Jan Schuemann, Harvard University
A L. McNamara, Harvard University
J Warmenhoven, University of Manchester
N Henthorn, University of Manchester
K Kirkby, University of Manchester
M Merchant, University of Manchester
S Ingram, University of Manchester
Harald Paganetti, Harvard UniversityFollow
Kathryn D. Held, Harvard University
J Ramos-Mendez, University of California
B Faddegon, University of California
J Perl, Slac
D Goodhead, Medical Research Council
I Plante, KBRWyle
Hans Rabus, Physikalisch-Technische Bundesanstalt GermanyFollow
Heidi Nettelbeck, Physikalisch-Technische BundesanstaltFollow
W Friedland, Helmholtz Zentrum Munchen, GmbH
P Kundrat, Helmholtz Zentrum Munchen, GmbH
A Ottolenghi, University of Pavia
G Baiocco, University of Pavia
S Barbieri, University of Pavia
M Dingfelder, East Carolina University
Sebastien Incerti, University of BordeauxFollow
Carmen Villagrasa, IRSN
M Bueno, IRSN
M A. Bernal, Universidade Estadual de Campinas
Susanna Guatelli, University of WollongongFollow
Dosatsu Sakata, University of BordeauxFollow
J Brown, Delft University of Technology
Z Francis, Universite Saint Joseph
Ioanna Kyriakou, University of Ioannina Medical School
N Lampe, CNRS
F Ballarini, University of Pavia
M Carante, University of Pavia
M Davidkova, Nuclear Physics Institute ACSR
V Stepan, Nuclear Physics Institute ACSR
X Jia, University of Texas
F. Cucinotta, University of Nevada
Reinhard W. Schulte, Loma Linda UniversityFollow
R Stewart, University of Washington
David Carlson, Yale University
S Galer, National Physical Laboratory
Zdenka Kuncic, University of SydneyFollow
S Lacombe, CNRS Centre National de la Recherche Scientifique
J Milligan
S Cho, University of Texas
G Sawakuchi, University of Texas
T Inaniwa, National Institute Of Radiological Sciences
T Sato, Japan Atomic Energy Agency
W Li, Helmholtz Zentrum Munchen, GmbH
Audrey V. Solov'Yov, Frankfurt Institute for Advanced Studies
Eugene Surdutovich, Oakland University
M Durante, GSI Helmholtz Center for Heavy Ion Research
Kevin M. Prise, Queen's University Belfast
Stephen J. McMahon, Queen's University Belfast



Publication Details

Schuemann, J., McNamara, A. L., Warmenhoven, J. W., Henthorn, N. T., Kirkby, K. J., Merchant, M. J., Ingram, S., Paganetti, H., Held, K. D., Ramos-Mendez, J., Faddegon, B., Perl, J., Goodhead, D. T., Plante, I., Rabus, H., Nettelbeck, H., Friedland, W., Kundrat, P., Ottolenghi, A., Baiocco, G., Barbieri, S., Dingfelder, M., Incerti, S., Villagrasa, C., Bueno, M., Bernal, M. A., Guatelli, S., Sakata, D., Brown, J. M. C., Francis, Z., Kyriakou, I., Lampe, N., Ballarini, F., Carante, M. P., Davidkova, M., Stepan, V., Jia, X., Cucinotta, F. A., Schulte, R., Stewart, R. D., Carlson, D. J., Galer, S., Kuncic, Z., Lacombe, S., Milligan, J., Cho, S. H., Sawakuchi, G., Inaniwa, T., Sato, T., Li, W., Solov'yov, A. V., Surdutovich, E., Durante, M., Prise, K. M. & McMahon, S. J. (2019). A New Standard DNA Damage (SDD) Data Format. Radiation Research, 191 (1), 76-92.


Our understanding of radiation-induced cellular damage has greatly improved over the past few decades. Despite this progress, there are still many obstacles to fully understand how radiation interacts with biologically relevant cellular components, such as DNA, to cause observable end points such as cell killing. Damage in DNA is identified as a major route of cell killing. One hurdle when modeling biological effects is the difficulty in directly comparing results generated by members of different research groups. Multiple Monte Carlo codes have been developed to simulate damage induction at the DNA scale, while at the same time various groups have developed models that describe DNA repair processes with varying levels of detail. These repair models are intrinsically linked to the damage model employed in their development, making it difficult to disentangle systematic effects in either part of the modeling chain. These modeling chains typically consist of track-structure Monte Carlo simulations of the physical interactions creating direct damages to DNA, followed by simulations of the production and initial reactions of chemical species causing so-called "indirect" damages. After the induction of DNA damage, DNA repair models combine the simulated damage patterns with biological models to determine the biological consequences of the damage. To date, the effect of the environment, such as molecular oxygen (normoxic vs. hypoxic), has been poorly considered. We propose a new standard DNA damage (SDD) data format to unify the interface between the simulation of damage induction in DNA and the biological modeling of DNA repair processes, and introduce the effect of the environment (molecular oxygen or other compounds) as a flexible parameter. Such a standard greatly facilitates inter-model comparisons, providing an ideal environment to tease out model assumptions and identify persistent, underlying mechanisms. Through inter-model comparisons, this unified standard has the potential to greatly advance our understanding of the underlying mechanisms of radiation-induced DNA damage and the resulting observable biological effects when radiation parameters and/or environmental conditions change.



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