Search results for "damage [radiation]"

showing 10 items of 101 documents

CHK1 inhibitor sensitizes resistant colorectal cancer stem cells to nortopsentin

2021

Summary Limited therapeutic options are available for advanced colorectal cancer (CRC). Herein, we report that exposure to a neo-synthetic bis(indolyl)thiazole alkaloid analog, nortopsentin 234 (NORA234), leads to an initial reduction of proliferative and clonogenic potential of CRC sphere cells (CR-CSphCs), followed by an adaptive response selecting the CR-CSphC-resistant compartment. Cells spared by the treatment with NORA234 express high levels of CD44v6, associated with a constitutive activation of Wnt pathway. In CR-CSphC-based organoids, NORA234 causes a genotoxic stress paralleled by G2-M cell cycle arrest and activation of CHK1, driving the DNA damage repair of CR-CSphCs, regardless…

0301 basic medicineCell cycle checkpointColorectal cancerScienceSettore MED/50 - Scienze Tecniche Mediche Applicate02 engineering and technologyGenotoxic StressArticleMolecular Physiology03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALERabusertibmedicineClonogenic assayCancerMultidisciplinarybusiness.industryQWnt signaling pathwayDrugsCancerCell Biology021001 nanoscience & nanotechnologymedicine.disease030104 developmental biologyCancer researchSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioStem cell0210 nano-technologybusinesscolorectal cancer cancer stem cells alkaloids DNA damage repair CHK1.iScience
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RINT1 Loss Impairs Retinogenesis Through TRP53-Mediated Apoptosis

2020

Genomic instability in the central nervous system (CNS) is associated with defective neurodevelopment and neurodegeneration. Congenital human syndromes that affect the CNS development originate from mutations in genes of the DNA damage response (DDR) pathways. RINT1 (Rad50-interacting protein 1) is a partner of RAD50, that participates in the cellular responses to DNA double-strand breaks (DSB). Recently, we showed that Rint1 regulates cell survival in the developing brain and its loss led to premature lethality associated with genomic stability. To bypass the lethality of Rint1 inactivation in the embryonic brain and better understand the roles of RINT1 in CNS development, we conditionally…

0301 basic medicineGenome instabilityDNA damagereplicative stressBiologyDNA damage responseRetinal ganglionganglion cellsCell and Developmental Biology03 medical and health sciences0302 clinical medicinemedicineoptic nerve hypoplasiaProgenitor celllcsh:QH301-705.5Original ResearchNeurogenesisNeurodegenerationneurodegenerationCell BiologyCell cyclemedicine.diseaseNeural stem cellCell biologyneurogenesis030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisvisual system developmentDevelopmental BiologyFrontiers in Cell and Developmental Biology
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
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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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Effects of air pollution particles (ultrafine and fine particulate matter) on mitochondrial function and oxidative stress – Implications for cardiova…

2020

Environmental pollution is a major cause of global mortality and burden of disease. All chemical pollution forms together may be responsible for up to 12 million annual excess deaths as estimated by the Lancet Commission on pollution and health as well as the World Health Organization. Ambient air pollution by particulate matter (PM) and ozone was found to be associated with an all-cause mortality rate of up to 9 million in the year 2015, with the majority being of cerebro- and cardiovascular nature (e.g. stroke and ischemic heart disease). Recent evidence suggests that exposure to airborne particles and gases contributes to and accelerates neurodegenerative diseases. Especially, airborne t…

0301 basic medicinePollutionmedia_common.quotation_subjectBiophysicsAir pollutionEnvironmental pollutionDiseasemedicine.disease_causeBiochemistry03 medical and health sciencesEnvironmental healthMedicineAnimalsHumansEnvironmental risk factorsNeurodegenerationMolecular Biologymedia_commonMitochondrial damage and dysfunctionAir Pollutants030102 biochemistry & molecular biologybusiness.industryMortality rateNeurodegenerationNeurodegenerative DiseasesParticulatesmedicine.diseaseCardiovascular diseaseMitochondriaOxidative Stress030104 developmental biologyCardiovascular DiseasesAmbient air pollution; Cardiovascular disease; Environmental risk factors; Mitochondrial damage and dysfunction; Neurodegeneration; Particulate matter; Air Pollutants; Animals; Cardiovascular Diseases; Humans; Mitochondria; Neurodegenerative Diseases; Oxidative Stress; Particulate MatterParticulate MatterAmbient air pollutionbusinessOxidative stress
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La delimitación del concepto de daño moral: un estudio de la cuestión en el ordenamiento jurídico español.

