Search results for "MSH2"

showing 10 items of 24 documents

Benzo[a]pyrene represses DNA repair through altered E2F1/E2F4 function marking an early event in DNA damage-induced cellular senescence

2020

AbstractTranscriptional regulation of DNA repair is of outmost importance for the restoration of DNA integrity upon genotoxic stress. Here we report that the potent environmental carcinogen benzo[a]pyrene (B[a]P) activates a cellular DNA damage response resulting in transcriptional repression of mismatch repair (MMR) genes (MSH2, MSH6, EXO1) and of RAD51, the central homologous recombination repair (HR) component, ultimately leading to downregulation of MMR and HR. B[a]P-induced gene repression is caused by abrogated E2F1 signalling. This occurs through proteasomal degradation of E2F1 in G2-arrested cells and downregulation of E2F1 mRNA expression in G1-arrested cells. Repression of E2F1-me…

Cyclin-Dependent Kinase Inhibitor p21SenescenceAcademicSubjects/SCI00010DNA repairDNA damageRAD51E2F4 Transcription FactorBiologyDNA Mismatch Repair03 medical and health sciences0302 clinical medicineCell Line TumorBenzo(a)pyreneGeneticsHumansCellular SenescenceCell Line Transformed030304 developmental biology0303 health sciencesGene regulation Chromatin and EpigeneticsRecombinational DNA RepairEpithelial CellsKv Channel-Interacting ProteinsCell Cycle CheckpointsDNAFibroblastsCell biologyDNA-Binding ProteinsRepressor ProteinsMSH6DNA Repair EnzymesExodeoxyribonucleasesMutS Homolog 2 ProteinGamma RaysMSH2030220 oncology & carcinogenesisCarcinogensMCF-7 CellsDNA mismatch repairRad51 RecombinaseCell agingE2F1 Transcription FactorDNA DamageSignal TransductionNucleic Acids Research
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Nuclear Translocation of Mismatch Repair Proteins MSH2 and MSH6 as a Response of Cells to Alkylating Agents

2000

Mammalian mismatch repair has been implicated in mismatch correction, the prevention of mutagenesis and cancer, and the induction of genotoxicity and apoptosis. Here, we show that treatment of cells specifically with agents inducing O(6)-methylguanine in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine and N-methyl-N-nitrosourea, elevates the level of MSH2 and MSH6 and increases GT mismatch binding activity in the nucleus. This inducible response occurs immediately after alkylation, is long-lasting and dose-dependent, and results from translocation of the preformed MutSalpha complex (composed of MSH2 and MSH6) from the cytoplasm into the nucleus. It is not caused by an increase in MSH2 gen…

CytoplasmDNA RepairBase Pair MismatchRNA StabilityChromosomal translocationmedicine.disease_causeBiochemistrychemistry.chemical_compoundMismatch Repair Endonuclease PMS2Adenosine TriphosphatasesNuclear ProteinsMethylnitrosoureaNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinDNA mismatch repairMutL Protein Homolog 1Protein BindingAlkylating AgentsMethylnitronitrosoguanidinecongenital hereditary and neonatal diseases and abnormalitiesGuanineActive Transport Cell NucleusBiologyCell LineO(6)-Methylguanine-DNA MethyltransferaseProto-Oncogene ProteinsDNA Repair ProteinmedicineHumansRNA MessengerneoplasmsMolecular BiologyAdaptor Proteins Signal TransducingCell NucleusMutagenesisnutritional and metabolic diseasesDNACell BiologyDNA MethylationMolecular biologydigestive system diseasesMSH6DNA Repair EnzymesGene Expression RegulationchemistryMSH2Carrier ProteinsGenotoxicityDNADNA DamageHeLa CellsJournal of Biological Chemistry
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Prognostic Role of Mismatch Repair Status, Histotype and High-Risk Pathologic Features in Stage II Small Bowel Adenocarcinomas

2020

Abstract Background Small bowel adenocarcinoma is a relatively rare cancer, often diagnosed in an advanced stage. In localized and resectable disease, surgery alone or in combination with adjuvant chemotherapy is the mainstay of treatment. In the recently published National Comprehensive Cancer Network Clinical Practice guidelines, criteria for selecting patients with stage II small bowel adenocarcinoma to receive adjuvant chemotherapy are provided, and they are mainly extrapolated from studies on colorectal cancer. Patients and Methods In the present study, we aimed to verify whether mismatch repair deficiency phenotype, high-risk pathologic features (including T4, positive resection margi…

