Search results for "DNA Repair"

showing 10 items of 295 documents

Transcriptional Upregulation of DNA Damage Response Genes in Bank Voles (Myodes glareolus) Inhabiting the Chernobyl Exclusion Zone

2018

Exposure to ionizing radiation (IR) from radionuclides released into the environment can damage DNA. An expected response to exposure to environmental radionuclides, therefore, is initiation of DNA damage response (DDR) pathways. Increased DNA damage is a characteristic of many organisms exposed to radionuclides but expression of DDR genes of wildlife inhabiting an area contaminated by radionuclides is poorly understood. We quantified expression of five central DDR genes Atm, Mre11, p53, Brca1, and p21 in the livers of the bank vole Myodes glareolus that inhabited areas within the Chernobyl Exclusion Zone (CEZ) that differed in levels of ambient radioactivity, and also from control areas ou…

0301 basic medicinevauriotDNA damagetuhotZoologyMyodes glareolusDNA repairBiologydnamedicine.disease_causeChernobyl03 medical and health sciencesDownregulation and upregulationkorjausmedicineMre11oxidative stressExclusion zoneGeneoksidatiivinen stressichernobyllcsh:Environmental sciencesGeneral Environmental Sciencelcsh:GE1-350ionising radiationionisoiva säteilyDNAbiology.organism_classificationBank volebody regions030104 developmental biologyAtmta1181DNA damageionizing radiationOxidative stressFrontiers in Environmental Science
researchProduct

The Role of p53 Signaling in Colorectal Cancer.

2021

Simple Summary The transcription factor p53 is a crucial tumor suppressor that regulates diverse cellular responses to protect against cancer development. Deactivating p53 signaling either by altering p53 regulators or by p53 mutations occurs frequently in human colorectal carcinoma (CRC). Forty-three percent of CRCs harbor p53 mutations that reduce wild-type p53 tumor suppressor activity and often provide neo-morphic functions, which contribute to tumorigenesis. In this review, we summarize wild-type p53 signaling, how it can be deregulated in CRC, and the functional and phenotypical effects of p53 mutations. We also discuss current therapeutic strategies of targeting p53. Abstract The tra…

0301 basic medicinewild type p53Cancer ResearchDNA repairCellular differentiationcolorectal cancerReview03 medical and health sciences0302 clinical medicinemedicineTranscription factorRC254-282gain-of-functionbiologyCell growthmutant p53CancerNeoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseaseUbiquitin ligasep53 signaling030104 developmental biologyOncology030220 oncology & carcinogenesisCancer cellbiology.proteinCancer researchMdm2cancer therapyp53 pathwayCancers
researchProduct

Flipping of alkylated DNA damage bridges base and nucleotide excision repair

2009

Alkyltransferase-like proteins (ATLs) share functional motifs with the cancer chemotherapy target O6-alkylguanine-DNA alkyltransferase (AGT) and paradoxically protect cells from the biological effects of DNA alkylation damage, despite lacking the reactive cysteine and alkyltransferase activity of AGT. Here we determine Schizosaccharomyces pombe ATL structures without and with damaged DNA containing the endogenous lesion O6-methylguanine or cigarette-smoke-derived O6-4-(3-pyridyl)-4-oxobutylguanine. These results reveal non-enzymatic DNA nucleotide flipping plus increased DNA distortion and binding pocket size compared to AGT. Our analysis of lesion-binding site conservation identifies new A…

0303 health sciencesMultidisciplinarybiologyDNA damageDNA repair030302 biochemistry & molecular biologybiology.organism_classification03 medical and health sciencesDNA Alkylationchemistry.chemical_compoundchemistryBiochemistryhemic and lymphatic diseasesparasitic diseasesSchizosaccharomyces pombeERCC1DNA030304 developmental biologyAlkyltransferaseNucleotide excision repairNature
researchProduct

Cytotoxicity of 35 medicinal plants from Sudan towards sensitive and multidrug-resistant cancer cells

2015

Abstract Background Cancer is a complex disease with multiple genetic and epigenetic alterations. Since decades, the hallmark of cancer therapy is chemotherapy. Cytotoxic drugs erase rapidly dividing cells without sufficient differentiation between normal and cancerous cells resulting in severe side effects in normal tissues. Recently, strategies for cancer treatment focused on targeting specific proteins involved in tumor growth and progression. The present study was designed to investigate the cytotoxicity of 65 crude extracts from 35 Sudanese medicinal plants towards various cancer cell lines expressing molecular mechanisms of resistance towards classical chemotherapeutics (two ATP-bindi…

