Search results for "MUTATIONS"

showing 10 items of 205 documents

Corps individuels, corps social : Nexus, le "roman à thèse" posthumain de Ramez Naam ?

2015

International audience; Cet article analyse comment la dissolution des frontières entre l'homme et la machine, mais aussi entre l'humain et le posthuman, se manifeste dans "Nexus", le premier volet de la trilogie de science-fiction de Ramez Naam, et comment celui-ci adapte son écriture à son propos. Cet ouvrage est lu, à la lumière des essais de Naam, comme un "roman à thèse" qui redéfinit humain et posthumain, en particulier grâce à des stratégies narratives innovantes.

[SHS.LITT] Humanities and Social Sciences/Literatureposthumain[SHS.LITT]Humanities and Social Sciences/Literaturetranshumain[ SHS.LITT ] Humanities and Social Sciences/LiteraturemutationsNaamNexus
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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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GSK-3 as potential target for therapeutic intervention in cancer

2014

// James A. McCubrey 1 , Linda S. Steelman 1 , Fred E. Bertrand 2 , Nicole M. Davis 1 , Melissa Sokolosky 1 , Steve L. Abrams 1 , Giuseppe Montalto 3 , Antonino B. D’Assoro 4 , Massimo Libra 5 , Ferdinando Nicoletti 5 , Roberta Maestro 6 , Jorg Basecke 7,8 , Dariusz Rakus 9 , Agnieszka Gizak 9 Zoya Demidenko 10 , Lucio Cocco 11 , Alberto M. Martelli 11 and Melchiorre Cervello 12 1 Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University Greenville, NC, USA 2 Department of Oncology, Brody School of Medicine at East Carolina University Greenville, NC, USA 3 Biomedical Department of Internal Medicine and Specialties, University of Palermo, Palermo, Italy …

cancer stem cellsNotchmedicine.medical_treatmentReviewmacromolecular substancesPI3KTargeted therapyGlycogen Synthase Kinase 3GSK-3Cancer stem cellNeoplasmsmedicinePTENAnimalsHumansRapamycinProtein kinase BPI3K/AKT/mTOR pathwayGSK-3; cancer stem cells; Wnt/beta-catenin; PI3K; Akt; mTOR; Hedgehog; Notch; Targeted Therapy; Therapy Resistance; Mutations RapamycinGSK-3Roswell Park Cancer InstitutebiologyAkt; Cancer stem cells; GSK-3; Hedgehog; MTOR; Mutations; Notch; PI3K; Rapamycin; Targeted therapy; Therapy resistance; Wnt/beta-cateninAnimalAktWnt/beta-cateninCancerTargeted TherapyTherapy Resistancemedicine.disease3. Good healthOncologybiology.proteinCancer researchmTORHedgehogMutationsHuman
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Body Weight, Physical Activity, and Risk of Cancer in Lynch Syndrome

2021

Simple Summary Lifestyle modifies cancer risk in the general public. How lifestyle modifies cancer risk in individuals carrying the inherited pathogenic gene variants in DNA mismatch repair genes (Lynch syndrome) remains understudied. We conducted a retrospective study with cancer register data to investigate associations between body weight, physical activity, and cancer risk among Finnish Lynch syndrome carriers (n = 465, 54% women). The results of our study indicated that longitudinal weight gain increases cancer risk, whereas being highly physically active during adulthood could decrease cancer risk in men. Further, women were observed to be less prone to lifestyle-related risk factors …

elintavatperinnölliset tauditMENOPAUSElifestyleMUTATIONS3122 Cancershereditary non-polyposis colorectal cancerylipainoEXERCISEsuolistosyövätriskitekijätlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282ArticleCOLORECTAL-CANCERESTROGENADIPOSE-TISSUEMASS INDEXAGEDEFINED FAMILIAL RISKepidemiologyepidemiologiaLynchin oireyhtymäfyysinen aktiivisuusASSOCIATIONSCancers
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Dynamics and toxicity of proteins with a high homology of sequences: approach by molecular dynamics and ab-initio calculations

2008

The elucidation of the structure and the biological function of proteins is a major stake for its implications in the biomedical research as well as in biotechnologies. In addition, there is a glass or dynamical transition for the proteins which occurs at around 200K: it has been observed by Neutron Scattering, X-ray diffraction and Mossbauer spectroscopy for different proteins. Above the transition temperature, the biological function is activated as the protein may diffuse between conformational sub-states. The microscopic origin of this transition is still debated in spite of significant advances in recent years showing the significant role of hydration. By using all-atoms classical mole…

flexibilitédynamical transitiontransition dynamiquetoxicitymutationsmolecular dynamicsproteinsflexibilityDynamique moléculaireprotéinestoxicitéthioninesstructure[PHYS.COND]Physics [physics]/Condensed Matter [cond-mat]thionins[ PHYS.COND ] Physics [physics]/Condensed Matter [cond-mat][PHYS.COND] Physics [physics]/Condensed Matter [cond-mat]
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Rencontres du Clos-Vougeot 2012 - Crises, mutations, innovations : le devenir du monde vitivinicole

2013

International audience

innovations[SHS.PHIL] Humanities and Social Sciences/Philosophy[ SHS.PHIL ] Humanities and Social Sciences/PhilosophyClos-VougeotCrisesRencontresmonde vitivinicoledevenir[SHS.PHIL]Humanities and Social Sciences/PhilosophymutationsComputingMilieux_MISCELLANEOUS
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Colorectal cancer incidences in Lynch syndrome: a comparison of results from the prospective lynch syndrome database and the international mismatch r…

