Search results for "mutations"

showing 10 items of 205 documents

Impact of Different Selection Approaches for Identifying Lynch Syndrome-Related Colorectal Cancer Patients: Unity Is Strength

2022

Lynch syndrome (LS) is an inherited genetic condition associated with increased predisposition to colorectal cancer (CRC) and other tumors and is caused by germline mutations in Mismatch Repair (MMR) or EPCAM genes. The identification of LS carriers is currently based on germline testing of subjects with MMR-deficient (dMMR) tumors or fulfilling clinical criteria, but the most efficient strategies to select patients who should be offered genetic testing are yet not well defined. In order to assess the most suitable selection mode to identify LS-related CRC patients, we retrospectively collected and analyzed all clinical and molecular information of 854 CRC patients, recruited from 2013 to 2…

Cancer Researchmismatch repair genesSettore MED/06 - Oncologia MedicaMMR-deficiency[SDV]Life Sciences [q-bio]MLH1Neoplasms. Tumors. Oncology. Including cancer and carcinogenscolorectal cancerdigestive system diseasesMSH2Lynch syndromeOncologygermline mutationsmicrosatellite instabilityRC254-282Frontiers in Oncology
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KRAS-G12C Mutation in One Real-Life and Three Population-Based Nordic Cohorts of Metastatic Colorectal Cancer

2022

Background: KRAS mutations, present in over 40% of metastatic colorectal cancer (mCRC), are negative predictive factors for anti-EGFR therapy. Mutations in KRAS-G12C have a cysteine residue for which drugs have been developed. Published data on this specific mutation are conflicting; thus, we studied the frequency and clinical characteristics in a real-world and population-based setting. Methods: Patients from three Nordic population-based cohorts and the real-life RAXO-study were combined. RAS and BRAF tests were performed in routine healthcare, except for one cohort. The dataset consisted of 2,559 patients, of which 1,871 could be accurately classified as KRAS, NRAS, and BRAF-V600E. Demog…

Cancer och onkologireal-worldendocrine system diseasesEGFR3122 CancersKRAS mutationKRAS-G12C mutationKRAS MUTATIONScolorectal cancersuolistosyövät3126 Surgery anesthesiology intensive care radiologyTUMORSdigestive system diseasesetäpesäkkeetmetastaticpopulation-basedPOOLED ANALYSISRAS MUTATIONSsyöpägeenitCancer and Oncologymutaatiotkohorttitutkimusneoplasmspaksusuolisyöpä
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Exacerbated experimental autoimmune encephalomyelitis in mast-cell-deficient KitW-sh/W-sh mice

2011

Mast cell (MC)-deficient c-Kit mutant Kit(W/W-v) mice are protected against experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis, suggesting a detrimental role for MCs in this disease. To further investigate the role of MCs in EAE, we took advantage of a recently characterized model of MC deficiency, Kit(W-sh/W-sh). Surprisingly, we observed that myelin oligodendrocyte glycoprotein (MOG)(35-55)-induced chronic EAE was exacerbated in Kit(W-sh/W-sh) compared with Kit(+/+) mice. Kit(W-sh/W-sh) mice showed more inflammatory foci in the central nervous system (CNS) and increased T-cell response against myelin. To understand whether the discrepant results obtaine…

Central Nervous SystemT-LymphocytesEncephalomyelitisexperimental autoimmune encephalomyelitismast cellsInbred C57BLSeverity of Illness IndeximmunologyMiceMyelinPeptide Fragmentimmune system diseasesMast CellEncephalomyelitisMyelin SheathbiologyExperimental autoimmune encephalomyelitisMast cellProto-Oncogene Proteins c-kitPhenotypemedicine.anatomical_structuremastcell-deficient miceBone Marrow Cellgenetics/immunology/pathology/prevention /&/ controlc-kit mutationsc-kit mutations; experimental autoimmune encephalomyelitis; granulocytes; mast cellsEncephalomyelitis Autoimmune ExperimentalCentral nervous systemBone Marrow CellsPathology and Forensic MedicineMyelin oligodendrocyte glycoproteinExperimentalAnimals Antibody Formation Bone Marrow Cells; pathology Central Nervous System; pathology Encephalomyelitis; Autoimmune; Experimental; genetics/immunology/pathology/prevention /&/ control Glycoproteins; immunology Granulocytes; pathology Immunization Mast Cells; pathology Mice Mice; Inbred C57BL Mutation Myelin Sheath; immunology Myelin-Oligodendrocyte Glycoprotein Peptide Fragments; immunology Phenotype Proto-Oncogene Proteins c-kit; deficiency/genetics/metabolism Severity of Illness Index T-Lymphocytes; pathologyAntigendeficiency/genetics/metabolismmedicineAnimalsMolecular BiologyGlycoproteinsAnimalMultiple sclerosismast-cell-deficient Kit W-sh/W-sh mice.Experimental autoimmune encephalomyelitis; mast-cell-deficient Kit W-sh/W-sh mice.GranulocytegranulocytesCell Biologymedicine.diseaseEncephalomyelitiExperimental autoimmune encephalomyelitiPeptide FragmentsMice Inbred C57BLT-LymphocyteAntibody FormationMutationImmunologybiology.proteinexperimental autoimmune encephalomyelitis; mastcell-deficient mice; mast cellspathologyImmunizationMyelin-Oligodendrocyte GlycoproteinGlycoproteinAutoimmuneLaboratory Investigation
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Genetic instability in calamondin (Citrus madurensis Lour.) plants derived from somatic embryogenesis induced by diphenylurea derivative