MaleOncologyColorectal cancerDNA Mismatch RepairCOLORECTAL-CANCERSettore MED/120302 clinical medicinePMS2small bowel adenocarcinomaMismatch Repair Endonuclease PMS20303 health sciencesPrognosisMMRMutS Homolog 2 ProteinOncologyCARCINOMAS030220 oncology & carcinogenesisimmunohistochemistryMismatch Repair Status small bowel adenocarcinomaFemaleMicrosatellite InstabilityDNA mismatch repairMutL Protein Homolog 1Colorectal Neoplasmsstage IImedicine.medical_specialtyhigh-risk pathologic featuresDNA Mismatch Repair; Female; Humans; Male; Microsatellite Instability; Mismatch Repair Endonuclease PMS2; MutL Protein Homolog 1; MutS Homolog 2 Protein; Prognosis; Adenocarcinoma; Colorectal Neoplasmssmall bowel adenocarcinoma; mismatch repair statusAdenocarcinomaNO03 medical and health sciencessmall bowel carcinomahistotypeInternal medicineTranslational ResearchmedicineHumansmismatch repair status030304 developmental biologysmall bowel adenocarcinomasbusiness.industryCancerMicrosatellite instabilityMismatch Repair ProteinAdenocarcinoma IBD Cancermedicine.diseasedigestive system diseasesMSH6COLORECTAL-CANCER; CARCINOMAS; CONSENSUSsmall bowel carcinoma MMR immunohistochemistryMismatch repair Small bowel AdenocarcinomaMSH2Mismatch repair status; stage II; small bowel adenocarcinomas; histotype; high-risk pathologic featuresSurgeryCONSENSUSbusiness
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Contribution of Large Genomic Rearrangements in Italian Lynch Syndrome Patients: Characterization of a Novel Alu-Mediated Deletion

2012

Lynch syndrome is associated with germ-line mutations in the DNA mismatch repair (MMR) genes, mainlyMLH1andMSH2. Most of the mutations reported in these genes to date are point mutations, small deletions, and insertions. Large genomic rearrangements in the MMR genes predisposing to Lynch syndrome also occur, but the frequency varies depending on the population studied on average from 5 to 20%. The aim of this study was to examine the contribution of large rearrangements in theMLH1andMSH2genes in a well-characterised series of 63 unrelated Southern Italian Lynch syndrome patients who were negative for pathogenic point mutations in theMLH1,MSH2, andMSH6genes. We identified a large novel delet…

Malecongenital hereditary and neonatal diseases and abnormalitiesgenomic rearragementArticle SubjectPopulationlcsh:MedicineSettore BIO/11 - Biologia MolecolareBiologyMLH1General Biochemistry Genetics and Molecular Biologynovel Alu-mediated deletionAlu ElementsmedicineHumanseducationneoplasmsAdaptor Proteins Signal TransducingSequence DeletionGene RearrangementGeneticseducation.field_of_studyGeneral Immunology and MicrobiologyPoint mutationlcsh:RNuclear ProteinsLynch syndrome; genomic rearragements; novel Alu-mediated deletionnutritional and metabolic diseasesGeneral MedicineGene rearrangementmedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisMolecular biologyLynch syndromedigestive system diseasesDNA-Binding ProteinsMSH6Settore MED/18 - Chirurgia GeneraleLynch syndromeMutS Homolog 2 ProteinItalyMSH2FemaleDNA mismatch repairMutL Protein Homolog 1Research ArticleBioMed Research International
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Distinct Mutational Profile of Lynch Syndrome Colorectal Cancers Diagnosed under Regular Colonoscopy Surveillance

2021

Regular colonoscopy even with short intervals does not prevent all colorectal cancers (CRC) in Lynch syndrome (LS). In the present study, we asked whether cancers detected under regular colonoscopy surveillance (incident cancers) are phenotypically different from cancers detected at first colonoscopy (prevalent cancers). We analyzed clinical, histological, immunological and mutational characteristics, including panel sequencing and high-throughput coding microsatellite (cMS) analysis, in 28 incident and 67 prevalent LS CRCs (n total = 95). Incident cancers presented with lower UICC and T stage compared to prevalent cancers (p &lt