2022

Abstract Objective To compare colorectal cancer (CRC) incidences in carriers of pathogenic variants of the MMR genes in the PLSD and IMRC cohorts, of which only the former included mandatory colonoscopy surveillance for all participants. Methods CRC incidences were calculated in an intervention group comprising a cohort of confirmed carriers of pathogenic or likely pathogenic variants in mismatch repair genes (path_MMR) followed prospectively by the Prospective Lynch Syndrome Database (PLSD). All had colonoscopy surveillance, with polypectomy when polyps were identified. Comparison was made with a retrospective cohort reported by the International Mismatch Repair Consortium (IMRC). This com…

koloskopiaEuropean Hereditary Tumour Group (EHTG) and the International Mismatch Repair Consortium (IMRC)Epidemiology3122 Cancersehkäisycolorectal cancerPenetrancesegregaatioläpäisevyyssuolistosyövätGUIDELINESover-diagnosisSDG 3 - Good Health and Well-beingpreventionTumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14]1112 Oncology and CarcinogenesisOncology & CarcinogenesispenetranceLynchin oireyhtymäEpidemiologiaSegregation analysisOver-diagnosiGenetics (clinical)segregation analysisScience & TechnologyIncidencePreventionColonoscòpiaGERMLINE MUTATIONSColonoscopyprospectiveCARRIERSColorectal cancer3142 Public health care science environmental and occupational healthProspectiveLynch syndromeOncologyLynch SyndromeOver-diagnosisincidence/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingCLINICAL MANAGEMENTilmaantuvuusLife Sciences & Biomedicine
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Neoantigens Generated by Individual Mutations and Their Role in Cancer Immunity and Immunotherapy

2017

Recent preclinical and clinical studies have proved the long-standing hypothesis that tumors elicit adaptive immune responses and that the antigens driving effective T-cell response are neoantigens, i.e., peptides that are generated from somatically mutated genes. Hence, the characterization of neoantigens and the identification of the immunogenic ones are of utmost importance for improving cancer immunotherapy and broadening its efficacy to a larger fraction of patients. In this review, we first introduce the methods used for the quantification of neoantigens using next-generation sequencing data and then summarize results obtained using these tools to characterize the neoantigen landscape…

lcsh:Immunologic diseases. Allergyimmunoeditingintegumentary systemImmunologytumor heterogeneityImmunology and Allergysomatic mutationsnext-generation sequencingReviewlcsh:RC581-607cancer vaccinesFrontiers in Immunology
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Mutant HRAS as novel target for MEK and mTOR inhibitors.

2015

HRAS is a frequently mutated oncogene in cancer. However, mutant HRAS as drug target has not been investigated so far. Here, we show that mutant HRAS hyperactivates the RAS and the mTOR pathway in various cancer cell lines including lung, bladder and esophageal cancer. HRAS mutation sensitized toward growth inhibition by the MEK inhibitors AZD6244, MEK162 and PD0325901. Further, we found that MEK inhibitors induce apoptosis in mutant HRAS cell lines but not in cell lines lacking RAS mutations. In addition, knockdown of HRAS by siRNA blocked cell growth in mutant HRAS cell lines. Inhibition of the PI3K pathway alone or in combination with MEK inhibitors did not alter signaling nor had an imp…

mTOR inhibitorMutantBlotting Western610 Medicine & healthApoptosisMice SCIDCell LineProto-Oncogene Proteins p21(ras)chemistry.chemical_compoundCell Line TumorNeoplasmsMedicineAnimalsHumansHRASHRAS mutationsProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationGeneticsMitogen-Activated Protein Kinase KinasesMEK inhibitorOncogeneCell growthbusiness.industryMEK inhibitorTOR Serine-Threonine KinasesDiphenylamineXenograft Model Antitumor AssaysTumor Burdenlung cancer10219 Clinic for Gastroenterology and HepatologyCell Transformation NeoplasticOncologychemistry10032 Clinic for Oncology and HematologyBenzamidesMutationCancer researchbladder cancer2730 OncologyBenzimidazolesRNA InterferenceSignal transductionGrowth inhibitionbusinessSignal TransductionResearch PaperOncotarget
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New loci associated with kidney function and chronic kidney disease

2010

Chronic kidney disease (CKD) is a significant public health problem, and recent genetic studies have identified common CKD susceptibility variants. The CKDGen consortium performed a meta-analysis of genome-wide association data in 67,093 individuals of European ancestry from 20 predominantly population-based studies in order to identify new susceptibility loci for reduced renal function as estimated by serum creatinine (eGFRcrea), serum cystatin c (eGFRcys) and CKD (eGFRcrea 60 ml/min/1.73 m 2; n = 5,807 individuals with CKD (cases)). Follow-up of the 23 new genome-wide-significant loci (P 5 × 10 8) in 22,982 replication samples identified 13 new loci affecting renal function and CKD (in or…

medicine.medical_specialtyGENOME-WIDE ASSOCIATION ; SERUM CREATININE ; PROTEIN ; GENE ; MUTATIONS ; VARIANTS ; POPULATION ; CANDIDATE ; HOMOLOG ; MEGALINPopulationRenal functionGenome-wide association studyBiologyKidneyurologic and male genital diseasesCohort Studieschemistry.chemical_compoundSDG 3 - Good Health and Well-beingRisk FactorsInternal medicineGenetic MarkermedicineGeneticsHumansCystatin CeducationCystatin C/geneticsddc:616Genetic Markers/geneticsCreatinineKidneyeducation.field_of_studyModels GeneticRisk Factorchronic kidney disease; loci; SNPCreatinine/bloodmedicine.diseaseDietEuropeKidney/*physiologyEndocrinologymedicine.anatomical_structurechemistryCystatin CRenal physiologyCreatininebiology.proteinKidney Failure ChronicKidney Failure Chronic/ethnology/*geneticsCohort StudieKidney diseaseHumanGenome-Wide Association StudyGlomerular Filtration Rate
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