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Title: A New Standard DNA Damage (SDD) Data Format

Abstract

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.more » 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 significantly 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.« less

Authors:
 [1];  [1];  [2];  [2];  [2];  [2];  [2];  [1];  [1];  [3];  [3];  [4];  [5];  [6];  [7];  [7];  [8];  [9];  [10];  [8] more »;  [8];  [11];  [12];  [8];  [13];  [14];  [15];  [15];  [16];  [17];  [18];  [12];  [10];  [10];  [19];  [19];  [20];  [21];  [22];  [23];  [24];  [25];  [26];  [27];  [28];  [29];  [28];  [30];  [31];  [9];  [32];  [33];  [34];  [35];  [35] « less
  1. Massachusetts General Hospital and Harvard Medical School, Boston, MA (United States)
  2. Univ. of Manchester (United Kingdom)
  3. Univ. of California, San Francisco, CA (United States)
  4. SLAC National Accelerator Lab., Menlo Park, CA (United States)
  5. Medical Research Council, Harwell (United Kingdom)
  6. KBRwyle, Houston, TX (United States)
  7. Physikalisch-Technische Bundesanstalt (PTB), Braunschweig (Germany)
  8. European Radiation Dosimetry Group, Neuherberg (Germany)
  9. Helmholtz Zentrum München-German Research Center for Environmental Health, Neuherberg (Germany)
  10. Univ. of Pavia (Italy)
  11. East Carolina Univ., Greenville, NC (United States)
  12. French National Centre for Scientific Research (CNRS), Gradignan (France)
  13. Institute of Radiation Protection and Safety (IRSN), Fontenay-aux-Roses (France)
  14. State Univ. of Campinas, Campinas, SP (Brazil)
  15. Univ. of Wollongong, Wollongong, NSW (Australia)
  16. Delft Univ. of Technology (Netherlands)
  17. Saint Joseph Univ., Beirut (Lebanon)
  18. Univ. of Ioannina Medical School (Greece)
  19. Nuclear Physics Inst. of the CAS, Řež (Czech Republic)
  20. Univ. of Texas Southwestern Medical Center, Dallas, TX (United States)
  21. Univ. of Nevada, Las Vegas, NV (United States)
  22. Loma Linda Univ., CA (United States)
  23. Univ. of Washington, Seattle, WA (United States)
  24. Yale Univ. School of Medicine, New Haven, CT (United States)
  25. National Physical Lab., Teddington (United Kingdom)
  26. School of Physics, University of Sydney, Sydney, NSW, Australia
  27. Institut des Sciences Moléculaires d'Orsay (UMR 8214) University Paris-Sud, CNRS, University Paris-Saclay, 91405 Orsay Cedex, France
  28. Retired
  29. Univ. of Texas MD Anderson Cancer Center, Houston, TX (United States)
  30. National Inst. of Radiological Sciences, Chiba (Japan)
  31. Japan Atomic Energy Agency (JAEA), Tokai (Japan)
  32. MBN Research Center, Frankfurt am Main (Germany)
  33. Oakland Univ., Rochester, MI (United States)
  34. GSI Helmholtzzentrum für Schwerionenforschung, Darmstadt (Germany)
  35. Queens Univ., Belfast (United Kingdom)
Publication Date:
Research Org.:
SLAC National Accelerator Lab., Menlo Park, CA (United States)
Sponsoring Org.:
USDOE; National Institutes of Health (NIH)
OSTI Identifier:
1529498
Grant/Contract Number:  
AC02-76SF00515
Resource Type:
Accepted Manuscript
Journal Name:
Radiation Research
Additional Journal Information:
Journal Volume: 191; Journal Issue: 1; Journal ID: ISSN 0033-7587
Publisher:
Radiation Research Society
Country of Publication:
United States
Language:
English

Citation Formats

Schuemann, J., McNamara, A. L., Warmenhoven, J. W., Henthorn, N. T., Kirkby, K. J., Merchant, Michael 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., Kundrát, 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., Davídková, M., Štěpán, 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., and McMahon, Stephen J. A New Standard DNA Damage (SDD) Data Format. United States: N. p., 2018. Web. doi:10.1667/RR15209.1.
Schuemann, J., McNamara, A. L., Warmenhoven, J. W., Henthorn, N. T., Kirkby, K. J., Merchant, Michael 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., Kundrát, 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., Davídková, M., Štěpán, 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, Stephen J. A New Standard DNA Damage (SDD) Data Format. United States. doi:10.1667/RR15209.1.
Schuemann, J., McNamara, A. L., Warmenhoven, J. W., Henthorn, N. T., Kirkby, K. J., Merchant, Michael 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., Kundrát, 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., Davídková, M., Štěpán, 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., and McMahon, Stephen J. Thu . "A New Standard DNA Damage (SDD) Data Format". United States. doi:10.1667/RR15209.1. https://www.osti.gov/servlets/purl/1529498.
@article{osti_1529498,
title = {A New Standard DNA Damage (SDD) Data Format},
author = {Schuemann, J. and McNamara, A. L. and Warmenhoven, J. W. and Henthorn, N. T. and Kirkby, K. J. and Merchant, Michael J. and Ingram, S. and Paganetti, H. and Held, K. D. and Ramos-Mendez, J. and Faddegon, B. and Perl, J. and Goodhead, D. T. and Plante, I. and Rabus, H. and Nettelbeck, H. and Friedland, W. and Kundrát, P. and Ottolenghi, A. and Baiocco, G. and Barbieri, S. and Dingfelder, M. and Incerti, S. and Villagrasa, C. and Bueno, M. and Bernal, M. A. and Guatelli, S. and Sakata, D. and Brown, J. M. C. and Francis, Z. and Kyriakou, I. and Lampe, N. and Ballarini, F. and Carante, M. P. and Davídková, M. and Štěpán, V. and Jia, X. and Cucinotta, F. A. and Schulte, R. and Stewart, R. D. and Carlson, D. J. and Galer, S. and Kuncic, Z. and Lacombe, S. and Milligan, J. and Cho, S. H. and Sawakuchi, G. and Inaniwa, T. and Sato, T. and Li, W. and Solov'yov, A. V. and Surdutovich, E. and Durante, M. and Prise, K. M. and McMahon, Stephen J.},
abstractNote = {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 significantly 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.},
doi = {10.1667/RR15209.1},
journal = {Radiation Research},
number = 1,
volume = 191,
place = {United States},
year = {2018},
month = {11}
}

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