Search results for "Repair"

showing 10 items of 747 documents

Inactivation of O(6)-methylguanine-DNA methyltransferase by glucose-conjugated inhibitors.

2001

The DNA-repair protein O6-methylguanine-DNA methyltransferase (MGMT) is a decisive determinant of resistance of tumor cells to methylating and chloroethylating anti-cancer drugs. Therefore, selective inhibition of MGMT in tumors is expected to cause tumor sensitization. Several inhibitors of MGMT have been developed which function in both tumors and normal tissue. To deplete MGMT preferentially in tumors, strategies to target the inhibitor to the tumor tissue need to be developed. Here, we report on the properties of glucose-conjugated MGMT inhibitors that might be useful for tumor targeting since tumor cells frequently over-express glucose transporter. O6-Benzylguanine (O6BG), 8-aza-O6-ben…

Cancer ResearchMethyltransferaseGuaninebiologyDNA repairGlucose transporterbiology.organism_classificationDNA methyltransferaseMolecular biologydigestive system diseasesHeLaO(6)-Methylguanine-DNA MethyltransferaseGlucoseOncologyTargeted drug deliveryEnzyme inhibitorbiology.proteinTumor Cells CulturedHumansEnzyme InhibitorsneoplasmsAlkyltransferaseHeLa CellsInternational journal of cancer
researchProduct

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
researchProduct

DNA repair protein MGMT protects against N-methyl-N-nitrosourea-induced conversion of benign into malignant tumors

2003

Tumor formation is a multi-step process that can be divided into the stages of tumor initiation, promotion and progression. Previously, we showed that overexpression in skin of mice of the DNA repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) protects against N-methyl-N-nitrosourea (MNU)-induced tumor initiation without affecting tumor promotion. This indicated that O(6)-methylguanine, which is specifically repaired by MGMT, is a major tumor-initiating lesion. Here we extended this transgenic approach to the study of tumor progression. Benign papillomas that arose on the skin of CkMGMT transgenic mice upon initiation with 7,12-dimethylbenz[a]anthracene (DMBA) and promotion by 1…

Cancer ResearchPathologymedicine.medical_specialtySkin NeoplasmsMethyltransferaseDNA RepairDNA repairDMBAMice TransgenicTumor initiationBiologymedicine.disease_causeMiceO(6)-Methylguanine-DNA MethyltransferaseDNA Repair ProteinmedicineAnimalsneoplasmsPapillomaMethylnitrosoureaGeneral MedicineTumor progressionCarcinogensCancer researchTumor promotionCarcinogenesisCarcinogenesis
researchProduct

Nupr1-Aurora Kinase A Pathway Provides Protection against Metabolic Stress-Mediated Autophagic-Associated Cell Death

2012

Abstract Purpose: The limited supply of oxygen and nutrients is thought to result in rigorous selection of cells that will eventually form the tumor. Experimental Design: Nupr1 expression pattern was analyzed in human tissue microarray (TMA) and correlated with survival time of the patient. Microarray analysis was conducted on MiaPaCa2 cells subjected to metabolic stress in Nupr1-silenced conditions. DNA repair and cell cycle–associated gene expression was confirmed by real-time quantitative PCR (qRT-PCR). Nupr1 and AURKA protective role were analyzed using RNA interference (RNAi) silencing or overexpression. DNA damage and autophagy were analyzed by Western blot analysis and immunofluoresc…

Cancer ResearchProgrammed cell deathCell SurvivalDNA damageDNA repairAdenocarcinomaProtein Serine-Threonine KinasesBiologyAurora KinasesStress PhysiologicalCell Line TumorAutophagyBasic Helix-Loop-Helix Transcription FactorsHumansGene silencingAurora Kinase ARegulation of gene expressionGene knockdownMicroarray analysis techniquesAURKA GeneMolecular biologyCell HypoxiaNeoplasm ProteinsCell biologyGene Expression Regulation NeoplasticGlucoseOncologyRNA InterferenceCarcinoma Pancreatic DuctalClinical Cancer Research
researchProduct

Lovastatin protects human endothelial cells from killing by ionizing radiation without impairing induction and repair of DNA double-strand breaks.

