Search results for "Repair"

showing 10 items of 747 documents

Réparations et appropriation. Quelques considérations sur des épées personnalisées du Bronze final

2019

International audience; Repair is an action aiming at giving an object is functionality back. This is of course an economic process: if it is not possible to use an artefact for the purpose it was designed for, for example if it is flawed or worn out, then it needs to be smelted or repaired. But the cultural aspect of functionality shall not be forgotten. In Bronze Age societies, all items crafted had to look a certain way, and not another, varying according to the considered regions or time periods.Bronze Age swords are no exception to the rule. The shape of the hilt is particularly standardized, contributing to the visual identity of the weapon. For example, at the end of the Bronze Age (…

Bronze Age[SHS.ARCHEO] Humanities and Social Sciences/Archaeology and Prehistory[SHS.ARCHEO]Humanities and Social Sciences/Archaeology and PrehistorySwordMaterial cultureRepair
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Genetic and pharmacological modulation of DNA mismatch repair heterogeneous tumors promotes immune surveillance.

2023

Patients affected by colorectal cancer (CRC) with DNA mismatch repair deficiency (MMRd), often respond to immune checkpoint blockade therapies, while those with mismatch repair-proficient (MMRp) tumors generally do not. Interestingly, a subset of MMRp CRCs contains variable fractions of MMRd cells, but it is unknown how their presence impacts immune surveillance. We asked whether modulation of the MMRd fraction in MMR heterogeneous tumors acts as an endogenous cancer vaccine by promoting immune surveillance. To test this hypothesis, we use isogenic MMRp (Mlh1+/+) and MMRd (Mlh1-/-) mouse CRC cells. MMRp/MMRd cells mixed at different ratios are injected in immunocompetent mice and tumor reje…

Cancer Research6-thioguaninemismatch repairOncology6-thioguanine; heterogeneity; immune checkpoint blockade; immune evasion; immune surveillance; microsatellite unstable tumors (MSI); mismatch repair; temozolomide6-thioguanine heterogeneity immune checkpoint blockade immune evasion immune surveillance microsatellite unstable tumors (MSI) mismatch repair temozolomideimmune surveillancemicrosatellite unstable tumors (MSI)temozolomideheterogeneityimmune checkpoint blockadeSettore MED/08 - Anatomia Patologicaimmune evasionCancer cell
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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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Functional impact and evolution of a novel human polymorphic inversion that disrupts a gene and creates a fusion transcript

2015

Despite many years of study into inversions, very little is known about their functional consequences, especially in humans. A common hypothesis is that the selective value of inversions stems in part from their effects on nearby genes, although evidence of this in natural populations is almost nonexistent. Here we present a global analysis of a new 415-kb polymorphic inversion that is among the longest ones found in humans and is the first with clear position effects. This inversion is located in chromosome 19 and has been generated by non-homologous end joining between blocks of transposable elements with low identity. PCR genotyping in 541 individuals from eight different human populatio…

Cancer ResearchDNA End-Joining Repairlcsh:QH426-470GenotypeChromosome inversionPopulationChromosome BreakpointsBiologyChromosome breakpointsGenoma humàPolymorphism Single NucleotideEvolution MolecularChromosome Breakpoints03 medical and health sciences0302 clinical medicinePolymorphism Single nucleotideChromosome 19DNA end-joining repairGeneticsTranscription factorsHumansAlleleeducationMolecular BiologyGeneGenetics (clinical)Ecology Evolution Behavior and Systematics030304 developmental biologyChromosomal inversionGeneticsGene expression regulation0303 health scienceseducation.field_of_studyGenètica de poblacionsHaplotypelcsh:GeneticsDNA transposable elementsGenetics PopulationGene Expression RegulationFusion transcriptChromosome InversionDNA Transposable ElementsChromosomes Human Pair 19030217 neurology & neurosurgeryResearch ArticleTranscription Factors
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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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