OncologyColorectal cancerColonoscopybiomarkkeritHEREDITARYGUIDELINESTp53 mutationmedicine.disease_causeMolecular level0302 clinical medicineRISKincident cancercancer preventionmedicine.diagnostic_testRGeneral MedicineTUMORSLynch syndrome3. Good healthsyöpäsolutCARCINOMAS030220 oncology & carcinogenesisMedicineDNA mismatch repair030211 gastroenterology & hepatologyKRAScarcinogenesiskoloskopiamedicine.medical_specialtyDATABASEcolorectal cancersuolistosyövätmikrosatelliititArticle03 medical and health sciencescolonoscopy screeningInternal medicinemutational profilingmedicineLynchin oireyhtymäPathologicalpaksusuolisyöpäCancer preventionmismatch repair deficiencybusiness.industryMicrosatellite instabilitySCREENING INTERVAL3126 Surgery anesthesiology intensive care radiologymedicine.diseasedigestive system diseasesMSH2Lynch syndromeMSH23121 General medicine internal medicine and other clinical medicineT-stageCLINICAL MANAGEMENTmicrosatellite instabilitymutaatiotbusinessJournal of Clinical Medicine
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Correction:Cancer risks by gene, age, and gender in 6350 carriers of pathogenic mismatch repair variants: findings from the Prospective Lynch Syndrom…

2020

Lynch syndrome (LS) results from pathogenic variants in the mismatch repair (MMR) genes and is the most common hereditary cancer syndrome, affecting an estimated 1 in 300 individuals. Pathogenic variants in each of the MMR genes path_MLH1, path_MSH2, path_MSH6, and path_PMS2 result in different risks for cancers in organs including the colorectum, endometrium, ovaries, stomach, small bowel, bile duct, pancreas, and upper urinary tract. Accurate estimates of these risks are essential for planning appropriate approaches to the prevention or early diagnosis of cancers but the robustness of previous studies has been limited by factors including retrospective design,1,2 lack of validation in ind…

OncologyMaleColorectal cancer*Lynch syndromePenetranceDNA Mismatch Repair0302 clinical medicineDatabases GeneticMalalties hereditàriesProspective StudiesCàncer*PMS2Genetics (clinical)Mismatch Repair Endonuclease PMS2Cancer0303 health sciencesSex CharacteristicsFactors de risc en les malalties1184 Genetics developmental biology physiologyMLH1Middle Aged16. Peace & justiceLynch syndrome3. Good healthDNA-Binding ProteinsMutS Homolog 2 Proteinsyöpägeenit*MSH2030220 oncology & carcinogenesis*MSH6030211 gastroenterology & hepatologyDNA mismatch repairFemalegeneettiset tekijätMutL Protein Homolog 1Genetic diseasesAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesRisk factors in diseasessuolistosyövätMUTATION CARRIERSMLH1Risk AssessmentArticlesukupuoliAge and gender03 medical and health sciencesInternal medicinemedicineHumansGenetic Predisposition to DiseaseLynchin oireyhtymäGene030304 developmental biologyAgedbusiness.industryEndometrial cancerCorrectionnutritional and metabolic diseasesCancer*MLH1MSH6medicine.diseaseColorectal Neoplasms Hereditary NonpolyposisSurvival Analysisdigestive system diseasesMSH2MSH6Lynch syndromePMS2MSH2Mutation3111 BiomedicineikäbusinessOvarian cancer
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Hereditary ovarian cancer.

2008

Apoptosis is a form of cell death that permits the removal of damaged, senescent or unwanted cells in multicellular organisms, without damage to the cellular microenvironment. Defective apoptosis represents a major causative factor in the development and progression of cancer. The majority of chemotherapeutic agents, as well as radiation, utilize the apoptotic pathway to induce cancer cell death. Resistance to standard chemotherapeutic strategies also seems to be due to alterations in the apoptotic pathway of cancer cells. Recent knowledge on apoptosis has provided the basis for novel targeted therapies that exploit apoptosis to treat cancer. These new target include those acting in the ext…

