Search results for " Repair"

showing 10 items of 721 documents

The Use and Abuse of LexA by Mobile Genetic Elements

2016

The SOS response is an essential process for responding to DNA damage in bacteria. The expression of SOS genes is under the control of LexA, a global transcription factor that undergoes self-cleavage during stress to allow the expression of DNA repair functions and delay cell division until the damage is rectified. LexA also regulates genes that are not part of this cell rescue program, and the induction of bacteriophages, the movement of pathogenicity islands, and the expression of virulence factors and bacteriocins are all controlled by this important transcription factor. Recently it has emerged that when regulating the expression of genes from mobile genetic elements (MGEs), LexA often …

0301 basic medicineMicrobiology (medical)Transcription GeneticDNA repair030106 microbiologyRegulatorBiologyRegulonMicrobiology03 medical and health sciencesBacterial ProteinsVirologyGene expressionBacteriophagesSOS responseSOS Response GeneticsTranscription factorGeneGeneticsSerine Endopeptidasesbiochemical phenomena metabolism and nutritionInterspersed Repetitive Sequencesenzymes and coenzymes (carbohydrates)Infectious DiseasesbacteriaRepressor lexACorepressorDNA DamageTrends in Microbiology
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Analysis of DNA Polymerases Reveals Specific Genes Expansion in Leishmania and Trypanosoma spp.

2020

Leishmaniasis and trypanosomiasis are largely neglected diseases prevailing in tropical and subtropical conditions. These are an arthropod-borne zoonosis that affects humans and some animals and is caused by infection with protozoan of the genera Leishmania and Trypanosoma, respectively. These parasites present high genomic plasticity and are able to adapt themselves to adverse conditions like the attack of host cells or toxicity induced by drug exposure. Different mechanisms allow these adapting responses induced by stress, such as mutation, chromosomal rearrangements, establishment of mosaic ploidies, and gene expansion. Here we describe how a subset of genes encoding for DNA polymerases …

0301 basic medicineMicrobiology (medical)TrypanosomaDNA polymeraseDNA repairgene amplification030106 microbiologyImmunologylcsh:QR1-502DNA repairtrypanosomatidsDNA-Directed DNA Polymerasemedicine.disease_causeMicrobiologylcsh:Microbiology03 medical and health sciencesDNA polymerasesCellular and Infection MicrobiologyTrypanosomiasisGene duplicationTrypanosomatidamedicineAnimalsHumanstranslesion synthesisGeneLeishmaniasisGeneticsLeishmaniaMutationbiologyLeishmaniabiology.organism_classification030104 developmental biologyInfectious DiseasesPerspectivebiology.proteinTrypanosomagenome stabilityFrontiers in Cellular and Infection Microbiology
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Mechanisms of viral mutation

2016

The remarkable capacity of some viruses to adapt to new hosts and environments is highly dependent on their ability to generate de novo diversity in a short period of time. Rates of spontaneous mutation vary amply among viruses. RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate. Viral mutation rates are modulated at different levels, including polymerase fidelity, sequence context, template secondary structure, cellular microenvironment, replication mechanisms, proofreading, and access to post-replicative repair. Additionally, massive numbers of mutations can be intro…

0301 basic medicineMutation rateEvolutionMutation ratevirusesGenome ViralReviewBiologyVirus ReplicationGenetic diversityVirus03 medical and health sciencesCellular and Molecular NeuroscienceMolecular BiologySuppressor mutationRecombination GeneticPharmacologyGeneticsCell BiologyResistance mutationVirologyReplication fidelityVirusPost-replicative repair030104 developmental biologyViral replicationViral evolutionMutationVirusesMutation (genetic algorithm)Dynamic mutationMolecular MedicineHyper-mutationCellular and Molecular Life Sciences
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The shared frameshift mutation landscape of microsatellite-unstable cancers suggests immunoediting during tumor evolution

2020

The immune system can recognize and attack cancer cells, especially those with a high load of mutation-induced neoantigens. Such neoantigens are abundant in DNA mismatch repair (MMR)-deficient, microsatellite-unstable (MSI) cancers. MMR deficiency leads to insertion/deletion (indel) mutations at coding microsatellites (cMS) and to neoantigen-inducing translational frameshifts. Here, we develop a tool to quantify frameshift mutations in MSI colorectal and endometrial cancer. Our results show that frameshift mutation frequency is negatively correlated to the predicted immunogenicity of the resulting peptides, suggesting counterselection of cell clones with highly immunogenic frameshift peptid…

