Search results for "DNA breaks"

showing 10 items of 37 documents

High resistance to X-rays and therapeutic carbon ions in glioblastoma cells bearing dysfunctional ATM associates with intrinsic chromosomal instabili…

2014

To investigate chromosomal instability and radiation response mechanisms in glioblastoma cells.We undertook a comparative analysis of two patient-derived glioblastoma cell lines. Their resistance to low and high linear energy transfer (LET) radiation was assessed using clonogenic survival assay and their intrinsic chromosome instability status using fluorescence in situ hybridization. DNA damage was analyzed by pulsed-field gel electrophoresis and by γ-H2AX foci quantification. Expression of DNA damage response proteins was assessed by immunoblot.Increased radioresistance to X-rays as well as carbon ions was observed in glioblastoma cells exhibiting high levels of naturally occurring chromo…

Genome instabilityDNA RepairDNA damageLinear energy transferHeavy Ion RadiotherapyAtaxia Telangiectasia Mutated ProteinsBiologyRadiation ToleranceCell Line TumorChromosomal InstabilityRadioresistanceChromosome instabilitymedicineHumansDNA Breaks Double-StrandedLinear Energy TransferRadiology Nuclear Medicine and imagingGel electrophoresisRadiological and Ultrasound Technologymedicine.diagnostic_testX-RaysCell CycleGenomicsMolecular biologyPhosphorylationGlioblastomaSignal TransductionFluorescence in situ hybridizationInternational Journal of Radiation Biology
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Three-dimensional invasion of human glioblastoma cells remains unchanged by X-ray and carbon ion irradiation in vitro.

2012

Purpose Cell invasion represents one of the major determinants that treatment has failed for patients suffering from glioblastoma. Contrary findings have been reported for cell migration upon exposure to ionizing radiation. Here, the migration and invasion capability of glioblastoma cells on and in collagen type I were evaluated upon irradiation with X-rays or carbon ions. Methods and Materials Migration on and invasion in collagen type I were evaluated in four established human glioblastoma cell lines exposed to either X-rays or carbon ions. Furthermore, clonogenic radiation survival, proliferation (5-bromo-2-deoxyuridine positivity), DNA double-strand breaks (γH2AX/53BP1-positive foci), a…

MAPK/ERK pathwayCancer ResearchCell signalingMMP2MAP Kinase Kinase 4p38 Mitogen-Activated Protein KinasesCollagen Type IExtracellular matrixHistonesPhosphatidylinositol 3-KinasesCell MovementMedicineHumansRadiology Nuclear Medicine and imagingDNA Breaks Double-StrandedNeoplasm InvasivenessClonogenic assayPI3K/AKT/mTOR pathwayCell ProliferationRadiationbusiness.industryCell growthBrain NeoplasmsIntegrin beta1Intracellular Signaling Peptides and ProteinsCell migrationCarbonOncologyBromodeoxyuridineImmunologyCancer researchbusinessCell Migration AssaysGlioblastomaTumor Suppressor p53-Binding Protein 1International journal of radiation oncology, biology, physics
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A novel form of ataxia oculomotor apraxia characterized by oxidative stress and apoptosis resistance

2007

Several different autosomal recessive genetic disorders characterized by ataxia with oculomotor apraxia (AOA) have been identified with the unifying feature of defective DNA damage recognition and/or repair. We describe here the characterization of a novel form of AOA showing increased sensitivity to agents that cause single-strand breaks (SSBs) in DNA but having no gross defect in the repair of these breaks. Evidence for the presence of residual SSBs in DNA was provided by dramatically increased levels of poly (ADP-ribose)polymerase (PARP-1) auto-poly (ADP-ribosyl)ation, the detection of increased levels of reactive oxygen/nitrogen species (ROS/RNS) and oxidative damage to DNA in the patie…

MaleMethylnitronitrosoguanidineProgrammed cell deathAtaxiaDNA RepairApraxiasDNA damageMitomycinBlotting WesternPoly (ADP-Ribose) Polymerase-1Apoptosismedicine.disease_causeAntioxidantschemistry.chemical_compoundRadiation IonizingmedicineHumansDNA Breaks Single-StrandedOculomotor apraxiaMolecular BiologyCells CulturedEtoposideMembrane Potential MitochondrialbiologyCytochrome cHydrogen PeroxideCell BiologyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicReactive Nitrogen SpeciesMolecular biologyOxidative StresschemistryApoptosisbiology.proteinAtaxiaCamptothecinFemalePoly(ADP-ribose) Polymerasesmedicine.symptomDNAOxidative stressDNA DamageCell Death & Differentiation
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Genotoxic effects of zinc oxide nanoparticles

2015

The potential toxicity of nanoparticles has currently provoked public and scientific discussions, and attempts to develop generally accepted handling procedures for nanoparticles are under way. The investigation of the impact of nanoparticles on human health is overdue and reliable test systems accounting for the special properties of nanomaterials must be developed. Nanoparticular zinc oxide (ZnO) may be internalised through ambient air or the topical application of cosmetics, only to name a few, with unpredictable health effects. Therefore, we analysed the determinants of ZnO nanoparticle (NP) genotoxicity. ZnO NPs (15-18 nm in diameter) were investigated at concentrations of 0.1, 10 and …

