@misc{oai:repo.qst.go.jp:00070503,
 author = {Okayasu, Ryuichi and Hirakawa, Hirokazu and Noguchi, Miho and Yu, Dong and Hirayama, Ryoichi and Fujimori, Akira and et.al and 岡安 隆一 and 平川 博一 and 野口 実穂 and 于 冬 and 平山 亮一 and 藤森 亮},
 month = {Sep},
 note = {17AAG, an Hsp90 inhibitor was shown to radiosensitize certain human tumor cells exposed to X-rays, while this sensitization was not clearly observed in normal human cells.  The mechanism of this was suggested to come from inhibition of DNA double strand break (DSB) repair, particularly impairment of homologous recombination repair (HRR) pathway by this drug (Noguchi et al 2006). Key proteins associated with HRR seem to be affected by this inhibitor. To our surprise, tumor radiosensitization with 17 AAG was also observed in cells exposed to high LET carbon ions (70 kev/um). Independently we also found that knockdown of BRCA2, a key HRR protein significantly radiosensitized human tumor cells. These results indicate that there seem to be a radio-sensitization mechanism associated with the combination of HRR inhibition and high LET radiation, and this may occur particularly in S-phase cells. Furthermore, we also used mouse xenograft model to examine the combined effect of 17AAG and high LET carbon irradiation. For this purpose, SQ5 human lung tumor cells were implanted on the leg of nude mice and the tumor growth was observed in the combined treatment as compared with radiation or drug treatment alone. Our preliminary results indicate that tumor growth was more inhibited in the 17AAG and carbon irradiation than carbon or 17AAG treatment alone. These data suggest that an effective tumor control might be obtained by combining an HRR inhibitor with high LET carbon irradiation., 14th ICRR 2011},
 title = {Radiosensitization by inhibition of homologous recombination repair combined with high LET heavy ion irradiation},
 year = {2011}
}