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Friedrich, T.* ; Ilicic, K. ; Greubel, C.* ; Girst, S.* ; Reindl, J.* ; Sammer, M.* ; Schwarz, B.* ; Siebenwirth, C.* ; Walsh, D.W.M.* ; Schmid, T.E. ; Scholz, M.* ; Dollinger, G.*

DNA damage interactions on both nanometer and micrometer scale determine overall cellular damage.

Sci. Rep. 8:16063 (2018)
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Open Access Gold
Creative Commons Lizenzvertrag
DNA double strand breaks (DSB) play a pivotal role for cellular damage, which is a hazard encountered in toxicology and radiation protection, but also exploited e.g. in eradicating tumors in radiation therapy. It is still debated whether and in how far clustering of such DNA lesions leads to an enhanced severity of induced damage. Here we investigate - using focused spots of ionizing radiation as damaging agent - the spatial extension of DNA lesion patterns causing cell inactivation. We find that clustering of DNA damage on both the nm and pm scale leads to enhanced inactivation compared to more homogeneous lesion distributions. A biophysical model interprets these observations in terms of enhanced DSB production and DSB interaction, respectively. We decompose the overall effects quantitatively into contributions from these lesion formation processes, concluding that both processes coexist and need to be considered for determining the resulting damage on the cellular level.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Double-strand Breaks; Lethal Radiation-damage; Repair Pathway Choice; 20 Mev Protons; Track-structure; Human-cells; Irradiation; Chromatin; Complexity; Survival
Language english
Publication Year 2018
HGF-reported in Year 2018
ISSN (print) / ISBN 2045-2322
e-ISSN 2045-2322
Journal Scientific Reports
Quellenangaben Volume: 8, Issue: 1, Pages: , Article Number: 16063 Supplement: ,
Publisher Nature Publishing Group
Publishing Place London
Reviewing status Peer reviewed
Institute(s) Institute of Radiation Medicine (IRM)
POF-Topic(s) 30203 - Molecular Targets and Therapies
Research field(s) Radiation Sciences
PSP Element(s) G-501300-001
DOI 10.1038/s41598-018-34323-9
WOS ID WOS:000448746100002
Scopus ID 85055617211
Erfassungsdatum 2018-11-05
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