ATP Binding Cassette Transporter Subfamily BCytoskeleton organizationCell SurvivalDNA repairBiologyPharmacologySudanSesquiterpenes GuaianeImmune systemCell Line TumorOxazinesDrug DiscoveryHumansATP Binding Cassette Transporter Subfamily B Member 1EpigeneticsCytotoxicityPharmacologyPlants MedicinalComputational BiologyAntineoplastic Agents PhytogenicDrug Resistance MultipleGene expression profilingXanthenesDrug Resistance NeoplasmPharmacogeneticsCell cultureCancer cellCancer researchIndicators and ReagentsTumor Suppressor Protein p53SesquiterpenesJournal of Ethnopharmacology
researchProduct

In vitro model for DNA double‐strand break repair analysis in breast cancer reveals cell type–specific associations with age and prognosis

2016

Dysfunction of homologous recombination is a common denominator of changes associated with breast cancer-predisposing mutations. In our previous work, we identified a functional signature in peripheral blood lymphocytes from women who were predisposed that indicated a shift from homologous recombination to alternative, error-prone DNA double-strand break (DSB) repair pathways. To capture both hereditary and nonhereditary factors, we newly established a protocol for isolation and ex vivo analysis of epithelial cells, epithelial-mesenchymal transition cells (EMTs), and fibroblasts from breast cancer specimens (147 patients). By applying a fluorescence-based test system, we analyzed the error-…

Adult0301 basic medicinePathologymedicine.medical_specialtyEpithelial-Mesenchymal TransitionDNA RepairDNA repairCellBreast NeoplasmsBiologymedicine.disease_causeBiochemistry03 medical and health sciences0302 clinical medicineBreast cancerCell Line TumorGeneticsmedicineHumansDNA Breaks Double-StrandedGenetic Predisposition to DiseaseBreastEpithelial–mesenchymal transitionHomologous RecombinationMolecular BiologyAgedAged 80 and overAdenosine Diphosphate RiboseMutationAge FactorsMiddle AgedDNA repair protein XRCC4Prognosismedicine.diseaseDouble Strand Break Repair030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisMutationCancer researchFemaleHomologous recombinationBiotechnologyThe FASEB Journal
researchProduct

Induction of heme oxygenase-1 and adaptive protection against the induction of DNA damage after hyperbaric oxygen treatment.

2000

Hyperbaric oxygen (HBO) treatment of human subjects (i.e. exposure to 100% oxygen at a pressure of 2.5 ATA for a total period of 3 x 20 min) caused clear and reproducible DNA damage in lymphocytes, as detected with the comet assay (single cell gel electrophoresis). Induction of DNA damage was found only after the first HBO exposure and not after further treatments of the same individuals. Furthermore, blood taken 24 h after HBO treatment was significantly protected against the induction of DNA damage by hydrogen peroxide (H(2)O(2)) in vitro, indicating that adaptation occurred due to induction of antioxidant defenses. The cells were not significantly protected against the genotoxic effects …

AdultCancer ResearchDNA RepairDNA repairDNA damageCarbon-Oxygen LyasesBiologymedicine.disease_causeSuperoxide dismutasemedicineDNA-(Apurinic or Apyrimidinic Site) LyaseHumansLymphocytesDNA Polymerase betachemistry.chemical_classificationReactive oxygen speciesHyperbaric OxygenationSuperoxide DismutaseMembrane ProteinsGeneral MedicineHydrogen PeroxideCatalaseMolecular biologyDNA-(apurinic or apyrimidinic site) lyaseAdaptation PhysiologicalDeoxyribonuclease IV (Phage T4-Induced)Comet assayOxidative StresschemistryBiochemistryCatalaseEnzyme InductionHeme Oxygenase (Decyclizing)biology.proteinOxidative stressHeme Oxygenase-1DNA DamageCarcinogenesis
researchProduct

Extent and patterns of MGMT promoter methylation in glioblastoma- and respective glioblastoma-derived spheres.

2010

Abstract Purpose: Quantitative methylation-specific tests suggest that not all cells in a glioblastoma with detectable promoter methylation of the O6-methylguanine DNA methyltransferase (MGMT) gene carry a methylated MGMT allele. This observation may indicate cell subpopulations with distinct MGMT status, raising the question of the clinically relevant cutoff of MGMT methylation therapy. Epigenetic silencing of the MGMT gene by promoter methylation blunts repair of O6-methyl guanine and has been shown to be a predictive factor for benefit from alkylating agent therapy in glioblastoma. Experimental Design: Ten paired samples of glioblastoma and respective glioblastoma-derived spheres (GS), c…

AdultMaleCancer ResearchMethyltransferaseDNA repairBiologyDNA methyltransferaseGene dosageO(6)-Methylguanine-DNA MethyltransferaseGene FrequencyTumor Cells CulturedHumansPromoter Regions GeneticneoplasmsAgedAged 80 and overBrain NeoplasmsO-6-methylguanine-DNA methyltransferaseMethylationDNA MethylationMiddle AgedMolecular biologydigestive system diseasesChromatinOncologyCpG siteDNA methylationFemaleGlioblastomaClinical cancer research : an official journal of the American Association for Cancer Research
researchProduct

O6-methylguanine-DNA methyltransferase activity in breast and brain tumors.

