Search results for "mismatch repair"

showing 10 items of 81 documents

Incident colorectal cancer in Lynch syndrome is usually not preceded by compromised quality of colonoscopy

2019

AbstractBackground: Lifetime incidence of colorectal cancer (CRC) especially in carriers of MLH1 and MSH2 pathogenic germline variants in mismatch repair genes is high despite ongoing colonoscopy s...

AdenomaAdultMaleOncologycongenital hereditary and neonatal diseases and abnormalitiesmedicine.medical_specialtyHereditary non-polyposis colorectal cancerCOLONOSCOPYColorectal cancersurveillance colonoscopyeducationColonoscopycolorectal cancerMLH1Germline03 medical and health sciences0302 clinical medicineInternal medicinemedicineHumansRegistriesneoplasmsFinlandAgedNeoplasm StagingRetrospective Studiesmedicine.diagnostic_testbusiness.industryIncidenceIncidence (epidemiology)LYNCH SYNDROMEGastroenterologynutritional and metabolic diseasesMiddle Agedmedicine.diseaseColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasesLynch syndrome3. Good healthMSH2Population Surveillance030220 oncology & carcinogenesis3121 General medicine internal medicine and other clinical medicineFemale030211 gastroenterology & hepatologyDNA mismatch repairColorectal Neoplasmsbusiness
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Retinoblastoma epidemiology: Does the evidence matter?

2007

It has been proposed that retinoblastoma is 'caused' by two sequential mutations affecting the RB1 gene, but this is a rather outdated view of cancer aetiology that does not take into account a large amount of new acquisitions such as chromosomal and epigenetic alterations. Retinoblastoma remains probably the only cancer in which the rather simplistic 'two hit' mutational model is still considered of value, although cancer is known to be associated with genomic and microsatellite instability, defects of the DNA mismatch repair system, alterations of DNA methylation and hystone acethylation/deacethylation, and aneuploidy. Moreover, as it is shown herein, the predictions made by the 'two hit'…

AdultCancer ResearchAdolescentRetinal NeoplasmsRetinoblastoma Aneuploidy Two hit theoryDiseaseBiologyAge DistributionChromosome instabilitymedicineHumansEpigeneticsAge of OnsetChildGerm-Line MutationGeneticsRetinoblastomaRetinoblastomaMicrosatellite instabilityCancerInfantMiddle Agedmedicine.diseasePedigreeSettore BIO/18 - GeneticaOncologyChild PreschoolDNA methylationDNA mismatch repair
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Loss of SMARCB1 expression in colon carcinoma

2020

International audience; SMARCB1 is a tumor suppressor gene, which is part of SWI/SNF complex involved in transcriptional regulation. Recently, loss of SMARCB1 expression has been reported in gastrointestinal carcinomas. Our purpose was to evaluate the incidence and prognostic value of SMARCB1 loss in colon carcinoma (CC). Patients with stage III CC (n = 1695), and a second cohort of 23 patients with poorly differentiated CC were analyzed. Immunohistochemistry for SMARCB1 was performed on tissue microarrays, and cases with loss of expression were controlled on whole sections. Loss of SMARCB1 was compared with the clinico-pathological and molecular characteristics, and the prognostic value wa…

AdultMaleCancer ResearchPathologymedicine.medical_specialtyMedullary cavityTumor suppressor geneSMARCB1[SDV.CAN]Life Sciences [q-bio]/Cancercolon carcinomaYoung AdultGeneticsmedicineHumans0501 psychology and cognitive sciencesStage (cooking)SMARCB1AgedNeoplasm Staging0505 lawTissue microarrayBRAF V600Emismatch repair deficiencybusiness.industry05 social sciencesHistologySMARCB1 ProteinGeneral MedicineMiddle Agedmedicine.diseaseImmunohistochemistry3. Good healthOncologyMedullary carcinomaColonic Neoplasms050501 criminologyImmunohistochemistryFemalebusiness050104 developmental & child psychologyCancer Biomarkers
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Adjuvant Fluorouracil, Leucovorin, and Oxaliplatin in Stage II to III Colon Cancer: Updated 10-Year Survival and Outcomes According to BRAF Mutation …

2015

Purpose The MOSAIC (Multicenter International Study of Oxaliplatin/Fluorouracil/Leucovorin in the Adjuvant Treatment of Colon Cancer) study has demonstrated 3-year disease-free survival (DFS) and 6-year overall survival (OS) benefit of adjuvant oxaliplatin in stage II to III resected colon cancer. This update presents 10-year OS and OS and DFS by mismatch repair (MMR) status and BRAF mutation. Methods Survival actualization after 10-year follow-up was performed in 2,246 patients with resected stage II to III colon cancer. We assessed MMR status and BRAF mutation in 1,008 formalin-fixed paraffin-embedded specimens. Results After a median follow-up of 9.5 years, 10-year OS rates in the bolus/…

AdultMaleProto-Oncogene Proteins B-rafOncologyCancer Researchmedicine.medical_specialtyOrganoplatinum CompoundsColorectal cancermedicine.medical_treatmentPopulationLeucovorinGlutamic AcidKaplan-Meier EstimateDNA Mismatch RepairDisease-Free SurvivalInternal medicineAntineoplastic Combined Chemotherapy ProtocolsOdds RatiomedicineHumansStage (cooking)Infusions IntravenouseducationAgedNeoplasm Stagingeducation.field_of_studyChemotherapybusiness.industryHazard ratioValineMiddle AgedPrognosismedicine.diseasedigestive system diseasesSurgeryOxaliplatinTreatment OutcomeOncologyChemotherapy AdjuvantFluorouracilColonic NeoplasmsInjections IntravenousMutationFemaleFluorouracilbusinessAdjuvantFollow-Up Studiesmedicine.drugJournal of Clinical Oncology
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Repair of oxidatively generated DNA damage in Cockayne syndrome

