Search results for "DNA Repair"

showing 10 items of 295 documents

TP53 mutations and hepatocellular carcinoma: insights into the etiology and pathogenesis of liver cancer.

2007

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide and the major risk factors include chronic infections with the hepatitis B (HBV) or C (HCV) virus, and exposure to dietary aflatoxin B(1) (AFB(1)) or alcohol consumption. Multiple genetic and epigenetic changes are involved in the molecular pathogenesis of HCC, for example, somatic mutations in the p53 tumor suppressor gene (TP53) and the activation of the WNT signal transduction pathway. AFB(1) frequently induces G:C to T:A transversions at the third base in codon 249 of TP53 and cooperates with HBV in causing p53 mutations in HCC. The detection of TP53 mutant DNA in plasma is a biomarker of both AFB(1) exposur…

Cancer ResearchAflatoxin B1Carcinoma HepatocellularTumor suppressor geneDNA damageDNA repairBiologymedicine.disease_causeHepatitis VirusesGeneticsmedicineHumansGenetic Predisposition to DiseaseEpigeneticsMolecular BiologyGeneHepatitis ChronicIncidenceLiver Neoplasmsmedicine.diseaseVirologydigestive system diseasesHBxMutagenesisHepatocellular carcinomaMutationCancer researchTumor Suppressor Protein p53CarcinogenesisOncogene
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Induction of the alkyltransferase (MGMT) gene by DNA damaging agents and the glucocorticoid dexamethasone and comparison with the response of base ex…

1996

Repair of alkylated bases in DNA is performed by O6-methylguanine-DNA methyltransferase (MGMT) and a set of enzymes of the base excision repair pathway involving N-methylpurine-DNA glycosylase (MPG), apurinic endonuclease (APE), DNA polymerase beta (Pol beta) and DNA ligase. The level of expression of these enzymes may exert a profound effect on resistance of cells towards alkylating drugs. We have comparatively analyzed the expression of MGMT and the different base excision repair genes in rat hepatoma cells (line H4IIE) after exposure to alkylating agents, X-rays and the glucocorticoid hormone dexamethasone. Furthermore, the effect of these agents on the activity of the cloned human MGMT …

Cancer ResearchAlkylationDNA RepairDNA damageDNA polymerase betaBiologyDexamethasoneGene Expression Regulation Enzymologicchemistry.chemical_compoundO(6)-Methylguanine-DNA MethyltransferaseLiver Neoplasms ExperimentalAnimalsRNA MessengerPromoter Regions GeneticneoplasmsAntineoplastic Agents AlkylatingGlucocorticoidschemistry.chemical_classificationDNA ligaseO-6-methylguanine-DNA methyltransferaseGeneral MedicineBase excision repairDNA NeoplasmMethyltransferasesMolecular biologyDNA-(apurinic or apyrimidinic site) lyasedigestive system diseasesRatsUp-RegulationGene Expression Regulation NeoplasticKineticschemistryDNA glycosylaseEnzyme InductionAlkyltransferaseDNA DamageCarcinogenesis
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Why do results conflict regarding the prognostic value of the methylation status in colon cancers? The role of the preservation method.

2012

Abstract Background In colorectal carcinoma, extensive gene promoter hypermethylation is called the CpG island methylator phenotype (CIMP). Explaining why studies on CIMP and survival yield conflicting results is essential. Most experiments to measure DNA methylation rely on the sodium bisulfite conversion of unmethylated cytosines into uracils. No study has evaluated the performance of bisulfite conversion and methylation levels from matched cryo-preserved and Formalin-Fixed Paraffin Embedded (FFPE) samples using pyrosequencing. Methods Couples of matched cryo-preserved and FFPE samples from 40 colon adenocarcinomas were analyzed. Rates of bisulfite conversion and levels of methylation of …