2021

El presente estudio tiene como objetivo realizar una aproximación al concepto de daño moral en el derecho español porque, a diferencia del daño patrimonial, el Código Civil no proporciona un concepto sobre él. Para la articulación de un concepto de daño moral es necesario analizar los supuestos de reconocimiento legal, la interpretación que los órganos judiciales han hecho y el tratamiento proporcionado en los Principios de derecho contractual europeo y de derecho de daños europeo. El trabajo finaliza con una valoración sobre la actual configuración del daño moral. The present study aims to make an approximation to the concept of non-pecuniary damage in Spanish law because, unlike property …

:CIENCIAS JURÍDICAS [UNESCO]Principios de derecho contractual europeo2070-8157 22082 Revista Boliviana de Derecho 584568 2021 32 8055224 La delimitacion del concepto de daño moral un estudio de la cuestión en el ordenamiento jurídico español Mate SatuéPrincipios de derecho de daños europeoPrinciples of European Tort Law 278 313Principles of European Contract LawCivil Code does not provide a concept about it. For the articulation of a concept of non-pecuniary damageNon-material damageLoreto Carmen The present study aims to make an approximation to the concept of non-pecuniary damage in Spanish law becauseit is necessary to analyze the assumptions of legal recognitionUNESCO::CIENCIAS JURÍDICASDaño moralthe interpretation that the judicial bodies have made and the treatment of non-pecuniary damage in the Principles of European contract law and European tort law. The work ends with an assessment of the current configuration of non-pecuniary damage. Responsabilidad civilunlike property damage
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Hypoxia-Inducible Factor 2α Mutation-Related Paragangliomas Classify as Discrete Pseudohypoxic Subcluster

2016

Contains fulltext : 172720.pdf (Publisher’s version ) (Open Access) Recently, activating mutations of the hypoxia-inducible factor 2alpha gene (HIF2A/EPAS1) have been recognized to predispose to multiple paragangliomas (PGLs) and duodenal somatostatinomas associated with polycythemia, and ocular abnormalities. Previously, mutations in the SDHA/B/C/D, SDHAF2, VHL, FH, PHD1, and PHD2 genes have been associated with HIF activation and the development of pseudohypoxic (cluster-1) PGLs. These tumors overlap in terms of tumor location, syndromic presentation, and noradrenergic phenotype to a certain extent. However, they also differ especially by clinical outcome and by presence of other tumors o…

AdultMale0301 basic medicineOriginal articleCancer ResearchAdolescentMicroarraySDHBSDHABiologylcsh:RC254-282Oxidative PhosphorylationParagangliomaYoung Adult03 medical and health sciences0302 clinical medicineParagangliomaBasic Helix-Loop-Helix Transcription FactorsmedicineJournal ArticleCluster AnalysisHumansChildHypoxiaAgedGeneticsGene Expression ProfilingVascular damage Radboud Institute for Molecular Life Sciences [Radboudumc 16]Middle Agedlcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensmedicine.diseasePhenotypeGene Expression Regulation NeoplasticGene expression profiling030104 developmental biologyHypoxia-inducible factors030220 oncology & carcinogenesisMutationFemaleSDHDTranscriptomeProtein BindingNeoplasia
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Reperfusion therapy for ST elevation acute myocardial infarction 2010/2011:current status in 37 ESC countries

