Ability to repair DNA double-strand breaks related to cancer susceptibility and radiosensitivity

被引：54

作者：

Sakata K.-I. ^{[1
]}

Someya M. ^{[1
]}

Matsumoto Y. ^{[2
]}

Hareyama M. ^{[1
]}

机构：

[1] Department of Radiology, Sapporo Medical University School of Medicine, Chuo-ku, Sapporo 060-8543, West 16

[2] Tokyo Institute of Technology, Research Laboratory for Nuclear Reactors, Tokyo

来源：

Radiation Medicine | 2007年 / 25卷 / 9期

关键词：

Cancer susceptibility; DNA double-strand break; DNA-PK; NBS1; focus; Nonhomologous end joining;

D O I：

10.1007/s11604-007-0161-3

中图分类号：

学科分类号：

摘要：

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. © 2007 Japan Radiological Society.

引用

页码：433 / 438

页数：5

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