Search results for " Mismatch"

showing 10 items of 140 documents

An extensive pattern of atypical neural speech-sound discrimination in newborns at risk of dyslexia.

2019

Objective: Identifying early signs of developmental dyslexia, associated with deficient speech-sound processing, is paramount to establish early interventions. We aimed to find early speech-sound processing deficiencies in dyslexia, expecting diminished and atypically lateralized event-related potentials (ERP) and mismatch responses (MMR) in newborns at dyslexia risk. Methods: ERPs were recorded to a pseudoword and its variants (vowel-duration, vowel-identity, and syllable-frequency changes) from 88 newborns at high or no familial risk. The response significance was tested, and group, laterality, and frontality effects were assessed with repeated-measures ANOVA. Results: An early positive a…

6162 Cognitive scienceMaleSpeech soundAudiologyEvent-related potential (ERP)Dyslexia0302 clinical medicineEARLY LANGUAGE-ACQUISITIONnewbornMedicineFAMILIAL RISKAuditoryBRAIN RESPONSES05 social sciencesevent-related potential (ERP)ElectroencephalographySensory SystemsLanguage developmentNeurologyLateralityEvoked Potentials AuditorySpeech PerceptionFemaleAnalysis of variancespeech soundpsychological phenomena and processesmedicine.medical_specialty515 PsychologyMISMATCH NEGATIVITY MMNCORTICAL RESPONSESEVENT-RELATED POTENTIALSGENETIC RISKbehavioral disciplines and activities050105 experimental psychology03 medical and health sciencesSpeech discriminationEvent-related potentialPhoneticsPhysiology (medical)Vowelotorhinolaryngologic diseasesdysleksiaHumansSpeech0501 psychology and cognitive sciencesauditoryAUDITORY-DISCRIMINATIONMismatch response (MMR)vastasyntyneetAuditory Cortexbusiness.industrypuheääni3112 NeurosciencesDyslexiaInfant NewbornNewbornmismatch response (MMR)medicine.diseaseta3124PseudowordPHONEME MISMATCHAcoustic StimulationDEVELOPMENTAL DYSLEXIANeurology (clinical)business030217 neurology & neurosurgeryClinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology
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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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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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Prenatal diagnosis of a rhodopsin mutation using chemical cleavage of the mismatch

2002

Objective: Mutations of the rhodopsin gene are responsible for autosomal dominant or recessive retinitis pigmentosa (RP). The present study reports the first prenatal diagnosis performed on chorionic villi biopsy of a pregnant woman affected by a severe form of autosomal dominant transmitted RP, due to the Arg135Trp substitution. Methods: The rhodopsin gene was analysed by automated direct sequencing and, for the first time, by fluorescence-assisted mismatch analysis (FAMA). The latter is an inexpensive, rapid and particularly sensitive method, based on the chemical cleavage of the mismatch in heteroduplex DNA molecules marked with strand-specific fluorophores. Results: FAMA is a feasible p…

AdultRhodopsinrhodopsin geneBase Pair MismatchSettore MED/30 - Malattie Apparato VisivoDNA Mutational Analysisfama; retinitis pigmentosa; rhodopsin geneDNAHeteroduplex AnalysisPolymerase Chain ReactionSettore BIO/18 - GeneticaChorionic Villi SamplingPregnancyretinitis pigmentosaMutationHumansFemalefama
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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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Quantification of the Detrimental Effect of a Single Primer-Template Mismatch by Real-Time PCR Using the 16S rRNA Gene as an Example

2008

ABSTRACT We investigated the effects of internal primer-template mismatches on the efficiency of PCR amplification using the 16S rRNA gene as the model template DNA. We observed that the presence of a single mismatch in the second half of the primer extension sequence can result in an underestimation of up to 1,000-fold of the gene copy number, depending on the primer and position of the mismatch.

Base Pair MismatchGene DosageBiologyPolymerase Chain ReactionApplied Microbiology and BiotechnologyPrimer extensionlaw.inventionDNA POLYMERASElawRNA Ribosomal 16SMethodsCopy-number variationGenePolymerase chain reactionDNA PrimersADN CIBLE[SDV.EE]Life Sciences [q-bio]/Ecology environmentGeneticsEcologyRibosomal RNA16S ribosomal RNACOPIE DE GENEReal-time polymerase chain reactionPseudomonas aeruginosaPrimer (molecular biology)Food ScienceBiotechnologyApplied and Environmental Microbiology
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