Ability to repair DNA double-strand breaks related to cancer susceptibility and radiosensitivity |
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Authors: | Sakata Koh-Ichi Someya Masanori Matsumoto Yoshihisa Hareyama Masato |
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Institution: | (1) Department of Radiology, Sapporo Medical University School of Medicine, West 16, North 1, Chuo-ku, Sapporo 060-8543, Japan;(2) Tokyo Institute of Technology, Research Laboratory for Nuclear Reactors, Tokyo, Japan |
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Abstract: | Traditional radiobiology has aimed at elucidating the mechanism of radiosensitivity of cancer cells and normal cells. Because
the mechanism of DNA double-strand break (DSB) repair, which is inherently important to radiosensitivity, was unknown, it
has been difficult to obtain results applicable to clinical radiotherapy from traditional radiobiology research. Today, however,
the molecular mechanism of DNA DSB repair has been elucidated because of the rapid advances in molecular biology. In DNA DSB
repair, at least two major repair mechanisms, homologous recombination and nonhomologous end joining (NHEJ) have been reported.
In the NHEJ pathway, DSBs are directly, or after processing of the DNA ends, rejoined at an appropriate chromosomal end. DNA-dependent
protein kinase (DNA-PK) plays an important role in DNA DSB repair by NHEJ. We have investigated how the ability of repair
of DNA DSB influences cancer susceptibility and the radiosensitivity of tumors and normal tissues by focusing on the activity
of DNA-PK. In the near future, research on DNA DSB repair mechanism will be able to be applied to research on carcinogenesis,
prediction of radiosensitivity of tumors and normal cells, and sensitization of tumor cells. |
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Keywords: | DNA double-strand break DNA-PK Nonhomologous end joining Cancer susceptibility NBS1 focus |
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