Search results for "Chromosome instability"

showing 10 items of 38 documents

Senataxin defective in ataxia oculomotor apraxia type 2 is involved in the defence against oxidative DNA damage

2007

Adefective response to DNA damage is observed in several human autosomal recessive ataxias with oculomotor apraxia, including ataxia-telangiectasia. We report that senataxin, defective in ataxia oculomotor apraxia (AOA) type 2, is a nuclear protein involved in the DNA damage response. AOA2 cells are sensitive to H2O2, camptothecin, and mitomycin C, but not to ionizing radiation, and sensitivity was rescued with full-length SETX cDNA. AOA2 cells exhibited constitutive oxidative DNA damage and enhanced chromosomal instability in response to H2O2. Rejoining of H2O2-induced DNA double-strand breaks (DSBs) was significantly reduced in AOA2 cells compared to controls, and there was no evidence fo…

Ataxiagenetic structuresDNA RepairDNA damageApraxiasBiologyArticlechemistry.chemical_compoundComplementary DNAChromosome instabilitymedicineHumansDNA Breaks Double-StrandedOculomotor apraxiaCells CulturedResearch ArticlesNeurodegenerationMitomycin CDNA HelicasesCell BiologyHydrogen Peroxidemedicine.diseaseMolecular biologyMultifunctional EnzymesOxidative StresschemistryAtaxiamedicine.symptomDNARNA HelicasesDNA Damage
researchProduct

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
researchProduct

RB acute loss induces centrosome amplification and aneuploidy in murine primary fibroblasts

2006

AbstractBackgroundIncorrect segregation of whole chromosomes or parts of chromosome leads to aneuploidy commonly observed in cancer. The correct centrosome duplication, assuring assembly of a bipolar mitotic spindle, is essential for chromosome segregation fidelity and preventing aneuploidy. Alteration of p53 and pRb functions by expression of HPV16-E6 and E7 oncoproteins has been associated with centrosome amplification. However, these last findings could be the result of targeting cellular proteins in addition to pRb by HPV16-E7 oncoprotein. To get a more detailed picture on the role of pRb in chromosomal instability and centrosome amplification, we analyzed the effects of the acute loss …

Cancer ResearchTime FactorsTranscription GeneticRbCentrosomes AneuploidyGene ExpressionMitosisAneuploidyBiologyRetinoblastoma Proteinlcsh:RC254-282Chromosome segregationMiceChromosome instabilityGene duplicationmedicineAnimalsCentrosome duplicationMitosisCells CulturedCentrosomeResearchGene AmplificationFibroblastsAneuploidylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseSettore BIO/18 - GeneticaSpindle checkpointOncologyCentrosomeCancer researchMolecular MedicineMolecular Cancer
researchProduct

Cytogenetic analysis and metabolic profiling reveal a subgroup of benign meningiomas with chromosomal instabilities and aggressive metabolism

2010

Meningiomas add up to 30% of Central Nervous System (CNS) tumours. Atypical meningiomas show a high index of recurrence 5 years after complete resection. Sometimes, meningiomas with histological diagnosis of benign meningioma show genetics characteristics of atypical meningioma. Aberrations of chromosomes 1, 14, and 22 are the most frequently reported abnormalities in meningiomas. In this communication we used cytogenetic, FISH, and NMR metabolic profiling for a molecular characterization of a series of 46 meningiomas. Tumor samples were obtained from 46 patients with meningioma (36 benign and 12 atypical) from the Clinic Hospital of Valencia. Cytogenetic analyses were performed by short-te…

Cancer Researchmedicine.medical_specialtyPathologyTissue microarrayKaryotypeBiologymedicine.diseaseBioinformaticsCXCR4nervous system diseasesMeningiomaChromosome instabilityBenign Meningiomaotorhinolaryngologic diseasesGeneticsmedicineHistopathologyRhabdomyosarcomaneoplasmsMolecular BiologyCancer Genetics and Cytogenetics
researchProduct

FISH and CHIPs: Colorful Clues to Radiation-Induced Chromosomal Instability

2004

Radiation produces a variety of clonal and non-clonal chromosome aberrations that can be characterized by fluorescence in situ hybridization (FISH). Epigenetic changes affecting the expression of an essential DNA repair gene(s) may be an importantant mechanism for radiation-induced chromosomal instability. Expression profiling with specialized cDNA chips promises to identify candidate genes for the delayed effects of radiation and to provide new insights into the manifold and complex cellular responses to DNA damage. Much progress can be made by using FISH and CHIPs to study the mechanisms and biological consequences of ionizing radiation.

