genetic and epigenetic alterations in tumor suppressor genes and oncogenes. It is widely accepted that GC can follow at least two major genomic instability pathways, microsatellite instability (MSI) and chromosome instability (CIN). MSI is responsible for a well-defined subset of GCs. CIN represents a more common pathway comprising heterogeneous subsets of GC. In addition to MSI and CIN, the CpG islands methylator phenotype (CIMP) plays an important role in gastric carcinogenesis. CIMP may lead to th…

Genome instabilitybusiness.industrygastric cancer genomic instability microsatellite instability (MSI) chromosomal instability (CIN) CpG island methylator phenotype (CIMP) clinical implicationsMicrosatellite instabilityHematologyDNA Methylationmedicine.diseasemedicine.disease_causedigestive system diseasesDNA demethylationOncologyCpG siteStomach NeoplasmsChromosomal InstabilityChromosome instabilityDNA methylationmedicineCancer researchHumansCpG IslandsMicrosatellite InstabilityEpigeneticsbusinessCarcinogenesisneoplasms
researchProduct

Differential diagnosis problems in a patient with dysphonia and chronic lymphocytic leukemia

2014

SUMMARY Dysphonia is frequently an expression of laryngitis, especially when it comes in the evolution of an immunosuppressed patient, as happens in chronic lymphoproliferation. But other causes of dysphonia should also not be forgotten, including the possibility of new malignancies, especially due to the fact that these patients have genomic instability that predisposes to appearance of a second or even a third cancer. We present the case of a patient who developed dysphonia during chronic lymphocytic leukemia evolution. Its etiology was a mediastinal compression through lymph nodes, not linked to leukemia, but produced by metastases of a bronchopulmonary cancer, appeared recently. Dysphon…

Genomic instabilitymedicine.medical_specialtyPediatricsbusiness.industryChronic lymphocytic leukemiaMediastinumCancerCase ReportGeneral MedicineLaryngitisDysphoniaMediastinal compressionmedicine.diseaseSurgeryLeukemiamedicine.anatomical_structureotorhinolaryngologic diseasesmedicineVocal cord dysfunctionEtiologyChronic lymphocytic leukemiaLung cancerDifferential diagnosisbusiness
researchProduct

Immune pathway upregulation and lower genomic instability distinguish EBV-positive nodal T/NK-cell lymphoma from ENKTL and PTCL-NOS

2022

Primary Epstein-Barr virus (EBV)-positive nodal T/NK-cell lymphoma (PTCL-EBV) is a poorly understood disease which shows features resembling extranodal NK/T-cell lymphoma (ENKTL) and is currently not recognized as a distinct entity but categorized as a variant of primary T-cell lymphoma not otherwise specified (PTCL-NOS). Herein, we analyzed copynumber aberrations (n=77) with a focus on global measures of genomic instability and homologous recombination deficiency and performed gene expression (n=84) and EBV miRNA expression (n=24) profiling as well as targeted mutational analysis (n=16) to further characterize PTCL-EBV in relation to ENKTL and PTCL-NOS. Multivariate analysis revealed that …

Lymphoma Extranodal NK-T-CellEpstein-Barr Virus InfectionsHerpesvirus 4 HumanMicroRNAsgenomic instability EBV-positive nodal T/NK-cell lymphoma T cell lymphomahemic and lymphatic diseasesHumansLymphoma T-Cell PeripheralHematologySettore MED/08 - Anatomia PatologicaGenomic InstabilityUp-Regulation
researchProduct

Imbalance between genomic gain and loss identifies high-risk neuroblastoma patients with worse outcomes

2021

Survival in high-risk neuroblastoma (HR-NB) patients remains poor despite multimodal treatment. We aimed to identify HR-NB patients with worse outcomes by analyzing the genomic instability derived from segmental chromosomal aberrations. We calculated 3 genomic instability indexes for primary tumor SNP array profiles from 127 HR-NB patients: (1) Copy number aberration burden (%gainslength+%losseslength), (2) copy number load (CNL) (%gainslength-%losseslength) and (3) net genomic load (NGL) (%gainsamount-%lossesamount). Tumors were classified according to positive or negative CNL and NGL genomic subtypes. The impact of the genomic instability indexes on overall survival (OS) was assessed with…

Male0301 basic medicineGenome instabilityOncologyCancer ResearchCopy number loadSNPa single nucleotide polymorphism arrayNeuroblastoma0302 clinical medicineHigh risk neuroblastomaSegmental chromosomal aberrationsHR high-riskCNA copy number aberrationTumor biologyCNL copy number loaddNGL decreased net genomic loadlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensPrognosisPrimary tumornCNL negative copy number loadGI genomic instabilityHomogeneous030220 oncology & carcinogenesisMNA MYCN-amplificationFemaleHR-NB high-risk neuroblastomaNB neuroblastomaSNP arrayOriginal articlemedicine.medical_specialtyDNA Copy Number VariationsiNGL increased net genomic loadpCNL positive copy number loadhetMNA heterogeneous MYCN-amplificationlcsh:RC254-282Polymorphism Single NucleotideGenomic InstabilityUHR ultra-high-riskOS overall survivalNet genomic load03 medical and health sciencesSCA segmental chromosomal aberrationInternal medicineNeuroblastomamedicineHumansNGL net genomic loadGenetic Predisposition to DiseaseGenomic imbalanceGenetic Association StudiesEFS event-free survivalProportional Hazards ModelsChromosome AberrationsPloidieshomMNA homogeneous MYCN-amplificationProportional hazards modelbusiness.industryGene AmplificationGenetic Variationmedicine.diseasePatient Outcome AssessmentCopy number aberration burden030104 developmental biologybusinessNeoplasia
researchProduct