Materials scienceCell SurvivalDNA damageMetal Nanoparticleschemistry.chemical_elementNanoparticleNanotechnologyZincmedicine.disease_causechemistry.chemical_compoundChloridesMicroscopy Electron TransmissionCell Line TumormedicineHumansDNA Breaks Double-StrandedGeneral Materials ScienceAcetylcysteinechemistryZinc CompoundsCell cultureToxicityBiophysicsZinc OxideReactive Oxygen SpeciesDNAGenotoxicityIntracellularNanoscale
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Apoptosis in malignant glioma cells triggered by the temozolomide-induced DNA lesion O6-methylguanine

2006

Methylating drugs such as temozolomide (TMZ) are widely used in the treatment of brain tumours (malignant gliomas). The mechanism of TMZ-induced glioma cell death is unknown. Here, we show that malignant glioma cells undergo apoptosis following treatment with the methylating agents N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and TMZ. Cell death determined by colony formation and apoptosis following methylation is greatly stimulated by p53. Transfection experiments with O(6)-methylguanine-DNA methyltransferase (MGMT) and depletion of MGMT by O(6)-benzylguanine showed that, in gliomas, the apoptotic signal originates from O(6)-methylguanine (O(6)MeG) and that repair of O(6)MeG by MGMT prevent…

MethylnitronitrosoguanidineCancer ResearchProgrammed cell deathFas Ligand ProteinGuanineDNA repairFas-Associated Death Domain ProteinBlotting WesternApoptosisBiologymedicine.disease_causeO(6)-Methylguanine-DNA MethyltransferaseGliomaTemozolomideTumor Cells CulturedGeneticsmedicineHumansDNA Breaks Double-StrandedRNA Small InterferingAntineoplastic Agents AlkylatingneoplasmsMolecular BiologyTumor Stem Cell AssayCell ProliferationTemozolomideBrain NeoplasmsCell CycleGliomaCell cycleFlow CytometryFas receptormedicine.diseaseDacarbazineProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesCancer researchTumor Suppressor Protein p53CarcinogenesisDNA Damagemedicine.drugOncogene
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DNA strand breaks induced by nuclear hijacking of neuronal NOS as an anti-cancer effect of 2-methoxyestradiol

2015

2-Methoxyestradiol (2-ME) is a physiological metabolite of 17β-estradiol. At pharmacological concentrations, 2-ME inhibits colon, breast and lung cancer in tumor models. Here we investigated the effect of physiologically relevant concentrations of 2-ME in osteosarcoma cell model. We demonstrated that 2-ME increased nuclear localization of neuronal nitric oxide synthase, resulting in nitro-oxidative DNA damage. This in turn caused cell cycle arrest and apoptosis in osteosarcoma cells. We suggest that 2-ME is a naturally occurring hormone with potential anti-cancer properties.

Pathologymedicine.medical_specialtyneuronal nitric oxide synthaseCell cycle checkpoint2-methoxyestradiolDNA damageAntineoplastic AgentsApoptosisBone NeoplasmsNitric Oxide Synthase Type Imedicine.disease_causeNitric OxideNitric oxidechemistry.chemical_compoundReactive nitrogen specieCell Line TumormedicineHumans2-MethoxyestradiolReactive nitrogen speciesCytokinesisOsteosarcomaEstradiolbusiness.industryDNA BreaksIntracellular Signaling Peptides and ProteinsCancermedicine.diseaseReactive Nitrogen SpeciesG2 Phase Cell Cycle CheckpointsOxidative StressOncologychemistryApoptosis2-methoxyestradiol; Neuronal nitric oxide synthase; Nitric oxide; Osteosarcoma; Reactive nitrogen species; OncologyCancer researchM Phase Cell Cycle CheckpointsbusinessTumor Suppressor p53-Binding Protein 1Oxidative stressmedicine.drugResearch Paper
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Brca2/Xrcc2 dependent HR, but not NHEJ, is required for protection against O6-methylguanine triggered apoptosis, DSBs and chromosomal aberrations by …

2008

Abstract O 6 -methylguanine (O 6 MeG) is a highly critical DNA adduct induced by methylating carcinogens and anticancer drugs such as temozolomide, streptozotocine, procarbazine and dacarbazine. Induction of cell death by O 6 MeG lesions requires mismatch repair (MMR) and cell proliferation and is thought to be dependent on the formation of DNA double-strand breaks (DSBs) or, according to an alternative hypothesis, direct signaling by the MMR complex. Given a role for DSBs in this process, either homologous recombination (HR) or non-homologous end joining (NHEJ) or both might protect against O 6 MeG. Here, we compared the response of cells mutated in HR and NHEJ proteins to temozolomide and…