Candidate genemedicine.diagnostic_testDNA repairbusiness.industryDNA damageChromosomeBiologyBiotechnologyCell biologyGene expression profilingChromosome instabilitymedicineEpigeneticsbusinessFluorescence in situ hybridization
researchProduct

Simultaneous reduction of MAD2 and BUBR1 expression induces mitotic spindle alterations associated with p53 dependent cell cycle arrest and death

2014

Most human tumors are characterized by aneuploidy that is believed to be the consequence of chromosomal instability (CIN). The mechanism(s) leading to aneuploidy and the pathways that allow its tolerance are not completely understood. The Spindle Assembly Checkpoint (SAC) is a cellular surveillance mechanism working during mitosis, and alterations of genes that encode components of the SAC weakening the mitotic checkpoint, induce aneuploidy by chromosome mis-segregation. We induced aneuploidy in near-diploid tumor cells by simultaneous depletion of the SAC proteins MAD2 and BUBR1 by RNA interference in the attempt to gain further insight on the cellular responses to aneuploidy. Individual r…

Cell cycle checkpointMad2AneuploidyCell BiologyGeneral MedicineCell cycleBiologymedicine.diseaseSpindle apparatusCell biologySpindle checkpointChromosome instabilitymedicineMitosisCell Biology International
researchProduct

Compromised repair of radiation-induced DNA double-strand breaks in Fanconi anemia fibroblasts in G2

2020

Fanconi anemia (FA) is a rare chromosomal instability syndrome with various clinical features and high cancer incidence. Despite being a DNA repair disorder syndrome and a frequently observed clinical hypersensitivity of FA patients towards ionizing radiation, the experimental evidence regarding the efficiency of radiation-induced DNA double-strand break (DSB) repair in FA is very controversial. Here, we performed a thorough analysis of the repair of radiation-induced DSBs in G1 and G2 in FA fibroblasts of complementation groups A, C, D1 (BRCA2), D2, E, F, G and P (SLX4) in comparison to normal human lung and skin fibroblasts. γH2AX, 53BP1, or RPA foci quantification after X-irradiation was…

DNA End-Joining RepairBiologyBiochemistryFanconi Anemia Complementation Group F ProteinHistonesRecombinases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineFanconi anemiaChromosome instabilitymedicineHumansDNA Breaks Double-StrandedFanconi Anemia Complementation Group G ProteinMolecular BiologyCells Cultured030304 developmental biologyBRCA2 ProteinChromosome Aberrations0303 health sciencesFanconi Anemia Complementation Group A ProteinFanconi Anemia Complementation Group D2 ProteinX-RaysCell CycleFanconi Anemia Complementation Group C ProteinRecombinational DNA RepairChromosomeDNACell BiologyFibroblastsCell cyclemedicine.diseaseFanconi Anemia Complementation Group E ProteinComplementationKineticsenzymes and coenzymes (carbohydrates)Fanconi Anemiachemistry030220 oncology & carcinogenesisPremature chromosome condensationMutationCancer researchChromatidTumor Suppressor p53-Binding Protein 1DNADNA Repair
researchProduct

Functional Inactivation of pRB Results in Aneuploid Mammalian Cells After Release From a Mitotic Block

2002

AbstractThe widespread chromosome instability observed in tumors and in early stage carcinomas suggests that aneuploidy could be a prerequisite for cellular transformation and tumor initiation. Defects in tumor suppressers and genes that are part of mitotic checkpoints are likely candidates for the aneuploid phenotype. By using flow cytometric, cytogenetic, immunocytochemistry techniques we investigated whether pRB deficiency could drive perpetual aneuploidy in normal human and mouse fibroblasts after mitotic checkpoint challenge by microtubule-destabilizing drugs. Both mouse and human pRB-deficient primary fibroblasts resulted, upon release from a mitotic block, in proliferating aneuploid …