Cancer ResearchBisulfite sequencing[SDV.CAN]Life Sciences [q-bio]/CancerAdenocarcinomaBiologyMLH1lcsh:RC254-282[ SDV.CAN ] Life Sciences [q-bio]/Cancerchemistry.chemical_compound[SDV.CAN] Life Sciences [q-bio]/CancerPredictive Value of TestsBiomarkers TumorGeneticsHumansSulfitesDNA Modification MethylasesAdaptor Proteins Signal TransducingCryopreservationParaffin EmbeddingTumor Suppressor ProteinsNuclear ProteinsReproducibility of ResultsDNA NeoplasmMethylationDNA MethylationPrognosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensMolecular biologydigestive system diseasesNeoplasm ProteinsBisulfiteDNA Repair EnzymesLong Interspersed Nucleotide ElementsPhenotypeOncologyCpG sitechemistrySodium bisulfiteColonic NeoplasmsDNA methylationFeasibility StudiesPyrosequencingCpG IslandsMutL Protein Homolog 1Research Article
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The “unnatural” history of colorectal cancer in Lynch syndrome : lessons from colonoscopy surveillance

2021

Individuals with Lynch syndrome (LS), one of the most common inherited cancer syndromes, are at increased risk of developing malignancies, in particular colorectal cancer (CRC). Regular colonoscopy with polypectomy is recommended to reduce CRC risk in LS individuals. However, recent independent studies demonstrated that a substantial proportion of LS individuals develop CRC despite regular colonoscopy. The reasons for this surprising observation confirmed by large prospective studies are a matter of debate. In this review, we collect existing evidence from clinical, epidemiological and molecular studies and interpret them with regard to the origins and progression of LS-associated CRC. Alon…

Cancer ResearchColorectal cancermedicine.medical_treatmentColonoscopyDNA Mismatch RepairADENOMA DETECTION0302 clinical medicineRisk FactorsEpidemiologyMass ScreeningProspective cohort studyMUTATIONRISKmedicine.diagnostic_testincident cancer riskColonoscopyTUMORSLynch syndrome3. Good healthOncology030220 oncology & carcinogenesisPopulation SurveillancesyöpätauditColorectal Neoplasmskoloskopiamedicine.medical_specialtyLONG-TERM3122 Cancerscolorectal cancersuolistosyövätINTERVAL CANCERS03 medical and health sciencesINTESTINAL MICROBIOTACàncer colorectalCOLONmedicineMANAGEMENTHumansLynchin oireyhtymäIntensive care medicinepaksusuolisyöpäperinnölliset tauditseulontatutkimusbusiness.industrymismatch repair deficiencyMicrosatellite instabilityCancerColonoscòpiamedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisPolypectomydigestive system diseasesDNA Repair EnzymesLynch syndromemicrosatellite instabilitybusinesscolonoscopy surveillance
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Influence of nitric oxide on the generation and repair of oxidative DNA damage in mammalian cells

2002

We have analysed the effects of endogenously and exogenously generated nitric oxide (NO) in cultured mammalian fibroblasts on: (i) the steady-state (background) levels of oxidative DNA base modifications; (ii) the susceptibility of the cells to the induction of additional DNA damage and micronuclei by H(2)O(2); and (iii) the repair kinetics of various types of DNA modifications. Steady-state levels of oxidative DNA base modifications, measured by means of an alkaline elution assay in combination with the repair endonuclease Fpg protein, were similar in NO-overproducing B6 mouse fibroblasts stably transfected with an inducible NO synthase (iNOS) and in control cells. Increased oxidative dama…

Cancer ResearchDNA RepairDNA damageDNA repairNitric Oxide Synthase Type IIMutagenAlkenesBiologyNitric OxideTransfectionmedicine.disease_causeMicechemistry.chemical_compoundmedicineAnimalsNitric Oxide DonorsDose-Response Relationship DrugHydrogen PeroxideGeneral MedicineTransfectionFibroblastsCell biologyBiochemistrychemistryNitric Oxide SynthaseDNAGenotoxicityPeroxynitriteOxidative stressDNA DamageCarcinogenesis
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R-Roscovitine (Seliciclib) prevents DNA damage-induced cyclin A1 upregulation and hinders non-homologous end-joining (NHEJ) DNA repair.

