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Synchrotron Photoactivation of Cisplatin Elicits an Extra Number of DNA Breaks That Stimulate RAD51-mediated Repair Pathways¹

Equipe d’Accueil 2941 Rayonnement Synchrotron et Recherche Médicale, Unité IRM [S. C., J. B., H. E., A. J., M-C. B., J-F. A., A-M. C., J-F. L., F. E., N. F.], Département de Cancérologie et d’Hématologie [J. B.], and INSERM IFR 1 [H. E.], CHU A. Michallon, BP 217, F-38043 Grenoble cedex 09, France; European Synchrotron Radiation Facility, BP 220, F-38043 Grenoble, France [M. R., T. B.]; and Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton, BN19RQ, United Kingdom [N. F.]

Combination of cis-platinum with ionizing radiation is one of the most promising anticancer treatments that appears to be more efficient than radiotherapy alone. Unlike conventional X-ray emitters, accelerators of high energy particles like synchrotrons display powerful and monochromatizable radiation that makes the induction of an Auger electron cascade in cis-platinum molecules [also called photoactivation of cis-platinum (PAT-Plat)] theoretically possible. Here, we examined the molecular consequences of one of the first attempts of synchrotron PAT-Plat, performed at the European Synchrotron Research Facility (Grenoble-France). PAT-Plat was found to result in an extra number of slowly repairable DNA double-strand breaks, inhibition of DNA-protein kinase activity, dramatic nuclear relocalization of RAD51, hyperphosphorylation of the BRCA1 protein, and activation of proto-oncogenic c-Abl tyrosine kinase.

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