Search results for "DNA Repair"

showing 10 items of 295 documents

Coordinate mutation and transformation of mouse fibroblasts: induction by nitroquinoline oxide and modulation by caffeine

1981

Mutation and malignant transformation were followed in the same cells. Mouse fibroblasts (C3H 10T 1/2) were mutated and transformed by 4-nitroquinoline-1-oxide with similar, approximately linear dose-responses. The presence of caffeine immediately after exposure to 4-nitroquinoline-1-oxide potently inhibited mutation and transformation at high but not at low doses of 4-nitroquinoline-1-oxide. Whilst the coordinate induction of mutation and transformation could be explained by both a common target (DNA) or a common reactive species hitting several targets, the identical modulation by a DNA repair inhibitor of both end points suggests fundamental similarities in the nature of the lesions lead…

Cancer ResearchDNA repairDrug ResistanceBiologyMalignant transformationMicechemistry.chemical_compoundCaffeinemedicineAnimalsA-DNAOuabainFibroblastCells CulturedMice Inbred C3HNitroquinolinesDrug SynergismGeneral MedicineMolecular biology4-Nitroquinoline-1-oxideTransformation (genetics)Cell Transformation Neoplasticmedicine.anatomical_structurechemistryMutationMutation (genetic algorithm)Cancer researchCaffeineDNACarcinogenesis
researchProduct

GSK3β as a novel promising target to overcome chemoresistance in pancreatic cancer

2021

Pancreatic cancer is an aggressive malignancy with increasing incidence and poor prognosis due to its late diagnosis and intrinsic chemoresistance. Most pancreatic cancer patients present with locally advanced or metastatic disease characterized by inherent resistance to chemotherapy. These features pose a series of therapeutic challenges and new targets are urgently needed. Glycogen synthase kinase 3 beta (GSK3β) is a conserved serine/threonine kinase, which regulates key cellular processes including cell proliferation, DNA repair, cell cycle progression, signaling and metabolic pathways. GSK3β is implicated in non-malignant and malignant diseases including inflammation, neurodegenerative …

Cancer ResearchDNA repairDruggabilityDiseaseMalignancyPancreatic cancerHumansMedicinePharmacology (medical)GSK3BCell ProliferationPharmacologyGlycogen Synthase Kinase 3 betabusiness.industryKinaseGSK3βCancerTumor chromatin profilingOncogenesPancreatic cancermedicine.diseaseAnticancer drug combinationsPancreatic NeoplasmsInfectious DiseasesOncologyDrug Resistance NeoplasmCancer researchbusinessChemoresistanceDrug Resistance Updates
researchProduct

A new assay for O6-alkylguanine-DNA-alkyltransferase to determine DNA repair capacities using lambda-phage DNA as substrate.

1990

One O6-methylguanine (O6-meG) was introduced into each BamHI site of lambda-phage DNA as a substrate for the determination of the DNA repair protein O6-alkylguanine-DNA-alkyltransferase. A new assay using as the detection group 32P-labeled phosphate introduced at the 3' position of the modified nucleoside by incorporation of 32P-labeled TTP in the 3'-neighboring position proved highly sensitive: 10(-16) mol of the DNA lesion was still easily detectable. This DNA, which has greater than 1000 bp represents a good model for cellular DNA and was used as a substrate to measure the individual repair capacities for O6-meG in human lymphocytes of 20 healthy male and female donors. There were great …

Cancer ResearchGuanineDNA RepairDNA repairMolecular Sequence DataBiologySubstrate Specificitychemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseDNA Repair ProteinEscherichia coliHumansLymphocyteschemistry.chemical_classificationBase SequenceSubstrate (chemistry)General MedicineMethyltransferasesLambda phagebiology.organism_classificationBacteriophage lambdaIn vitroKineticsEnzymeBiochemistrychemistryDNA ViralBamHIDNACarcinogenesis
researchProduct

The Peroxisome Proliferator WY-14,643 Promotes Hepatocarcinogenesis Caused by Endogenously Generated Oxidative DNA Base Modifications in Repair-Defic…