Programmed cell deathGuanineKu80DNA RepairDown-RegulationFluorescent Antibody TechniqueApoptosisCHO CellsBiologyTransfectionBiochemistryMiceO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeDNA adductTemozolomideAnimalsDNA Breaks Double-StrandedMolecular BiologyBRCA2 ProteinChromosome AberrationsRecombination GeneticCell DeathCell growthCell BiologyTransfectionCell cycleMolecular biologyDNA-Binding ProteinsDacarbazineApoptosisMutationCancer researchHomologous recombinationSister Chromatid ExchangeDNA Repair
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Cytotoxicity and induction of DNA double-strand breaks by components leached from dental composites in primary human gingival fibroblasts

2012

Abstract Introduction The public interest steadily increases in the biological adverse effects caused by components released from resin-based dental restorations. Objective In this study, the cytotoxicity and the genotoxicity were investigated of following released components from dental resin restorations in human gingival fibroblasts (HGF): tetraethyleneglycol dimethacrylate (TEEGDMA), neopentylglycol dimethacrylate (Neopen), diphenyliodoniumchloride (DPIC), triphenyl-stibane (TPSB) and triphenylphosphane (TPP). Methods XTT based cell viability assay was used for cytotoxicity screening of substances. γ-H2AX assay was used for genotoxicity screening. In the γ-H2AX assay, HGFs were exposed …

Programmed cell deathMaterials scienceNecrosisCell SurvivalCell Culture TechniquesGingivaTetrazolium SaltsApoptosismedicine.disease_causeComposite ResinsCell LinePolyethylene GlycolsHistonesDental MaterialsNecrosisOnium CompoundsOrganophosphorus CompoundsPolymethacrylic AcidsMaterials TestingStilbenesmedicineHumansDNA Breaks Double-StrandedGeneral Materials ScienceViability assayCytotoxicityGeneral DentistryDose-Response Relationship DrugBiphenyl CompoundsFibroblastsMolecular biologyBiphenyl compoundMicroscopy FluorescenceMechanics of MaterialsApoptosisToxicityMethacrylatesIndicators and Reagentsmedicine.symptomGenotoxicityMutagensDental Materials
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A nanodosimetric model of radiation-induced clustered DNA damage yields

2010

International audience; We present a nanodosimetric model for predicting the yield of double strand breaks (DSBs) and non-DSB clustered damages induced in irradiated DNA. The model uses experimental ionization cluster size distributions measured in a gas model by an ion counting nanodosimeter or, alternatively, distributions simulated by a Monte Carlo track structure code developed to simulate the nanodosimeter. The model is based on a straightforward combinatorial approach translating ionizations, as measured or simulated in a sensitive gas volume, to lesions in a DNA segment of one-two helical turns considered equivalent to the sensitive volume of the nanodosimeter. The two model paramete…

Quantitative Biology::BiomoleculesAlgorithms Computer Simulation DNA/*radiation effects DNA Breaks[PHYS.PHYS.PHYS-MED-PH] Physics [physics]/Physics [physics]/Medical Physics [physics.med-ph][ PHYS.PHYS.PHYS-MED-PH ] Physics [physics]/Physics [physics]/Medical Physics [physics.med-ph]Genetic Monte Carlo Method Nanotechnology/instrumentation/*methods Plasmids/radiation effects Probability Protons/adverse effects Radiometry/instrumentation/*methods Reproducibility of Results Saccharomyces cerevisiae SoftwareDouble-Stranded/radiation effects DNA Damage/*radiation effects Helium/adverse effects *Models
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The contribution of hydrogen peroxide to the radiosensitizing effect of gold nanoparticles

2019

Abstract Plasmid DNA in aerated aqueous solution is used as a probe to determine whose of the reactive oxygen species (ROS) generated after absorption of ultra-soft X-rays (USX) take part in biomolecule damage in the presence and in absence of Gold Nano-Particles (GNP) and specific scavengers. Citrate-coated GNPs with core sizes of 6, 10 and 25 nm are synthetized and characterized, especially in terms of plasmon band shift, ζ-potential and hydrodynamic radii (respectively 9, 21 and 30 nm). We confirm the radiosensitizing effect of GNP and show that the SSB number per plasmid increases when, for a same mass of gold element, the core size of the gold nanoparticles decreases. Hydroxyl radicals…

Radiation-Sensitizing AgentsFormatesRadicalMetal Nanoparticles02 engineering and technologyPhotochemistry01 natural sciencesCitric AcidMetalchemistry.chemical_compoundColloid and Surface ChemistryPyruvic Acid0103 physical sciences[CHIM]Chemical SciencesMoleculeDimethyl SulfoxideDNA Breaks Single-StrandedParticle SizeTromethaminePhysical and Theoretical ChemistryHydrogen peroxideComputingMilieux_MISCELLANEOUSchemistry.chemical_classificationReactive oxygen speciesQuenching (fluorescence)Aqueous solution010304 chemical physicsHydroxyl RadicalX-RaysFree Radical ScavengersHydrogen PeroxideSurfaces and InterfacesGeneral Medicine021001 nanoscience & nanotechnologySolutionschemistryColloidal goldvisual_artvisual_art.visual_art_mediumGold0210 nano-technologyPlasmidsBiotechnologyColloids and Surfaces B: Biointerfaces
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