2006

Abstract Purpose: 3-hydroxy-3-methylglutaryl CoA reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they are reported to exert pleiotropic effects on cellular stress responses, proliferation, and apoptosis. Whether statins affect the sensitivity of primary human cells to ionizing radiation (IR) is still unknown. The present study aims at answering this question. Experimental Design: The effect of lovastatin on IR-provoked cytotoxicity was analyzed in primary human umbilical vein endothelial cells (HUVEC). To this end, cell viability, proliferation, and apoptosis as well as DNA damage–related stress responses were investigated. Results: The data show that lova…

Cancer ResearchProgrammed cell deathDNA RepairDNA repairDNA damageCell SurvivalApoptosisRadioresistanceRadiation Ionizingpolycyclic compoundsmedicineHumansLovastatinCells CulturedCell Proliferationbiologynutritional and metabolic diseasesEndothelial CellsDose-Response Relationship RadiationDNAMolecular biologyEndothelial stem cellOncologyApoptosisCytoprotectionHMG-CoA reductasebiology.proteinCancer researchlipids (amino acids peptides and proteins)Lovastatinmedicine.drugDNA DamageClinical cancer research : an official journal of the American Association for Cancer Research
researchProduct

Artesunate induces oxidative DNA damage, sustained DNA double-strand breaks, and the ATM/ATR damage response in cancer cells.

2011

Abstract Artesunate, the active agent from Artemisia annua L. used in the traditional Chinese medicine, is being applied as a first-line drug for malaria treatment, and trials are ongoing that include this drug in cancer therapy. Despite increasing interest in its therapeutic application, the mode of cell killing provoked by artesunate in human cells is unknown. Here, we show that artesunate is a powerful inducer of oxidative DNA damage, giving rise to formamidopyrimidine DNA glycosylase–sensitive sites and the formation of 8-oxoguanine and 1,N6-ethenoadenine. Oxidative DNA damage was induced in LN-229 human glioblastoma cells dose dependently and was paralleled by cell death executed by ap…

Cancer ResearchProgrammed cell deathDNA RepairRAD51Drug Evaluation PreclinicalArtesunateApoptosisCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiologyProtein Serine-Threonine KinasesModels Biologicalchemistry.chemical_compoundNeoplasmsTumor Cells CulturedHumansDNA Breaks Double-StrandedTumor Suppressor ProteinsMolecular biologyAntineoplastic Agents PhytogenicArtemisininsUp-RegulationNon-homologous end joiningDNA-Binding ProteinsOxidative StressCell killingOncologychemistryArtesunateApoptosisCancer cellHomologous recombinationDNA DamageMolecular cancer therapeutics
researchProduct

Differential Sensitivity of Malignant Glioma Cells to Methylating and Chloroethylating Anticancer Drugs: p53 Determines the Switch by Regulating xpc,…

2007

Abstract Glioblastoma multiforme is the most severe form of brain cancer. First line therapy includes the methylating agent temozolomide and/or the chloroethylating nitrosoureas [1-(2-chloroethyl)-1-nitrosourea; CNU] nimustine [1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea; ACNU], carmustine [1,3-bis(2-chloroethyl)-1-nitrosourea; BCNU], or lomustine [1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea; CCNU]. The mechanism of cell death after CNU treatment is largely unknown. Here we show that ACNU and BCNU induce apoptosis in U87MG [p53 wild-type (p53wt)] and U138MG [p53 mutant (p53mt)] glioma cells. However, contrary to what we observed previously for temozolomide, chl…

Cancer ResearchProgrammed cell deathDNA repairAntineoplastic AgentsBiologychemistry.chemical_compoundCell Line TumorGliomamedicineHumansRNA NeoplasmRNA Small InterferingneoplasmsCarmustineTemozolomideBrain Neoplasmsorganic chemicalsNimustineDNA NeoplasmDNA Methylationmedicine.diseaseDNA-Binding ProteinsOncologychemistryCell cultureApoptosisCancer researchTumor Suppressor Protein p53GlioblastomaDNA Damagemedicine.drugCancer Research
researchProduct

Temozolomide- and fotemustine-induced apoptosis in human malignant melanoma cells: response related to MGMT, MMR, DSBs, and p53

