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The mechanism of high biological effectiveness induced by accelerated heavy ions
https://repo.qst.go.jp/records/63159
https://repo.qst.go.jp/records/63159cc53a3d0-528b-4c59-99d0-93096951dd8b
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2009-07-15 | |||||
| タイトル | ||||||
| タイトル | The mechanism of high biological effectiveness induced by accelerated heavy ions | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
| 資源タイプ | conference object | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 著者 |
Okayasu, Ryuichi
× Okayasu, Ryuichi× Kato, Takamitsu× Fujimori, Akira× Noguchi, Miho× Fujii, Yoshihiro× Seo, Kentaro× 岡安 隆一× 加藤 宝光× 藤森 亮× 野口 実穂× 藤井 義大× 瀬尾 健太郎 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | At the National Institute of Radiological Sciences, thousands of cancer patients have been treated by carbon ion irradiation with satisfactory outcome. However, the biological basis for this effectiveness is not fully elucidated. In this presentation, we focus on several critical issues behind the high relative biological effectiveness (RBE) associated with heavy ion irradiation. Although repair of DNA double strand breaks (DSBs) is known to depend on LET values, the aspect of mis-repair (rejoining) has been less frequently studied. Our data using premature chromosome condensation (PCC) combined with fluorescence in situ hybridization (FISH) technique indicate that the frequency of mis-rejoining (in G1 cells) was also LET dependent in the range of 0-200 keV/um. This could partially explain the high RBE for high LET radiation. Another important aspect is the cell cycle dependency of cell killing by ionizing radiation. In mid-70s, Bird and Burki showed that the variation of cell survival rate was significantly reduced with high LET heavy ions produced by the Berkeley accelerator. However, this phenomenon has not been repeated with other heavy ion facilities. This time we have basically reproduced the historical Berkeley result using the heavy ion accelerator facility in Chiba (HIMAC); significantly less variation in cell survival throughout the cell cycle was observed. Furthermore, using non-homologous end joining (NHEJ) and homologous recombination repair (HRR) defective mutants of CHO cells, we also demonstrate that both of these repair pathways were affected by high LET irradiation. To confirm these significant findings, further studies on repair inhibition by heavy ions were currently under way at cellular and molecular levels. | |||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Heavy Ions in Therapy and Space Symposium | |||||
| 発表年月日 | ||||||
| 日付 | 2009-07-10 | |||||
| 日付タイプ | Issued | |||||