2013

Defects in the repair of endogenously (especially oxidatively) generated DNA modifications and the resulting genetic instability can potentially explain the clinical symptoms of Cockayne syndrome (CS), a hereditary disease characterized by developmental defects and neurological degeneration. In this review, we describe the evidence for the involvement of CSA and CSB proteins, which are mutated in most of the CS patients, in the repair and processing of DNA damage induced by reactive oxygen species and the implications for the induction of cell death and mutations. Taken together, the data demonstrate that CSA and CSB, in addition to their established role in transcription-coupled nucleotide…

AgingDNA RepairTranscription GeneticDNA damageDNA repairBiologymedicine.disease_causeCockayne syndromemedicineAnimalsHumansCockayne SyndromePoly-ADP-Ribose Binding ProteinsMutationDNA HelicasesBase excision repairmedicine.diseaseMolecular biologyCell biologyDNA Repair EnzymesMitochondrial DNA repairMutationDNA mismatch repairOxidation-ReductionDNA DamageTranscription FactorsDevelopmental BiologyNucleotide excision repairMechanisms of Ageing and Development
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Transgenic systems in studies on genotoxicity of alkylating agents: critical lesions, thresholds and defense mechanisms

1998

Abstract Transgenic systems, both cell lines and mice with gain or loss of function, are being used in order to modulate the expression of DNA repair proteins, thus allowing to assess their contribution to the defense against genotoxic mutagens and carcinogens. In this review, questions have been addressed concerning the use of transgenic systems in elucidating critical primary DNA lesions, their conversion into genotoxic endpoints, low-dose effects, and the relative contribution of individual cellular functions in defense. It has been shown that the repair protein alkyltransferase (MGMT) is decisive for protection against methylating and chloroethylating compounds. Protection pertains also…

Alkylating AgentsDNA repairDNA polymeraseHealth Toxicology and MutagenesisTransgeneMice Transgenicmedicine.disease_causeCell LineMiceGeneticsmedicineAnimalsHumansMolecular BiologyGeneticsbiologyMutagenicity TestsNeoplasms ExperimentalBase excision repairDNA glycosylaseCancer researchbiology.proteinDNA mismatch repairGenotoxicityMutagensAlkyltransferaseMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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MGMT: Key node in the battle against genotoxicity, carcinogenicity and apoptosis induced by alkylating agents

2007

O(6)-methylguanine-DNA methyltransferase (MGMT) plays a crucial role in the defense against alkylating agents that generate, among other lesions, O(6)-alkylguanine in DNA (collectively termed O(6)-alkylating agents [O(6)AA]). The defense is highly important, since O(6)AA are common environmental carcinogens, are formed endogenously during normal cellular metabolism and possibly inflammation, and are being used in cancer therapy. O(6)AA induced DNA damage is subject to repair, which is executed by MGMT, AlkB homologous proteins (ABH) and base excision repair (BER). Although this review focuses on MGMT, the mechanism of repair by ABH and BER will also be discussed. Experimental systems, in wh…

Alkylating AgentsMethyltransferaseAlkylationDNA RepairDNA repairDNA damageGene ExpressionApoptosisIn Vitro TechniquesBiologyDNA Mismatch RepairModels BiologicalBiochemistryNecrosisO(6)-Methylguanine-DNA MethyltransferaseNeoplasmsAnimalsHumansDNA Modification MethylasesneoplasmsMolecular BiologyCarcinogenChromosome AberrationsGeneticsTumor Suppressor ProteinsO-6-methylguanine-DNA methyltransferaseDNACell BiologyBase excision repairdigestive system diseasesDNA Repair EnzymesMutationCancer researchDNA mismatch repairSister Chromatid ExchangeDNA DamageAlkyltransferaseDNA Repair
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Mismatch G-T binding activity and MSH2 expression is quantitatively related to sensitivity of cells to methylating agents

1998

To elucidate mechanisms involved in alkylating drug resistance, Chinese hamster cells resistant to methylating agents have been generated upon transfection with human DNA. Here it is shown that these Chinese hamster ovary (CHO) variants exhibit the tolerance phenotype: they are alkyltransferase deficient (Mex-), cross-resistant to 6-thioguanine, exhibit reduced G-T binding (MutS alpha) activity and express the mismatch repair protein MSH2 at a significantly lower level than the corresponding control. By comparing wild-type cells with different tolerant strains that show gradual differences in resistance to methylating agents, it was shown that both the G-T binding activity and the amount of…

Alkylating Agentscongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA RepairHamsterCHO CellsBiologyMethylationChinese hamsterCricetinaeProto-Oncogene ProteinsAnimalsHumansRNA MessengerChinese hamster ovary cellCell CycleGeneral MedicineMismatch Repair ProteinTransfectionbiology.organism_classificationMolecular biologyDNA-Binding ProteinsMutS Homolog 2 ProteinMSH2DNA mismatch repairAlkyltransferaseCarcinogenesis
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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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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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