Search results for "DNA Repair"

showing 10 items of 295 documents

Promoter methylation of MGMT, MLH1 and RASSF1A tumor suppressor genes in head and neck squamous cell carcinoma: Pharmacological genome demethylation …

2012

Promoter hypermethylation of tumor suppressor genes (TSGs) is a common feature of primary cancer cells. However, to date the somatic epigenetic events that occur in head and neck squamous cell carcinoma (HNSCC) tumorigenesis have not been well-defined. In the present study, we analyzed the promoter methylation status of the genes mutL homolog 1 (MLH1), Ras-association domain family member 1 (RASSF1A) and O-6-methylguanine-DNA methyltransferase (MGMT) in 23 HNSCC samples, three control tissues and one HNSCC cell line (UM-SCC 33) using methylation-specific PCR (MSP). The expression of the three proteins was quantified by semi-quantitative immunohistochemical analysis. The cell line was treate…

MaleCancer Researchmedicine.disease_causePolymerase Chain Reactionchemistry.chemical_compoundRas association domain family member 1Genes Tumor Suppressortumor suppressor geneEnzyme InhibitorsPromoter Regions GeneticDNA Modification MethylasesAged 80 and overNuclear ProteinsArticlesGeneral MedicineMethylationMiddle AgedImmunohistochemistryPrimary tumorOncologyDealkylationHead and Neck NeoplasmsDNA methylationAzacitidineCarcinoma Squamous CellFemaleMutL Protein Homolog 1Molecular Sequence DataDown-RegulationBiologyhead and neck squamous cell carcinomamutL homolog 15-azacytidineCell Line TumormedicineHumansEpigeneticsneoplasmsO-6-methylguanine-DNA methyltransferaseAdaptor Proteins Signal TransducingAgedCell ProliferationBase SequenceDose-Response Relationship DrugTumor Suppressor ProteinsSequence Analysis DNADNA Methylationmedicine.diseaseHead and neck squamous-cell carcinomaMolecular biologyDemethylating agentSquamous carcinomastomatognathic diseasesDNA Repair EnzymeschemistryCase-Control StudiesCpG IslandsCarcinogenesisOncology Reports
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Immunoprofiles and DNA methylation of inflammatory marker genes in ulcerative colitis-associated colorectal tumorigenesis

2021

Immunological and epigenetic changes are interconnected and contribute to tumorigenesis. We determined the immunoprofiles and promoter methylation of inflammation-related genes for colitis-associated colorectal carcinomas (CA-CRC). The results were compared with Lynch syndrome (LS)-associated colorectal tumors, which are characterized by an active immune environment through inherited mismatch repair defects. CA-CRCs (n = 31) were immunohistochemically evaluated for immune cell scores (ICSs) and PDCD1 and CD274 expression. Seven inflammation-associated genes (CD274, NTSR1, PPARG, PTGS2, PYCARD, SOCS1, and SOCS2), the repair gene MGMT, and eight standard marker genes for the CpG Island Methyl…

MaleCarcinogenesismedicine.disease_causeBiochemistry0302 clinical medicineIntestinal MucosaDNA Modification Methylases0303 health sciencesMUCOSADNA methylationtulehdusinflammation-associated genesPYCARDMethylationMiddle AgedLynch syndromeQR1-502EPIGENETICS3. Good healthDNA-metylaatioGene Expression Regulation NeoplasticPhenotypecolon cancerepigenetiikka030220 oncology & carcinogenesisimmuunivasteDNA methylationFemaleColorectal NeoplasmsCANCERSINSTABILITYsuolistosyövätBiology3121 Internal medicineMicrobiologyArticle03 medical and health sciencesmedicineHumansEpigeneticsLynchin oireyhtymäMolecular Biologyneoplasms030304 developmental biologypaksusuolisyöpäulcerative colitisInflammationCpG Island Methylator PhenotypeTumor Suppressor Proteinshaavainen koliittimedicine.disease3126 Surgery anesthesiology intensive care radiologydigestive system diseasesDNA Repair EnzymesLynch syndrome3121 General medicine internal medicine and other clinical medicineMutationimmune cell scoreCancer research1182 Biochemistry cell and molecular biologyColitis UlcerativeCpG IslandsField cancerizationCarcinogenesisBiomarkers
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DNA repair activity of 8-oxoguanine DNA glycosylase 1 (OGG1) in human lymphocytes is not dependent on genetic polymorphism Ser326/Cys326.

