Search results for "MutS Homolog 2 Protein"

showing 10 items of 15 documents

Associations of Pathogenic Variants in MLH1, MSH2, and MSH6 With Risk of Colorectal Adenomas and Tumors and With Somatic Mutations in Patients With L…

2020

Contains fulltext : 220040.pdf (Publisher’s version ) (Closed access) BACKGROUND & AIMS: Lynch syndrome is caused by variants in DNA mismatch repair (MMR) genes and associated with an increased risk of colorectal cancer (CRC). In patients with Lynch syndrome, CRCs can develop via different pathways. We studied associations between Lynch syndrome-associated variants in MMR genes and risks of adenoma and CRC and somatic mutations in APC and CTNNB1 in tumors in an international cohort of patients. METHODS: We combined clinical and molecular data from 3 studies. We obtained clinical data from 2747 patients with Lynch syndrome associated with variants in MLH1, MSH2, or MSH6 from Germany, the Net…

0301 basic medicineOncologyMaleColorectal cancerDNA Mutational Analysisgenetic analysisHEREDITARYcancer riskGUIDELINESDNA Mismatch Repair0302 clinical medicineGermanyTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]Prospective Studiesprognostic factorFinlandbeta CateninNetherlandsOutcomePrognostic FactorGastroenterologyGenetic AnalysisColonoscopyMiddle AgedCANCERLynch syndromeCancer Risk3. Good healthDNA-Binding ProteinsDEFICIENCYMutS Homolog 2 Proteinsyöpägeenitoutcome030211 gastroenterology & hepatologyDNA mismatch repairFemaleMutL Protein Homolog 1geenitutkimusAdenomaAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdenoma3122 CancersAdenomatous Polyposis Coli ProteinINSTABILITYSOCIETYMLH103 medical and health sciencesInternal medicinemedicineMANAGEMENTHumansLynchin oireyhtymäneoplasmspaksusuolisyöpäHepatologybusiness.industryCancernutritional and metabolic diseasesennusteetmedicine.diseaseColorectal Neoplasms Hereditary Nonpolyposisdigestive system diseasesMSH6030104 developmental biologyMSH2Mutationbusiness
researchProduct

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
researchProduct

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
researchProduct

Factors associated with decision-making on prophylactic hysterectomy and attitudes towards gynecological surveillance among women with Lynch syndrome…

2020

AbstractTo prevent endometrial carcinoma in Lynch syndrome (LS), regular gynecological surveillance visits and prophylactic surgery are recommended. Previous data have shown that prophylactic hysterectomy is an effective means of cancer prevention, while the advantages and disadvantages of surveillance are somewhat unclear. We aimed to evaluate female LS carriers’ attitudes towards regular gynecological surveillance and factors influencing their decision-making on prophylactic surgery that have not been well documented. Pain experienced during endometrial biopsies was also evaluated. Postal questionnaires were sent to LS carriers undergoing regular gynecological surveillance. Questionnaires…

Cancer ResearchSURGERYmedicine.medical_treatmentPain Procedural0302 clinical medicineSurveys and QuestionnairesEpidemiologyProphylactic surgeryFinlandGenetics (clinical)Aged 80 and overRISKSurveillancemedicine.diagnostic_testObstetricsMiddle Aged16. Peace & justiceProphylactic SurgeryLynch syndrome3. Good healthDNA-Binding Proteinsprophylactic surgeryMutS Homolog 2 ProteinOncologyPatient Satisfaction030220 oncology & carcinogenesissurveillanceFemaleOriginal Article030211 gastroenterology & hepatologyMutL Protein Homolog 1AdultHeterozygotemedicine.medical_specialtyDecision Making3122 CancersHNPCCHysterectomyehkäisevä lääketiede03 medical and health sciencesSyöpätaudit - CancersGeneticsmedicineCarcinomaHumansGenetic TestingLynchin oireyhtymäAgedRetrospective StudiesHysterectomyCancer preventionbusiness.industryEndometrial cancerENDOMETRIAL CANCERmedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisEndometrial NeoplasmsLynch syndromebusinessEndometrial biopsy
researchProduct

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
researchProduct

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
researchProduct

Dysregulation of DNA methylation induced by past arsenic treatment causes persistent genomic instability in mammalian cells

2015

The mechanisms by which arsenic-induced genomic instability is initiated and maintained are poorly understood. To investigate potential epigenetic mechanisms, in this study we evaluated global DNA methylation levels in V79 cells and human HaCaT keratinocytes at several time points during expanded growth of cell cultures following removal of arsenite exposures. We have found altered genomic methylation patterns that persisted up to 40 cell generations in HaCaT cells after the treatments were withdrawn. Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, o…

DNA (Cytosine-5-)-Methyltransferase 1KeratinocytesDNA methylationArsenitesarsenicNuclear ProteinsFibroblastsgenomic instabilityArticleDNA Methyltransferase 3ASettore BIO/18 - GeneticaCricetulusLong Interspersed Nucleotide ElementsMutS Homolog 2 Protein5-MethylcytosineAnimalsDNA (Cytosine-5-)-MethyltransferasesMutL Protein Homolog 1Promoter Regions GeneticCells CulturedAdaptor Proteins Signal Transducing
researchProduct

The Different Immune Profiles of Normal Colonic Mucosa in Cancer-Free Lynch Syndrome Carriers and Lynch Syndrome Colorectal Cancer Patients.

2021

ABSTRACT Background and aims Due to the high load of immunogenic frameshift neoantigens, tumors arising in individuals with Lynch syndrome (LS), the most common inherited colorectal cancer (CRC) syndrome, are characterized by a pronounced immune infiltration. However, the immune status of normal colorectal mucosa in LS is not well characterized. We assessed the immune infiltrate in tumor-distant normal colorectal mucosa from LS CRC patients, sporadic microsatellite-unstable (MSI) and microsatellite-stable (MSS) CRC patients, and cancer-free LS carriers. Methods CD3-positive, FOXP3-positive and CD8-positive T cells were quantified in 219, 233 and 201 formalin-fixed paraffin-embedded (FFPE) n…

MaleCD3 ComplexColorectal cancerT-LymphocytesCD8-Positive T-LymphocytesT-Lymphocytes Regulatory0302 clinical medicineIntestinal MucosaMismatch Repair Endonuclease PMS2Aged 80 and over0303 health sciencesbiologyGastroenterologyFOXP3Forkhead Transcription FactorsMiddle AgedLynch syndrome3. Good healthDNA-Binding Proteinsmedicine.anatomical_structureMutS Homolog 2 Protein030220 oncology & carcinogenesisFemaleMicrosatellite InstabilityMutL Protein Homolog 1AdultHeterozygoteColonT cellCD303 medical and health sciencesYoung AdultImmune systemmedicineHumansLymphocyte Count030304 developmental biologyAgedHepatologybusiness.industryCarcinomaRectumCancerMicrosatellite instabilitymedicine.diseaseColorectal Neoplasms Hereditary NonpolyposisCancer researchbiology.proteinbusinessTranscriptomeGastroenterology
researchProduct

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
researchProduct

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
researchProduct