0301 basic medicineMutation rateGeneral Physics and Astronomymedicine.disease_causeCOLORECTAL-CANCER0302 clinical medicineINDEL MutationMutation RateimmunologiaHLA AntigensNeoplasmsFrameshift Mutationlcsh:ScienceImmunologic SurveillanceGeneticsMutationMultidisciplinaryMISMATCH REPAIR DEFICIENCYQPEPTIDES3. Good healthkohdunrungon syöpäsyöpäsolutimmuunivaste030220 oncology & carcinogenesisTumour immunologyMicrosatellite InstabilityDNA mismatch repairINDEL MutationEXPRESSIONcongenital hereditary and neonatal diseases and abnormalitieskasvaimetDATABASESciencegastrointestinal cancerINSTABILITY3122 CancerssuolistosyövätBiologycomplex mixturesArticleGeneral Biochemistry Genetics and Molecular BiologyFrameshift mutationGastrointestinal cancer03 medical and health sciencesAntigens NeoplasmCOLONmedicineHumansCELLSelection GeneticIndelSIGNATUREStumour immunologyMicrosatellite instabilityGeneral ChemistryDNAmedicine.disease3126 Surgery anesthesiology intensive care radiologydigestive system diseases030104 developmental biologyImmunoeditinglcsh:Qmutaatiotbeta 2-MicroglobulinMicrosatellite Repeats
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High Fidelity Deep Sequencing Reveals No Effect of ATM, ATR, and DNA-PK Cellular DNA Damage Response Pathways on Adenovirus Mutation Rate

2019

This article belongs to the Section Animal Viruses.

0301 basic medicineMutation ratemutation rateDNA RepairDNA damageMutation rateviruseslcsh:QR1-502Eukaryotic DNA replicationAtaxia Telangiectasia Mutated ProteinsDNA-Activated Protein KinaseHuman Adenovirus Type 5BiologyDNA damage responsemedicine.disease_causelcsh:MicrobiologyArticleDeep sequencingCell Line03 medical and health scienceschemistry.chemical_compoundVirologymedicineHumansexperimental evolutionPolymeraseMutation030102 biochemistry & molecular biologyAdenoviruses HumanHigh-Throughput Nucleotide SequencingDNA virus3. Good healthCell biologyHuman adenovirus type 5body regions030104 developmental biologyInfectious DiseasesExperimental evolutionchemistrybiology.proteinHuman Adenovirus Type 5.DNADNA DamageSignal TransductionViruses
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Inherited variants in XRCC2 and the risk of breast cancer

2019

Background XRCC2 participates in homologous recombination and in DNA repair. XRCC2 has been reported to be a breast cancer susceptibility gene and is now included in several breast cancer susceptibility gene panels. Methods We sequenced XRCC2 in 617 Polish women with familial breast cancer and found a founder mutation. We then genotyped 12,617 women with breast cancer and 4599 controls for the XRCC2 founder mutation. Results We identified a recurrent truncating mutation of XRCC2 (c.96delT, p.Phe32fs) in 3 of 617 patients with familial breast cancer who were sequenced. The c.96delT mutation was then detected in 29 of 12,617 unselected breast cancer cases (0.23%) compared to 11 of 4599 cancer…

0301 basic medicineOncologyAdultCancer Researchmedicine.medical_specialtyGenotypeXRCC2DNA repairEpidemiologyBreast NeoplasmsXRCC203 medical and health sciences0302 clinical medicineBreast cancerBreast cancerMutation RateInternal medicinemedicineHumansGenetic TestingAlleleMutation frequencyskin and connective tissue diseasesGeneAllelesGenetic Association StudiesAgedbusiness.industryMiddle Agedmedicine.diseaseDNA-Binding Proteins030104 developmental biologyHereditaryOncology030220 oncology & carcinogenesisMutation (genetic algorithm)MutationFemalePolandbusinessHomologous recombinationBreast Cancer Research and Treatment
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Prognostic value of methylator phenotype in stage III colon cancer treated with oxaliplatin-based adjuvant chemotherapy

2017

Abstract Purpose: There are conflicting results concerning the prognostic value of the CpG island methylator phenotype (CIMP) in patients with nonmetastatic colon cancer. We studied this phenotype in stage III colon cancer characterized for mismatch repair (MMR), RAS, and BRAF status, and treated with adjuvant FOLFOX-based regimen. Experimental Design: Tumor samples of 1,907 patients enrolled in the PETACC-8 adjuvant phase III trial were analyzed. The method used was methylation-specific PCR, where CIMP+ status was defined by methylation of at least 3 of 5 following genes: IGF2, CACNA1G, NEUROG1, SOCS1, and RUNX3. Association between CIMP status and overall survival (OS), disease-free survi…