2001

8-oxoguanine DNA glycosylase 1 (OGG1) is a DNA repair enzyme that excises 7,8-dihydro-8-oxoguanine (8oxoG) from DNA. Since 8oxoG is a highly mispairing lesion, decreased OGG1 expression level could lead to a higher background mutation frequency and could possibly increase the cancer risk of an individual under oxidative stress. In order to analyse the natural variation of OGG1, we measured the DNA repair activity in human lymphocytes of healthy individuals by means of an 8oxoG-containing oligonucleotide assay. The data obtained revealed a two fold interindividual variation of OGG1 activity in lymphocytes. There was no difference in OGG1 activity due to gender and smoking behaviour. Transcri…

MaleDNA RepairDNA damageDNA repairBiologyIn Vitro TechniquesToxicologyDNA-formamidopyrimidine glycosylasechemistry.chemical_compoundGene FrequencyMUTYHGeneticsHumansAmino Acid SequenceLymphocytesMolecular BiologyGeneN-Glycosyl HydrolasesAllelesDNA PrimersPolymorphism GeneticBase SequenceOligonucleotideReverse Transcriptase Polymerase Chain ReactionMolecular biologyIsoenzymeschemistryDNA-Formamidopyrimidine GlycosylaseDNA glycosylaseDNADNA DamageMutation research
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Expression of somatic DNA repair genes in human testes

2006

Meiosis is the key process for recombination and reduction of the diploid chromosome set to a haploid one. Many genes that have been found in yeast or mouse models to play a role in meiosis are also important for the repair of DNA damage in somatic cells. To study the DNA repair gene transcriptome during male germ cell development, we have developed a specialized cDNA microarray with 181 human genes which are involved in different somatic DNA repair pathways and/or cell cycle control and 45 control house-keeping genes. This DNA repair gene chip was used to quantify the mRNA expression levels in three human testes samples versus a fibroblast RNA pool. Two hundred twenty genes on the chip (in…

MaleDNA RepairDNA damageSomatic cellDNA repairBiologyBiochemistryTranscriptomeTestismedicineHumansMolecular BiologyGeneCells CulturedOligonucleotide Array Sequence AnalysisSkinReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell BiologyFibroblastsDNA repair protein XRCC4Molecular biologyMeiosismedicine.anatomical_structureGene Expression RegulationHuman genomeBiomarkersGerm cellJournal of Cellular Biochemistry
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Bone marrow cell transcripts from Fanconi anaemia patients revealin vivoalterations in mitochondrial, redox and DNA repair pathways

2013

Fanconi anaemia (FA) is a genetic cancer predisposition disorder associated with cytogenetic instability, bone marrow failure and a pleiotropic cellular phenotype, including low thresholds of responses to oxidative stress, cross-linking agents and selected cytokines. This study was aimed at defining the scope of abnormalities in gene expression using the publicly available FA Transcriptome Consortium (FTC) database (Gene Expression Omnibus, 2009 and publicly available as GSE16334). We evaluated the data set that included transcriptomal analyses on RNA obtained from low-density bone marrow cells (BMC) from 20 patients with FA and 11 healthy volunteers, by seeking to identify changes in expre…

MaleDNA Repairiron-chelating proteinsTranscriptome0302 clinical medicineFanconi anemiaGene expressioncytokineoxidative stressChildbioenergetic pathwayRegulation of gene expression0303 health sciencesHematologyGeneral Medicineheat-shock proteinMitochondria3. Good health030220 oncology & carcinogenesisFemaleFanconi anaemiaOxidation-ReductionSignal TransductionAdultiron-chelating proteinDNA repairDNA repairBone Marrow CellsBiologyProinflammatory cytokine03 medical and health sciencesmedicineHumanstranscriptsGene030304 developmental biologyoxidative streGene Expression Profilingheat-shock proteinsMolecular Sequence Annotationmedicine.diseaseMolecular biologycytokinesDNA repair Fanconi anaemia bioenergetic pathways cytokines heat-shock proteins iron-chelating proteins oxidative stress transcriptsGene expression profilingOxidative StressFanconi AnemiaCase-Control Studiesbioenergetic pathwaysTranscriptomeEuropean Journal of Haematology
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Increased Oxidative Damage Associated with Unfavorable Cytogenetic Subgroups in Chronic Lymphocytic Leukemia

2014

Oxidative stress contributes to genomic instability in chronic lymphocytic leukemia (CLL), but its relationship with the acquisition of specific chromosomal abnormalities is unknown. We recruited 55 untreated CLL patients and assessed 8-oxo-2′-deoxyguanosine (8-oxo-dG), glutathione, and malondialdehyde (MDA) levels, and we compared them among the cytogenetic subgroups established using fluorescence in situ hybridization (FISH). Significant increases in 8-oxo-dG and/or MDA were observed in patients with unfavorable cytogenetic aberrations (17p and 11q deletions) compared to the 13q deletion group.TP53deletion patients exhibited a diminished DNA repair efficiency. Finally, cases with normal F…