2009

Malignant melanomas are highly resistant to chemotherapy. First-line chemotherapeutics used in melanoma therapy are the methylating agents dacarbazine (DTIC) and temozolomide (TMZ) and the chloroethylating agents BCNU and fotemustine. Here, we determined the mode of cell death in 11 melanoma cell lines upon exposure to TMZ and fotemustine. We show for the first time that TMZ induces apoptosis in melanoma cells, using therapeutic doses. For both TMZ and fotemustine apoptosis is the dominant mode of cell death. The contribution of necrosis to total cell death varied between 10 and 40%. The O(6)-methylguanine-DNA methyltransferase (MGMT) activity in the cell lines was between 0 and 1100 fmol m…

Cancer ResearchProgrammed cell deathDNA repairDacarbazineBlotting WesternApoptosistemozolomideBiologyCollagen Type XIDNA Mismatch RepairNecrosisGliomaAntineoplastic Combined Chemotherapy ProtocolsTumor Cells CulturedmedicineHumansDNA Breaks Double-StrandedEverolimusPhosphorylationDNA Modification MethylasesMelanomaneoplasmsSirolimusTemozolomideTumor Suppressor ProteinsMelanomafotemustinemelanoma therapymedicine.diseaseDacarbazineEnzyme Activationmismatch repairDNA Repair EnzymesOncologyApoptosisCaspasesCancer researchFotemustineTumor Suppressor Protein p53Translational TherapeuticsMGMTmedicine.drugBritish Journal of Cancer
researchProduct

Induction of DNA breaks and apoptosis in crosslink-hypersensitive V79 cells by the cytostatic drug beta-D-glucosyl-ifosfamide mustard.

2001

To study molecular aspects of cytotoxicity of the anticancer drug β-D-glucose-ifosfamide mustard we investigated the potential of the agent to induce apoptosis and DNA breakage. Since β-D-glucose-ifosfamide mustard generates DNA interstrand crosslinks, we used as an in vitro model system a pair of isogenic Chinese hamster V79 cells differing in their sensitivity to crosslinking agents. CL-V5B cells are dramatically more sensitive (30-fold based on D10 values) to the cytotoxic effects of β-D-glucose-ifosfamide mustard as compared to parental V79B cells. After 48 h of pulse-treatment with the agent, sensitive cells but not the resistant parental line undergo apoptosis and necrosis, with apopt…

Cancer ResearchProgrammed cell deathNecrosisDNA damageDNA repairAntineoplastic AgentsBiologychemistry.chemical_compoundCricetinaemedicineCytotoxic T cellAnimalsExperimental TherapeuticsIfosfamideDNA breaksCytotoxicityapoptosisDNAPhosphoramide MustardMolecular biologyNitrogen mustardEnzyme ActivationCross-Linking ReagentsGlucoseOncologyBiochemistrychemistryApoptosisCaspasescancer therapyPhosphoramide Mustardscyclophosphamidemedicine.symptomDNA DamageBritish journal of cancer
researchProduct

Overexpression of Ogg1 in mammalian cells: effects on induced and spontaneous oxidative DNA damage and mutagenesis

1999

Chinese hamster ovary cell lines (AA8 and AS52) were stably transfected to overexpress hOgg1 protein, the human DNA repair glycosylase for 7,8-dihydro-8-oxoguanine (8-oxoG). In the transfectants, the repair rate of 8-oxoG residues induced by either potassium bromate or the photosensitizer [R]-1-[(10-chloro-4-oxo-3-phenyl-4H-benzo[a]quinolizin-1-yl)-carbo nyl ]-2-pyrrolidinemethanolplus light was up to 3-fold more rapid than in the parental cells. However, the improved repair had little effect on the mutagenicity of potassium bromate in the guanine phosphoribosyl transferase (gpt) locus of the OGG1-transfected AS52 cells. The steady-state (background) levels of DNA base modifications sensiti…

Cancer ResearchPyrrolidinesDNA RepairPhotochemistryDNA repairDNA damageBiologyTransfectionPolymerase Chain ReactionCell LineDNA-formamidopyrimidine glycosylasechemistry.chemical_compoundCricetulusGenes ReporterCricetinaeAnimalsheterocyclic compoundsN-Glycosyl HydrolasesPhotosensitizing AgentsBromatesChinese hamster ovary cellOvaryGeneral MedicineTransfectionDNA repair protein XRCC4OxidantsMolecular biologyOxidative StressDNA-Formamidopyrimidine GlycosylasechemistryGenes BacterialMutagenesisDNA glycosylaseEnzyme InductionFemaleQuinolizinesDNADNA DamageCarcinogenesis
researchProduct