Oncologymedicine.medical_specialtyendocrine system diseasesColorectal cancerMLH1Germline mutationNeoplastic Syndromes HereditaryInternal medicineGenetic predispositionMedicineHumansGenetic Predisposition to DiseaseGenetic testingOvarian Neoplasmsmedicine.diagnostic_testbusiness.industryBRCA mutationHematologymedicine.diseasePrognosisfemale genital diseases and pregnancy complicationsovarian cancerOncologyMSH2FemalebusinessOvarian cancer
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Identification and molecular characterization of a novel mutation in MSH2 gene in a lynch syndrome family

2017

Background and aim of the work: The Lynch Syndrome (LS) is associated with germline mutations in one of the MisMatch Repair (MMR) genes, including MLH1, MSH2, MSH6, PMS2, MLH3 and MSH3. The molecular characterization of mutations in these MMR genes facilitates the pre-symptomatic diagnosis of subjects at risk to develop a colon cancer or a cancer LS-related. Methods: DHPLC and direct sequencing were performed for the mutation detection analysis. Results: In this study, we identified a novel frame shift mutation, the named is c.170delT in MSH2 gene that determined a premature stop codon and consequently, the formation of a truncated protein (p. Val56Glyfs*7). This is a novel mutation, as it …

Settore MED/18 - Chirurgia GeneraleLynch syndromeNovel variant MSH2 geneHNPCCFrame-shift mutationMSH2 gene
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No Difference in Penetrance between Truncating and Missense/Aberrant Splicing Pathogenic Variants in MLH1 and MSH2: A Prospective Lynch Syndrome Data…

2021

Background. Lynch syndrome is the most common genetic predisposition for hereditary cancer. Carriers of pathogenic changes in mismatch repair (MMR) genes have an increased risk of developing colorectal (CRC), endometrial, ovarian, urinary tract, prostate, and other cancers, depending on which gene is malfunctioning. In Lynch syndrome, differences in cancer incidence (penetrance) according to the gene involved have led to the stratification of cancer surveillance. By contrast, any differences in penetrance determined by the type of pathogenic variant remain unknown. Objective. To determine cumulative incidences of cancer in carriers of truncating and missense or aberrant splicing pathogenic …

cancer incidence0302 clinical medicineMalalties hereditàriesMissense mutation8Q23.3CàncerCancerGenetics0303 health sciencesmedicine.diagnostic_testFactors de risc en les malaltiesMISMATCH REPAIR GENESRMLH1General MedicinePenetranceLynch syndrome3. Good healthsyöpägeenit030220 oncology & carcinogenesisMedicinesyöpätauditilmaantuvuusGenetic diseasescongenital hereditary and neonatal diseases and abnormalitiesmissense11Q23.1Risk factors in diseasesCANCER-RISKMLH1Articleaberrant splicing03 medical and health sciencesAGEmedicineGenetic predispositionddc:610<i>MSH2</i>Lynchin oireyhtymäpenetrance030304 developmental biologyGenetic testingMLH1; MSH2; penetrance; cancer incidence; truncating; missense; aberrant splicing; Lynch syndromeperinnölliset tauditbusiness.industryMUTATIONSHMSH2Cancernutritional and metabolic diseasesmedicine.diseasedigestive system diseasesMSH2Lynch syndromeMSH23121 General medicine internal medicine and other clinical medicine<i>MLH1</i>businesstruncating
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In the literature: April 2020

2020

Deficient DNA mismatch repair (dMMR) may be caused by germline or somatic mutations in mismatch repair genes ( MLH1 , MSH2 , MSH3 , MSH6 and PMS2 ) or through epigenetic silencing of MLH1 .1 dMMR induces a hypermutator phenotype, also known as microsatellite instability (MSI). Next-generation sequencing identifies MSI in 12 cancer types. The highest prevalence is seen in endometrial cancer (31.4%), followed by colorectal cancer (19.7%) and gastric cancer (GC, 19.1%). MSI was related to better prognosis for colorectal cancer and GC . Moreover, the dMMR/MSI hypermutator phenotype is thought to produce large numbers of immunogenic neoantigens that can be recognised by immune cells, leading to …

congenital hereditary and neonatal diseases and abnormalitiesCancer Researchbusiness.industryCancerMicrosatellite instabilityNewsmedicine.diseaseMLH1digestive system diseasesnot applicableMSH6OncologyMSH3MSH2medicineCancer researchPMS2DNA mismatch repair1506businessneoplasmsESMO Open
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