2010

Abstract Background CDK-inhibitors can diminish transcriptional levels of cell cycle-related cyclins through the inhibition of E2F family members and CDK7 and 9. Cyclin A1, an E2F-independent cyclin, is strongly upregulated under genotoxic conditions and functionally was shown to increase NHEJ activity. Cyclin A1 outcompetes with cyclin A2 for CDK2 binding, possibly redirecting its activity towards DNA repair. To see if we could therapeutically block this switch, we analyzed the effects of the CDK-inhibitor R-Roscovitine on the expression levels of cyclin A1 under genotoxic stress and observed subsequent DNA damage and repair mechanisms. Results We found that R-Roscovitine alone was unable …

Cancer ResearchDNA RepairDNA repairDNA damageSettore MED/06 - Oncologia MedicaCyclin DCyclin ACyclin BSettore BIO/11 - Biologia Molecolarelcsh:RC254-282RoscovitineProtein Kinase InhibitorsBIO/10 Biochimicaroscovitine doxorubicinbiologyResearchCyclin A1; Doxorubicin; Protein Kinase Inhibitors; Purines; Up-Regulation; DNA Damage; DNA Repair; Hydrogen-Ion Concentration; Cancer Research; Molecular Medicine; OncologyG2-M DNA damage checkpointHydrogen-Ion Concentrationlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensUp-RegulationOncologyDoxorubicinPurinesCancer researchbiology.proteinMolecular MedicineCyclin A1biological phenomena cell phenomena and immunityCyclin A1Cyclin A2DNA DamageMolecular cancer
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Ultraviolet light-induced DNA damage triggers apoptosis in nucleotide excision repair-deficient cells via Bcl-2 decline and caspase-3/-8 activation.

2001

Ultraviolet (UV) light is a potent mutagenic and genotoxic agent. Whereas DNA damage induced by UV light is known to be responsible for UV-induced genotoxicity, its role in triggering apoptosis is still unclear. We addressed this issue by comparing nucleotide excision repair (NER) deficient 27-1 and 43-3B Chinese hamster (CHO) cells with the corresponding wild-type and ERCC-1 complemented cells. It is shown that NER deficient cells are dramatically hypersensitive to UV-C induced apoptosis, indicating that DNA damage is the major stimulus for the apoptotic response. Apoptosis triggered by UV-C induced DNA damage is related to caspase- and proteosome-dependent degradation of Bcl-2 protein. Th…

Cancer ResearchDNA RepairDNA repairDNA damageUltraviolet RaysPoly ADP ribose polymeraseFas-Associated Death Domain ProteinApoptosisCHO CellsBiologyCysteine Proteinase InhibitorsCaspase 8TransfectionFas ligandMembrane PotentialsCricetinaeGeneticsUltraviolet lightAnimalsRNA MessengerMolecular BiologyAdaptor Proteins Signal TransducingCaspase 8Caspase 3Fas receptorMolecular biologyCaspase InhibitorsCaspase 9MitochondriaEnzyme ActivationProto-Oncogene Proteins c-bcl-2CaspasesPoly(ADP-ribose) PolymerasesCarrier ProteinsNucleotide excision repairDNA DamageOncogene
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Phosphorylation of the DNA repair protein APE/REF-1 by CKII affects redox regulation of AP-1

1999

The DNA repair protein apurinic endonuclease (APE/Ref-1) exerts several physiological functions such as cleavage of apurinic/apyrimidinic sites and redox regulation of the transcription factor AP-1, whose activation is part of the cellular response to DNA damaging treatments. Here we demonstrate that APE/Ref-1 is phosphorylated by casein kinase II (CKII). This was shown for both the recombinant APE/Ref-1 protein (Km=0.55 mM) and for APE/Ref-1 expressed in COS cells. Phosphorylation of APE/Ref-1 did not alter the repair activity of the enzyme, whereas it stimulated its redox capability towards AP-1, thus promoting DNA binding activity of AP-1. Inhibition of CKII mediated phosphorylation of A…