2007

Somatic embryos were regenerated in vitro from calamondin style-stigma explants cultured in the presence of N (6)-benzylaminopurine (BAP) cytokinin and three synthetic phenylurea derivatives, N-(2-chloro-4-pyridyl)-N-phenylurea (4-CPPU), N-phenyl-N'-benzothiazol-6-ylurea (PBU) and N,N'-bis-(2,3-methilendioxyphenyl)urea (2,3-MDPU). The phenylurea derivative compounds tested at micromolar level (12 muM) were able to induce a percentage of responsive explants significantly higher from that obtained with BAP and hormone-free (HF) conditions. In order to verify the genetic stability of the regenerants, 27 plants coming from different embryogenic events were randomly selected from each different …

CitrusSomatic embryogenesisMutantPlant ScienceBiologyGenetic polymorphismsSomaclonal variationTissue Culture Techniqueschemistry.chemical_compoundGene Expression Regulation PlantBotanygenetic polymorphismmolecular markerPolymorphism GeneticMolecular markersGeneral MedicineSomaclonal variabilitybiology.organism_classificationMolecular biologyIn vitroCulture MediaRutaceaechemistryMutagenesisCytokininmutationAgronomy and Crop ScienceCarbanilidesDNAMutationsExplant culturePlant regeneration
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Genome-Wide Association Study of Diabetic Kidney Disease Highlights Biology Involved in Glomerular Basement Membrane Collagen

2019

BACKGROUND: Although diabetic kidney disease demonstrates both familial clustering and single nucleotide polymorphism heritability, the specific genetic factors influencing risk remain largely unknown.METHODS: To identify genetic variants predisposing to diabetic kidney disease, we performed genome-wide association study (GWAS) analyses. Through collaboration with the Diabetes Nephropathy Collaborative Research Initiative, we assembled a large collection of type 1 diabetes cohorts with harmonized diabetic kidney disease phenotypes. We used a spectrum of ten diabetic kidney disease definitions based on albuminuria and renal function.RESULTS: Our GWAS meta-analysis included association result…

Collagen Type IVMale0301 basic medicineEXPRESSIONNEPHROPATHY030232 urology & nephrologyPROTEINGenome-wide association studyRECEPTOR TYROSINE KINASESBiologySUSCEPTIBILITYBioinformaticsurologic and male genital diseasesAutoantigensNephropathyEnd stage renal diseaseCohort StudiesDiabetic nephropathy03 medical and health sciences0302 clinical medicineSDG 3 - Good Health and Well-beingDiabetes mellitusGlomerular Basement MembranemedicineHumansDiabetic NephropathiesAlport syndromeLetter to the EditorCOMPLICATIONSNITRIC-OXIDEMUTATIONS1184 Genetics developmental biology physiologyGeneral Medicinemedicine.diseaseGENE3. Good healthDiabetes Mellitus Type 1030104 developmental biologyNephrology3121 General medicine internal medicine and other clinical medicineMutationAlbuminuria/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemale3111 Biomedicinemedicine.symptomCOLLECTIN 11 CL-11Genome-Wide Association StudyKidney disease
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Efficacy and safety of cyclic pyranopterin monophosphate substitution in severe molybdenum cofactor deficiency type A: a prospective cohort study.

2015

Summary Background Molybdenum cofactor deficiency (MoCD) is characterised by early, rapidly progressive postnatal encephalopathy and intractable seizures, leading to severe disability and early death. Previous treatment attempts have been unsuccessful. After a pioneering single treatment we now report the outcome of the complete first cohort of patients receiving substitution treatment with cyclic pyranopterin monophosphate (cPMP), a biosynthetic precursor of the cofactor. Methods In this observational prospective cohort study, newborn babies with clinical and biochemical evidence of MoCD were admitted to a compassionate-use programme at the request of their treating physicians. Intravenous…

