Titre :

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

Auteur(s) :

Sarma, Parvathy [Auteur]
Physique - IEMN [PHYSIQUE - IEMN]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Abbadie, Corinne [Auteur]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
De Launoit, Yvan [Auteur]
Hétérogénéité, Plasticité et Résistance aux Thérapies des Cancers = Cancer Heterogeneity, Plasticity and Resistance to Therapies - UMR 9020 - U 1277 [CANTHER]
Cleri, Fabrizio [Auteur]
Physique - IEMN [PHYSIQUE - IEMN]
Institut d’Électronique, de Microélectronique et de Nanotechnologie - UMR 8520 [IEMN]

Mot(s)-clé(s) en anglais :

Radiation-induced stress
Cell senescence DNA damage Radiotherapy DNA repair pathways Base-excision repair Single-strand breaks Radiation-induced stress
Cell senescence
DNA damage
Radiotherapy
DNA repair pathways
Base-excision repair
Single-strand breaks

Discipline(s) HAL :

Physique [physics]
Sciences du Vivant [q-bio]

Résumé en anglais : [en]

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 ...
Lire la suite >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.Lire moins >

Langue :

Anglais

Commentaire :

Article non encore soumis

Collections :

• Cancer Heterogeneity, Plasticity and Resistance to Therapies (CANTHER) - UMR 9020 - UMR 1277

Source :

Harvested from HAL