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Cell senescence and the DNA single-strand break damage repair pathway

Title: Cell senescence and the DNA single-strand break damage repair pathway
Authors: Sarma, Parvathy, A; Abbadie, Corinne; de Launoit, Yvan; Cleri, Fabrizio
Contributors: Physique - IEMN (PHYSIQUE - IEMN); Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 (IEMN); Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA); Université catholique de Lille (UCL)-Université catholique de Lille (UCL)-Centrale Lille-Université de Lille-Centre National de la Recherche Scientifique (CNRS)-Université Polytechnique Hauts-de-France (UPHF)-JUNIA (JUNIA); Université catholique de Lille (UCL)-Université catholique de Lille (UCL); Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 (CANTHER); Institut Pasteur de Lille; Pasteur Network (Réseau International des Instituts Pasteur)-Pasteur Network (Réseau International des Instituts Pasteur)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire CHU Lille (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS); Projet PEARL Université de Lille "SENESIMEX" Experiments and simulations of radiation-induced cell senescence"
Source: https://hal.science/hal-04759695 ; 2024.
Publisher Information: CCSD
Publication Year: 2024
Collection: LillOA (HAL Lille Open Archive, Université de Lille)
Subject Terms: DNA damage; Radiotherapy; DNA repair pathways; Base-excision repair; Single-strand breaks; Radiation-induced stress; Cell senescence; Cell senescence DNA damage Radiotherapy DNA repair pathways Base-excision repair Single-strand breaks Radiation-induced stress; [PHYS]Physics [physics]; [SDV]Life Sciences [q-bio]
Description: Article non encore soumis ; Cellular senescence is a response to endogenous and exogenous stresses, including telomere dysfunction, oncogene activation and persistent DNA damage. In particular, radiation damage induces oxidative base damage and bond breaking in the DNA double-helix structure, which are treated by dedicated enzymatic repair pathways. In this review we discuss the correlation between senescence and the accumulation of non-repaired single-strand breaks, as it could occur during radiation therapy treatments. Recent experiments of cell irradiation in vitro by high-energy photons showed that single-strand breaks may be preferentially produced at the borders of the irradiated region, thereby inducing senescence, in competition with the apoptosis end-point typically induced by double-strand breaks. Such a peculiar response to radiation damage has been proposed as a possible source of radiation-induced second primary cancers, when such cells with accumulated, non-repaired single-strand breaks evade the senescent state at much later times. The peculiarities of strand-break repair pathways are highlighted, also in relation with the base-excision pathway that repairs several different DNA oxidation defects.
Document Type: report
Language: English
Availability: https://hal.science/hal-04759695; https://hal.science/hal-04759695v1/document; https://hal.science/hal-04759695v1/file/senescence_DNA.pdf
Rights: https://creativecommons.org/licenses/by-nd/4.0/ ; info:eu-repo/semantics/OpenAccess
Accession Number: edsbas.A9A3BD03
Database: BASE