2007

Abstract Basal levels of endogenously generated oxidative DNA modifications such as 7,8-dihydro-8-oxoguanine (8-oxoG) are present in apparently all mammalian cells, but their relevance for the generation of spontaneous cancers remains to be established. Both the 8-oxoG levels and the resulting spontaneous mutations are increased in the livers of Csbm/m/Ogg1−/− mice, which are deficient in the repair of 8-oxoG. In order to determine the consequences of these additional oxidative DNA modifications and mutations and thus assess the tumor initiating potency of this type of endogenous DNA damage, we treated Csbm/m/Ogg1−/− mice and repair-proficient controls with the peroxisome proliferator WY-14…

Cancer ResearchGuanineDNA RepairRatónDNA damageEndogenyOxidative phosphorylationBiologymedicine.disease_causeDNA GlycosylasesMicechemistry.chemical_compoundLiver Neoplasms ExperimentalmedicineAnimalsPoly-ADP-Ribose Binding ProteinsCocarcinogenesisCell growthLiver cellMolecular biologyMice Inbred C57BLOxidative StressDNA Repair EnzymesPyrimidinesLiverOncologyBiochemistrychemistryMutationPeroxisome ProliferatorsCarcinogenesisPrecancerous ConditionsDNADNA DamageCancer Research
researchProduct

Acquired resistance of melanoma cells to the antineoplastic agent fotemustine is caused by reactivation of the DNA repair gene mgmt

2001

Acquired resistance to antineoplastic agents is a frequent obstacle in tumor therapy. Malignant melanoma cells are particularly well known for their unresponsiveness to chemotherapy; only about 30% of tumors exhibit a transient clinical response to treatment. In our study, we investigated the molecular mechanism of acquired resistance of melanoma cells (MeWo) to the chloroethylating drug fotemustine. Determination of O6-methylguanine-DNA methyltransferase (MGMT) activity showed that MeWo cells that acquired resistance to fotemustine upon repeated treatment with the drug display high MGMT activity, whereas the parental cell line had no detectable MGMT. The resistant cell lines exhibit cross-…

Cancer ResearchGuanineMethyltransferaseDNA RepairDNA repairmedicine.medical_treatmentGene ExpressionAntineoplastic AgentsDrug resistanceBiologyNitrosourea CompoundsO(6)-Methylguanine-DNA MethyltransferaseEnzyme ReactivatorsOrganophosphorus CompoundsTumor Cells CulturedmedicineHumansEnzyme InhibitorsPromoter Regions GeneticMelanomaneoplasmsChemotherapyMelanomaGene AmplificationDNA Methylationmedicine.diseaseVirologydigestive system diseasesEnzyme ActivationBlotting SouthernOncologyDrug Resistance NeoplasmDNA methylationAzacitidineCancer researchFotemustinemedicine.drugAlkyltransferaseInternational Journal of Cancer
researchProduct

Artesunate derived from traditional Chinese medicine induces DNA damage and repair.

2008

Abstract Artesunate is a semisynthetic derivative from artemisinin, a natural product from the Chinese herb Artemisia annua L. It exerts antimalarial activity, and, additionally, artemisinin and its derivatives are active against cancer cells. The active moiety is an endoperoxide bridge. Its cleavage leads to the formation of reactive oxygen species and carbon-centered radicals. These highly reactive molecules target several proteins in Plasmodia, which is thought to result in killing of the microorganism. DNA damage induced by artemisinins has not yet been described. Here, we show that artesunate induces apoptosis and necrosis. It also induces DNA breakage in a dose-dependent manner as sho…

Cancer ResearchKu80DNA RepairDNA repairDNA damageBlotting WesternArtesunateFluorescent Antibody TechniqueApoptosisBiologyCell Linechemistry.chemical_compoundCricetulusCricetinaeAnimalsMedicine Chinese TraditionalBase excision repairDNAMolecular biologyArtemisininsComet assayOncologychemistryArtesunateCancer cellComet AssayHomologous recombinationDNA DamageCancer research
researchProduct

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