2014

Item does not contain fulltext AIMS: Primary percutaneous coronary intervention (PPCI) is the preferred reperfusion therapy in ST-elevation myocardial infarction (STEMI). We conducted this study to evaluate the contemporary status on the use and type of reperfusion therapy in patients admitted with STEMI in the European Society of Cardiology (ESC) member countries. METHODS AND RESULTS: A cross-sectional descriptive study based on aggregated country-level data on the use of reperfusion therapy in patients admitted with STEMI during 2010 or 2011. Thirty-seven ESC countries were able to provide data from existing national or regional registries. In countries where no such registries exist, dat…

AdultMalemedicine.medical_specialtyCross-sectional studymedicine.medical_treatmentVascular damage Radboud Institute for Health Sciences [Radboudumc 16]PopulationCardiologyMyocardial Infarctionacute myocardial infarction610 Medicine & healthMyocardial ReperfusionPercutaneous Coronary InterventionReperfusion therapyHumansMedicineThrombolytic TherapyIn patientHospital MortalityRegistriescardiovascular diseasesMyocardial infarctioneducationAgededucation.field_of_studybusiness.industryST elevationCoronary Care UnitsPercutaneous coronary interventionThrombolysisMiddle Agedmedicine.disease3. Good healthEuropeCross-Sectional Studiessurgical procedures operativeEmergency medicineWorkforceFemaleHuman medicineMedical emergencyCardiology and Cardiovascular Medicinebusiness
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Angiotensin Receptor Neprilysin Inhibition Compared With Enalapril on the Risk of Clinical Progression in Surviving Patients With Heart Failure

2015

Background— Clinical trials in heart failure have focused on the improvement in symptoms or decreases in the risk of death and other cardiovascular events. Little is known about the effect of drugs on the risk of clinical deterioration in surviving patients. Methods and Results— We compared the angiotensin-neprilysin inhibitor LCZ696 (400 mg daily) with the angiotensin-converting enzyme inhibitor enalapril (20 mg daily) in 8399 patients with heart failure and reduced ejection fraction in a double-blind trial. The analyses focused on prespecified measures of nonfatal clinical deterioration. In comparison with the enalapril group, fewer LCZ696-treated patients required intensification of med…

Angiotensin receptorVascular damage Radboud Institute for Health Sciences [Radboudumc 16]receptorsTetrazolesheart failureAngiotensin-Converting Enzyme InhibitorsKaplan-Meier EstimateSacubitrilAngiotensin; Heart failure; Neprilysin; Receptors; Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Biomarkers; Double-Blind Method; Enalapril; Heart Failure; Humans; Kaplan-Meier Estimate; Natriuretic Peptide Brain; Neprilysin; Peptide Fragments; Risk Factors; Stroke Volume; Survivors; Tetrazoles; Treatment Outcome; Troponin; Disease Progression; Medicine (all); Cardiology and Cardiovascular Medicine; Physiology (medical)AngiotensinEnalaprilRisk FactorsEnalapril/therapeutic useNatriuretic Peptide BrainHeart Failure/bloodSurvivorsReceptorNeprilysinAminobutyrates: Systèmes cardiovasculaire & respiratoire [D03] [Sciences de la santé humaine]Troponin/bloodTroponinAngiotensin Receptor Antagonists/therapeutic useDrug CombinationsAngiotensin-Converting Enzyme Inhibitors/therapeutic useTreatment OutcomeTetrazoles/therapeutic useCardiologyDisease ProgressionValsartanNeprilysinHeart Failure/blood/drug therapy/physiopathologyCardiology and Cardiovascular Medicinemedicine.drugReceptormedicine.medical_specialtyHeart failureneprilysinAngiotensin Receptor Antagonistsreceptors angiotensinDouble-Blind MethodPhysiology (medical)Internal medicineRenin–angiotensin systemmedicineHumansheart failure neprilysin receptors angiotensinEnalaprilbusiness.industryBiphenyl CompoundsStroke Volumemedicine.diseasePeptide FragmentsEndocrinologyAminobutyrates/therapeutic useStroke Volume/physiologyHeart failureNatriuretic Peptide Brain/blood: Cardiovascular & respiratory systems [D03] [Human health sciences]businessNeprilysin/antagonists & inhibitorsPeptide Fragments/bloodSacubitril ValsartanBiomarkersBiomarkers/blood
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