MaleGenome instabilityArticle SubjectDNA RepairDNA damageDNA repairChronic lymphocytic leukemialcsh:MedicineBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyCohort Studieschemistry.chemical_compoundMalondialdehydemedicineHumansLymphocytesIn Situ Hybridization FluorescenceAgedAged 80 and overChromosome AberrationsGeneral Immunology and Microbiologymedicine.diagnostic_testlcsh:RDeoxyguanosineGeneral MedicineGlutathioneMiddle AgedMalondialdehydemedicine.diseaseGlutathioneLeukemia Lymphocytic Chronic B-CellOxidative Stresschemistry8-Hydroxy-2'-DeoxyguanosineImmunologyFemaleLipid PeroxidationReactive Oxygen SpeciesGene DeletionOxidative stressDNA DamageResearch ArticleFluorescence in situ hybridizationBioMed Research International
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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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DNA repair protein O6-methylguanine-DNA methyltransferase in testis and testicular tumors as determined by a novel nonradioactive assay

2003

The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT, alkyltransferase) is an important suicide enzyme involved in defense against O6-alkylating endogenous metabolites and environmental carcinogens. It also plays a pivotal role in primary and acquired resistance of tumors to alkylating anticancer drugs targeting the O6-position of guanine (i.e., methylating and chloroethylating agents). MGMT can thus be considered a crucial biomarker for individual susceptibility to alkylating carcinogens and tumor drug resistance. This implies a need for a fast and convenient method for determination of MGMT. Routinely, MGMT is being quantified by radioactive assays which are relatively labo…

MaleMethyltransferaseDNA RepairGuanineDNA repairBiophysicsEnzyme-Linked Immunosorbent AssayEndogenyBiologyBiochemistryDNA methyltransferaseAntibodiesO(6)-Methylguanine-DNA Methyltransferasechemistry.chemical_compoundTesticular NeoplasmsCell Line TumorTestisDNA Repair ProteinAnimalsHumansneoplasmsMolecular BiologyCarcinogenCell BiologyMolecular biologydigestive system diseasesGene Expression Regulation NeoplasticchemistryCattleAlkyltransferaseAnalytical Biochemistry
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The basal levels of 8-oxoG and other oxidative modifications in intact mitochondrial DNA are low even in repair-deficient (Ogg1(-/-)/Csb(-/-)) mice.

2007

Abstract Mitochondrial DNA (mtDNA) is assumed to be highly prone to damage by reactive oxygen species (ROS) because of its location in close proximity to the mitochondrial electron transport chain. Accordingly, mitochondrial oxidative DNA damage has been hypothesized to be responsible for various neurological diseases, ageing and cancer. Since 7,8-dihydro-8-oxoguanine (8-oxoG), one of the most frequent oxidative base modifications, is removed from the mitochondrial genome by the glycosylase OGG1, the basal levels of this lesion are expected to be highly elevated in Ogg1−/− mice. To investigate this hypothesis, we have used a mtDNA relaxation assay in combination with various repair enzymes …

MaleMitochondrial DNADNA RepairDNA repairHealth Toxicology and MutagenesisOxidative phosphorylationBiologyMitochondrionDNA MitochondrialDNA Glycosylaseschemistry.chemical_compoundMiceGeneticsAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyMice KnockoutGuanosinePlant ExtractsCorticoviridaeMolecular biologyNuclear DNAMice Inbred C57BLDNA Repair EnzymeschemistryDNA glycosylaseDNA ViralFemaleDNANucleotide excision repairDNA DamageMutation research
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Cancer in Children With Fanconi Anemia and Ataxia-Telangiectasia—A Nationwide Register-Based Cohort Study in Germany

2021

PURPOSE Fanconi anemia (FA) and ataxia-telangiectasia (AT) are rare inherited syndromes characterized by abnormal DNA damage response and caused by pathogenic variants in key DNA repair proteins that are also relevant in the pathogenesis of breast cancer and other cancer types. The risk of cancer in children with these diseases is poorly understood and has never been assessed in a population-based cohort before. METHODS We identified 421 patients with FA and 160 patients with AT diagnosed between 1973 and 2020 through German DNA repair disorder reference laboratories. We linked patients' laboratory data with childhood cancer data from the German Childhood Cancer Registry. RESULTS Among 421 …

MaleOncologyRegister basedCancer Researchmedicine.medical_specialtyTime FactorsAdolescentDNA damageAnemiaDNA repairRisk AssessmentAtaxia TelangiectasiaRisk FactorsFanconi anemiaGermanyNeoplasmsInternal medicinemedicineHumansRegistriesChildbusiness.industryIncidenceAge FactorsInfantCancerPrognosismedicine.diseaseFanconi AnemiaOncologyChild PreschoolAtaxia-telangiectasiaFemalebusinessCohort studyJournal of Clinical Oncology
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