A New Standard DNA Damage (SDD) Data Format


J. Schuemann, Massachusetts General Hospital and Harvard Medical School
A. L. McNamara, Massachusetts General Hospital and Harvard Medical School
J. W. Warmenhoven, The University of Manchester
N. T. Henthorn, The University of Manchester
K. J. Kirkby, The University of Manchester
M. J. Merchant, The University of Manchester
S. Ingram, The University of Manchester
H. Paganetti, Massachusetts General Hospital and Harvard Medical School
K. D. Held, Massachusetts General Hospital and Harvard Medical School
J. Ramos-Mendez, University of California San Francisco
B. Faddegon, University of California San Francisco
J. Perl, SLAC National Accelerator Laboratory
D. T. Goodhead, Medical Research Council, Harwell
I. Plante, KBRwyle
H. Rabus, Physikalisch-Technische Bundesanstalt (PTB)
H. Nettelbeck, Physikalisch-Technische Bundesanstalt (PTB)
W. Friedland, European Radiation Dosimetry Group e.V.
P. Kundrát, Institute of Radiation Protection, Helmholtz Zentrum München
A. Ottolenghi, University of Pavia
G. Baiocco, European Radiation Dosimetry Group e.V.
S. Barbieri, European Radiation Dosimetry Group e.V.
M. Dingfelder, East Carolina University
S. Incerti, CNRS, IN2P3, CENBG, UMR 5797, F-33170 Gradignan
C. Villagrasa, European Radiation Dosimetry Group e.V.,
M. Bueno, Institut de Radioprotection et Sûreté Nucléaire, F-92262 Fontenay aux Roses Cedex
M. A. Bernal, State University of Campinas
S. Guatelli, University of Wollongong
D. Sakata, University of Wollongong
J. M. C. Brown, Delft University of Technology
Z. Francis, Saint Joseph University
I. Kyriakou, University of Ioannina Medical School

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Radiation Research





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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 intermodel 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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