0301 basic medicineOncologyMaleCancer ResearchOrganoplatinum CompoundsAdjuvant chemotherapyColorectal cancermedicine.medical_treatmentLeucovorincolon cancer stage iiiKaplan-Meier EstimateDNA Mismatch Repair[ SDV.CAN ] Life Sciences [q-bio]/Cancer0302 clinical medicineFOLFOXAntineoplastic Combined Chemotherapy ProtocolsMethylator phenotypecolorectalCetuximabHematologyMiddle AgedColon cancer stage iiiPrognosisPhenotypeStage III Colon Cancer3. Good healthadjuvant chemotherapyChemotherapy Adjuvant030220 oncology & carcinogenesisColonic NeoplasmsoncologyFemaleFluorouracilmedicine.drugmedicine.medical_specialtyphenotype[SDV.CAN]Life Sciences [q-bio]/CancerGastrointestinal tumoursDisease-Free Survivalpatient prognosis03 medical and health sciencesInternal medicinemedicineHumansneoplasmsAgedNeoplasm StagingChemotherapyCpG Island Methylator Phenotypebusiness.industryProportional hazards modeloxaliplatinCancerDNA Methylationmedicine.diseasedigestive system diseasesOxaliplatin030104 developmental biologyMutationCpG IslandsNeoplasm Recurrence LocalbusinessValue (mathematics)030217 neurology & neurosurgery
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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
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Schlafen-11 (SLFN11): a step forward towards personalized medicine in small-cell lung cancer?

2018

Purpose Both temozolomide (TMZ) and poly (ADP-ribose) polymerase (PARP) inhibitors are active in small-cell lung cancer (SCLC). This phase II, randomized, double-blind study evaluated whether addition of the PARP inhibitor veliparib to TMZ improves 4-month progression-free survival (PFS). Patients and Methods A total of 104 patients with recurrent SCLC were randomly assigned 1:1 to oral veliparib or placebo 40 mg twice daily, days 1 to 7, and oral TMZ 150 to 200 mg/m

0301 basic medicineOncologyMaleLung NeoplasmsDNA Mutational AnalysisPoly (ADP-Ribose) Polymerase-1Placebos0302 clinical medicineAntineoplastic Combined Chemotherapy ProtocolsPromoter Regions GeneticDNA Modification MethylasesAged 80 and overStandard treatmentNuclear ProteinsMiddle AgedNeoplastic Cells CirculatingImmunohistochemistryhumanitiesEditorialOncology030220 oncology & carcinogenesisFemaleNon small cellAdultmedicine.medical_specialtyMEDLINEAggressive disease03 medical and health sciencesText miningDouble-Blind MethodInternal medicinemedicineBiomarkers TumorTemozolomideHumansLung cancerneoplasmsAntineoplastic Agents AlkylatingAgedbusiness.industryTumor Suppressor ProteinsDNA Methylationmedicine.diseaseSmall Cell Lung Carcinomarespiratory tract diseases030104 developmental biologyDNA Repair EnzymesBenzimidazolesPersonalized medicinebusiness
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Does breast carcinoma belong to the Lynch syndrome tumor spectrum? : Somatic mutational profiles vs. ovarian and colorectal carcinomas

2020

// Noora K. Porkka 1 , Alisa Olkinuora 1 , Teijo Kuopio 2 , 3 , Maarit Ahtiainen 4 , Samuli Eldfors 5 , Henrikki Almusa 5 , Jukka-Pekka Mecklin 6 , 7 , 8 and Paivi Peltomaki 1 1 Department of Medical and Clinical Genetics, University of Helsinki, Helsinki, Finland 2 Department of Pathology, Jyvaskyla Central Hospital, Jyvaskyla, Finland 3 Department of Biological and Environmental Science, University of Jyvaskyla, Jyvaskyla, Finland 4 Department of Education and Research, Jyvaskyla Central Hospital and University of Eastern Finland, Jyvaskyla, Finland 5 Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland 6 Faculty of Sport and Health Sciences, University of J…

0301 basic medicineOncologymedicine.medical_specialtyDNA mismatch repair3122 Cancersmedicine.disease_cause03 medical and health sciences0302 clinical medicineBreast cancerGermline mutationInternal medicinemedicinesomatic mutationbreast carcinomaLynchin oireyhtymäMSIperinnölliset tauditrintasyöpäbusiness.industryCancermedicine.diseaseLynch syndromedigestive system diseases3. Good health030104 developmental biologyLynch syndromeOncologysyöpägeenit030220 oncology & carcinogenesisMedical geneticsDNA mismatch repairsyöpätaudit3111 BiomedicinemutaatiotCarcinogenesisBreast carcinomabusinessResearch Paper
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