Compassionate Use TrialsMalePediatricsmedicine.medical_specialtyGENOMIC STRUCTUREFEATURESEncephalopathyMolybdopterin synthaseCyclic pyranopterin monophosphateDrug Administration ScheduleCohort Studieschemistry.chemical_compoundOrganophosphorus CompoundsmedicineURINEHumansBIOSYNTHESISProspective cohort studyAdverse effectMolybdenum cofactor deficiencyPRECURSORMetal Metabolism Inborn ErrorsMetal metabolismbusiness.industryMUTATIONSInfant NewbornGENES MOCS1CPMPMOLYBDOPTERIN SYNTHASEGeneral Medicinemedicine.diseasePterinsTreatment OutcomechemistryFemalebusinessCohort studyLancet (London, England)
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Clinical, molecular and functional characterization of two novel mutations associated to compound heterozygous FHBL

2012

Introduction. Primary hypobetalipoproteinemia (pHBL) is a monogenic heterogeneous condition characterized by total cholesterol (TC) and/or LDL cholesterol (LDL-C) levels below the 5th percentile of the reference population. Heterozygous APOB gene mutations are responsible for the majority of the dominant pHBL causing the familial hypobetalipoproteinemia (FHBL). The clinical phenotype of heterozygous FHBL is usually mild. The homozygous or compound heterozygous APOB mutations are in some cases responsible for a more severe biochemical and clinical phenotype, similar to the abetalipoproteinemia (ABL) due to homozygous mutations in the MTP gene, characterized by intestinal malabsorption, pigme…

Compound heterozygouSettore MED/09 - Medicina InternaFHBLsplicing mutations
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Boolean Networks: A Primer

2021

Abstract Autism Spectrum Disorders (ASDs) stand out as a relevant example where omics-data approaches have been extensively and successfully employed. For instance, an outstanding outcome of the Autism Genome Project relies in the identification of biomarkers and the mapping of biological processes potentially implicated in ASDs’ pathogenesis. Several of these mapped processes are related to molecular and cellular events (e.g., synaptogenesis and synapse function, axon growth and guidance, etc.) that are required for the development of a correct neuronal connectivity. Interestingly, these data are consistent with results of brain imaging studies of some patients. Despite these remarkable pr…

Computer scienceIn silicoAttractor Autism spectrum disorders (ASDs) Axon guidance Basin of attraction Boolean network BoolNet Computational model Copy number variants (CNVs) Growth cone In silico mutagenesis Mutations Neurodevelopmental disorders Systems biologyGenome projectComputational biologyGene mutationmedicine.diseasePhenotypeEndophenotypemental disordersmedicineAutismIdentification (biology)Function (biology)
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Fraser syndrome: epidemiological study in a European population

2013

Fraser syndrome is a rare autosomal recessive disorder characterized by cryptophthalmos, cutaneous syndactyly, laryngeal, and urogenital malformations. We present a population-based epidemiological study using data provided by the European Surveillance of Congenital Anomalies (EUROCAT) network of birth defect registries. Between January 1990 and December 2008, we identified 26 cases of Fraser syndrome in the monitored population of 12, 886, 464 births (minimal estimated prevalence of 0.20 per 100, 000 or 1:495, 633 births). Most cases (18/26 ; 69%) were registered in the western part of Europe, where the mean prevalence is 1 in 230, 695 births, compared to the prevalence 1 in 1, 091, 175 fo…

CryptophthalmosMalemedicine.medical_specialtyEpidemiologyAnorectal anomaliesPopulationprevalencePrevalencePrenatal diagnosisinduced abortionCongenital abnormalitiesPregnancyInduced abortionGeneticsPrevalenceMedicineHumansCRITERIASyndactylyRegistriesPRENATAL-DIAGNOSISeducationFraser syndromeRenal agenesisGenetics (clinical)education.field_of_studycongenital abnormalitiesprenatal diagnosisFraser syndrome; epidemiology; prevalence; congenital abnormalities; prenatal diagnosis; induced abortionbusiness.industryObstetricsMUTATIONSInfant Newbornmedicine.diseaseBilateral Renal AgenesisEuropeEpidemiologic StudiesCRYPTOPHTHALMOSFemaleepidemiologyFraser syndromebusiness
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Partitioning study of polycyclic aromatic hydrocarbons between water and some selected water-insoluble phases

2007

An investigation on the partitioning of naphthalene and phenanthrene between water and some water-insoluble phases has been carried out by Uv-vis-NIR spectrophotometry. The analysis of the experimental results emphasized the role of intermolecular interactions and structural features of the hosting phases as driving forces of the partitioning of these polycyclic aromatic hydrocarbons. The critical comparison of the resulting distribution constants allowed to evaluate the potentials of some extracting phases to set up sensitive analytical methods and/or effective environment remediation technologies.

DNA-ADDUCTSEXTRACTIONSpectroscopy Near-Infraredmedicine.diagnostic_testEnvironmental remediationChemistryMUTATIONSIntermolecular forcetechnology industry and agricultureWaterWater insolublePhenanthreneSensitivity and SpecificityAnalytical Chemistrychemistry.chemical_compoundSolubilityEnvironmental chemistrySpectrophotometrySOLUBILIZATIONmedicinePolycyclic CompoundsSpectrophotometry UltravioletGeneral Environmental ScienceNaphthalene
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