DNA ReplicationCancer ResearchBrief ArticleClone (cell biology)MitosisAneuploidyCre recombinaseSpindle Apparatuslcsh:RC254-282Retinoblastoma ProteinColony-Forming Units AssayMicechemistry.chemical_compoundChromosome instabilitymedicineAnimalsHumanscentrosomesCINGenes RetinoblastomaMitosisCells CulturedIn Situ Hybridization FluorescenceCentrosomeCell cycle controlbiologyColcemidChromosome FragilityCell CycleGINDemecolcineRetinoblastoma proteinAneuploidy; Cell cycle control; Centrosomes; CIN; PRB;FibroblastsCell cyclelcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensAneuploidyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicCell biologyCell Transformation NeoplasticPRBMicroscopy Fluorescencechemistrybiology.proteinFemaleNeoplasia
researchProduct

DNA polymeraseθ up-regulation is associated with poor survival in breast cancer, perturbs DNA replication, and promotes genetic instability

2010

“Replicative stress” is one of the main factors underlying neoplasia from its early stages. Genes involved in DNA synthesis may therefore represent an underexplored source of potential prognostic markers for cancer. To this aim, we generated gene expression profiles from two independent cohorts (France,n= 206; United Kingdom,n= 117) of patients with previously untreated primary breast cancers. We report here that among the 13 human nuclear DNA polymerase genes, DNA Polymerase θ (POLQ) is the only one significantly up-regulated in breast cancer compared with normal breast tissues. Importantly,POLQup-regulation significantly correlates with poor clinical outcome (4.3-fold increased risk of de…

DNA ReplicationGenome instabilityDNA damageDNA polymerase[SDV]Life Sciences [q-bio]DNA Polymerase ThetaBreast NeoplasmsDNA-Directed DNA PolymeraseKaplan-Meier Estimatemedicine.disease_causeBioinformaticsGenomic InstabilityCell LineCohort Studies03 medical and health sciences0302 clinical medicineBreast cancerCell Line TumorChromosome instabilityCyclin EmedicineHumansComputingMilieux_MISCELLANEOUS030304 developmental biology0303 health sciencesMultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCancerMiddle AgedBiological SciencesPrognosismedicine.diseaseUnited KingdomUp-RegulationGene Expression Regulation Neoplastic030220 oncology & carcinogenesisCancer researchbiology.proteinFemaleRNA InterferenceFranceCarcinogenesisDNA DamageProceedings of the National Academy of Sciences
researchProduct

Chromosomal instability, reproductive cell death and apoptosis induced by O6-methylguanine in Mex−, Mex+ and methylation-tolerant mismatch repair com…

1998

O6-Methylguanine (O6-MeG) is induced in DNA by methylating environmental carcinogens and various cytostatic drugs. It is repaired by O6-methylguanine-DNA methyltransferase (MGMT). If not repaired prior to replication, the lesion generates gene mutations and leads to cell death, sister chromatid exchanges (SCEs), chromosomal aberrations and malignant transformation. To address the question of how O6-MeG is transformed into genotoxic effects, isogenic Chinese hamster cell lines either not expressing MGMT (phenotypically Mex-), expressing MGMT (Mex+) or exhibiting the tolerance phenotype (Mex-, methylation resistant) were compared as to their clastogenic response. Mex- cells were more sensitiv…

DNA ReplicationMethylnitronitrosoguanidineGuanineDNA RepairDNA damageHealth Toxicology and MutagenesisDrug ResistanceApoptosisCHO CellsGene mutationBiologyChromosomesDNA AdductsO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeChromosome instabilityGeneticsAnimalsSister chromatidsMolecular BiologyMitosisChromosome AberrationsCell DeathModels GeneticMutagenicity TestsDNA replicationDNA MethylationMolecular biologyDNA methylationDNA mismatch repairSister Chromatid ExchangeMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
researchProduct