1995

The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is a main determinant of resistance of tumor cells to the cytostatic activity of chemotherapeutic alkylating agents (methylating and chloroethylating nitrosoureas) and is effective in protecting normal cells against genotoxic and carcinogenic effects resulting from DNA alkylation. Therefore, the level of expression of MGMT is significant for the response of both the tumor and the non-target tissue following application of nitrosoureas in tumor therapy. To determine the expression of MGMT in tumor tissue, we have assayed MGMT activity in 68 breast carcinomas and 38 brain tumors. There was a wide variation of MGMT expression…

AdultMaleCancer ResearchPathologymedicine.medical_specialtyMethyltransferaseDNA RepairMammary glandBlotting WesternBreast NeoplasmsBiologyAstrocytomaO(6)-Methylguanine-DNA MethyltransferaseGliomaDNA Repair ProteinmedicineCarcinomaHumansneoplasmsCarcinogenAgedEpitheliomaL-Lactate DehydrogenaseBrain NeoplasmsAstrocytomaMethyltransferasesMiddle Agedmedicine.diseasedigestive system diseasesmedicine.anatomical_structureOncologyCancer researchFemaleGlioblastomaHeLa CellsInternational journal of cancer
researchProduct

Increasing rates of DNA single-strand breaks in lymphocytes of clinical personnel handling cytostatic drugs

1993

A total of 27 persons, working in cancer stations with exposure to cytostatics, and 40 healthy control persons were examined for DNA single-strand breaks in peripheral lymphocytes. Non-smoking personnel from cancer stations were found to have an increased rate of DNA single-strand breaks compared to the non-smoking control subjects. In the case of smokers an increased rate of DNA single-strand breaks could be recorded for those working in cancer stations as well as with the controls. DNA single-strand breaks indicate reversible damage to DNA. As DNA repair is not perfect in every case, an increased number of DNA single-strand breaks leads to irreversible DNA damage.

AdultMaleCancer Researchmedicine.medical_specialtyDNA damageDNA repairLymphocyteDNA Single-StrandedAntineoplastic AgentsBiologyMedical Oncologychemistry.chemical_compoundInternal medicinemedicineHumansLymphocytesGeneticsDNA single strandHematologyCancerGeneral MedicineMiddle Agedmedicine.diseasePersonnel Hospitalmedicine.anatomical_structureOncologychemistryToxicityCancer researchFemaleDNADNA DamageJournal of Cancer Research and Clinical Oncology
researchProduct

Occupational exposure to metal-rich particulate matter modifies the expression of repair genes in foundry workers

2021

Foundry workers are exposed to numerous occupational health hazards, which may result in increased risk of cancer, respiratory disease, and other diseases. Oxidative stress is known to be involved in the pathogenesis of such diseases. The present study aimed to investigate the association between multiple occupational exposures in foundry workers and expression of deoxyribonucleic acid (DNA) repair genes as a biomarker of oxidative DNA damage. The study sample comprised 17 foundry workers and 27 matched control subjects. Expression of 8-oxoguanine DNA glycosylase-1 (OGG1), inosine triphosphate pyrophosphate (ITPA), and MutT homolog 1 (MTH1) in peripheral blood was examined using the real-t…

AdultMaleDNA repairThreshold limit valueHealth Toxicology and MutagenesisIran010501 environmental sciencesToxicologymedicine.disease_cause01 natural sciencesDNA Glycosylaseslaw.invention03 medical and health sciencesElectromagnetic FieldslawMetals HeavyOccupational ExposureHumansMedicinePyrophosphatasesGenePolymerase chain reaction030304 developmental biology0105 earth and related environmental sciences0303 health sciencesbusiness.industryPublic Health Environmental and Occupational HealthMiddle AgedPhosphoric Monoester HydrolasesOxidative StressDNA Repair EnzymesCase-Control StudiesMetallurgyImmunologyToxicityBiomarker (medicine)Particulate MatterITPAbusinessBiomarkersOxidative stressDNA DamageToxicology and Industrial Health
researchProduct