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Author Notes:

Correspondence to: Ya Wang, MD, PhD, Department of Radiation Oncology, Emory University School of Medicine, 1365 Clifton Rd NE Suite 5090, Atlanta, GA 30322, USA, Tel: (404) 778-1832, Fax: (404) 778-1750, ywang94@emory.edu. Lihua Dong, MD, Department of Radiation Oncology, The First Hospital, Jilin University, 71 Xinmin Street, Changchun, 130021, China, Tel: 011 86 431-8878-2468, Fax: 011 86 431-8878-6172, drlhdong@163.com

We thank Ms. Doreen Theune for editing the manuscript.

The authors report no conflict of interest.

The authors alone are responsible for the contents and writing of the paper.

Subjects:

Research Funding:

This work is supported by grants from the National Aeronautics and Space Administration (NNX11AC30G to Y.W.) and the National Cancer Institute (CA186129, CA185882, to Y.W. and P30CA138292 to the Institute).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Technology
  • Biology
  • Nuclear Science & Technology
  • Radiology, Nuclear Medicine & Medical Imaging
  • Life Sciences & Biomedicine - Other Topics
  • DNA double strand break (DSB)
  • DNA repair
  • homologous recombination repair (HRR)
  • ionizing radiation
  • non-homologous end-joining (NHEJ)
  • sublethal damage repair (SLDR)
  • potentially lethal damage repair (PLDR)
  • heavy ion
  • POTENTIALLY LETHAL DAMAGE
  • DEPENDENT PROTEIN-KINASE
  • STRAND BREAK REPAIR
  • HUMAN-TUMOR CELLS
  • HOMOLOGOUS RECOMBINATION
  • MAMMALIAN-CELLS
  • SUBLETHAL DAMAGE
  • RADIATION
  • CONTRIBUTES
  • SENSITIVITY

DNA repair pathway choice at various conditions immediately post irradiation

Tools:

Journal Title:

International Journal of Radiation Biology

Volume:

Volume 92, Number 12

Publisher:

, Pages 819-822

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Purpose: To clarify which DNA double-strand break repair pathway, non-homologous end-joining (NHEJ), homologous recombination repair (HRR) or both, plays a key role in potentially lethal damage repair (PLDR). Methods and materials: Combining published data and our new potentially lethal damage repair (PLDR) data, we explain whether similar to sublethal damage repair (SLDR), PLDR also mainly depends on NHEJ versus HRR. The PLDR data used the same cell lines: wild type, HRR or NHEJ-deficient fibroblast cells, as those SLDR data published by our laboratory previously. The PLDR condition that we used was as commonly described by many other groups: the cells were collected immediately or overnight post ionizing radiation for colony formation after cultured to a plateau phase with a low concentration of serum medium. Results: Enough data from other groups and our lab showed that wild type or HRR-deficient cells had efficient PLDR, but NHEJ deficient cells did not. Conclusion: NHEJ contributes more to PLDR than HRR in mammalian cells, which is similar to SLDR. Since both SLDR and PLDR are relevant to clinical tumor status while undergoing radiotherapy, such clarification may benefit radiotherapy in the near future.

Copyright information:

© 2016 Informa UK Limited, trading as Taylor & Francis Group.

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