Cancer ResearchDNA RepairProto-Oncogene Proteins c-junDNA repairDNA damageCarbon-Oxygen LyasesCHO CellsProtein Serine-Threonine KinasesBiologyTransfectionSubstrate SpecificityCricetinaeDNA Repair ProteinDNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsAnimalsHumansAP sitePhosphorylationCasein Kinase IIProtein kinase AMolecular BiologyMethyl MethanesulfonateCyclic AMP-Dependent Protein KinasesMolecular biologyDNA-(apurinic or apyrimidinic site) lyaseTranscription Factor AP-1COS CellsPhosphorylationCasein kinase 2Oxidation-ReductionDNA DamageHeLa CellsMutagensOncogene
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Expression of DNA repair proteins hMSH2, hMSH6, hMLH1,O6-methylguanine-DNA methyltransferase and N-methylpurine-DNA glycosylase in melanoma cells wit…

1999

Malignant melanoma is well known for its primary unresponsiveness to chemotherapy. The mechanisms conferring this intrinsic resistance are unclear. In this study, we investigated the role of genes involved in DNA repair in a panel of human melanoma cell variants exhibiting low and high levels of resistance to 4 commonly used drugs in melanoma treatment, i.e., vindesine, etoposide, fotemustine and cisplatin. We show that in melanoma cells exhibiting resistance to cisplatin, etoposide and vindesine, the nuclear content of each of the DNA mismatch repair (MMR) proteins hMLH1, hMSH2 and hMSH6 was reduced by 30–70%. A decreased expression level of up to 80% of mRNAs encoding hMLH1 and hMSH2 was …

Cancer ResearchDNA RepairTranscription GeneticVindesineDNA repairAntineoplastic AgentsBiologyNitrosourea CompoundsDNA GlycosylasesO(6)-Methylguanine-DNA MethyltransferaseOrganophosphorus CompoundsProto-Oncogene ProteinsmedicineHumansRNA MessengerPromoter Regions GeneticMelanomaN-Glycosyl HydrolasesneoplasmsEtoposideAdaptor Proteins Signal TransducingEtoposideCisplatinMelanomaNuclear Proteinsmedicine.diseaseMolecular biologyDrug Resistance Multipledigestive system diseasesNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinOncologyDNA glycosylaseFotemustineVindesineDNA mismatch repairCisplatinCarrier ProteinsMutL Protein Homolog 1medicine.drugInternational Journal of Cancer
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Aurora kinases in ovarian cancer

2020

Aurora kinases (AURK) are key regulators of the mitotic spindle formation. AURK is frequently overexpressed in ovarian cancer and this overexpression has been frequently associated with prognosis in these tumours. Interestingly, AURK have been shown to interact with DNA repair mechanisms and other cell cycle regulators. These functions have brought light to Aurora family as a potential target for anticancer therapy. In the last years, two clinical trials with different AURK inhibitors have shown activity in epithelial and clear-cell ovarian cancer. Although there is a lack of predictive factors of AURK inhibition activity, recent trials have identified some candidates. This review will focu…

Cancer ResearchDNA repairAurora inhibitorReviewCarcinoma Ovarian EpithelialProtein Serine-Threonine Kinaseslcsh:RC254-282aurora kinaseAurora kinaseAurora KinasesHumansMedicine1506Protein Kinase InhibitorsOvarian Neoplasmsbusiness.industryKinaseCell cyclemedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensSpindle apparatusClinical trialovarian cancerOncologyCancer researchFemalebusinessOvarian canceraurora inhibitorsESMO Open
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