@misc{oai:repo.qst.go.jp:00064047,
 author = {Okayasu, Ryuichi and Yu, Dong and Noguchi, Miho and Takahashi, Momoko and Fujimori, Akira and Hirakawa, Hirokazu and 岡安 隆一 and 于 冬 and 野口 実穂 and 高橋 桃子 and 藤森 亮 and 平川 博一},
 month = {Sep},
 note = {Hsp 90 inhibitor 17AAG has been shown to be an effective radio-sensitizer in vitro using several tumor cell lines. One attractive point of using this chemical with radiation is its sensitizing effectiveness in normal cells being significantly smaller than that in tumor cells. We have shown that inhibition of DNA double strand break (DSB) repair by 17AAG is one of the causes for this sensitization in X-irradiated tumor cells. (Noguchi et al 2006). Inactivation of proteins associated with homologous recombination repair was also described in the publication. In this report, in vivo studies of 17AAG combined with radiation are presented using a mouse xenograft model with human tumor cells. SQ5 lung carcinoma cells were transplanted into the leg of nude mice, and the mice were treated with either 17AAG alone, radiation alone (gamma-rays or carbon ions), or the combined 17AAG and radiation treatment. 17AAG doses of 80 mg/kg body weight was given i.p. for 3 consecutive days. With 17AAG treatment or 10 Gy of gamma-ray alone, tumor growth was delayed in comparison to the control. The combination of 17AAG (pre-treatment for 3 days) and gamma-rays caused further delay in tumor growth. With 5 Gy dose of carbon ions, the combined treatment showed a significant delay in tumor growth, but by 25 days after irradiation, the tumor growth became similar in 5 Gy carbon treatment alone and in the combined treatment. These data indicate that 17AAG is effective in enhancing radiation response in gamma-irradiated tumors in vivo. Furthermore, carbon ion irradiation alone is very effective in controlling tumors in vivo even at low radiation doses., Radiation Research Society 56th Annual Meeting},
 title = {Effectiveness of the combined treatment of Hsp90 inhibitor 17AAG with gamma-rays or carbon ions in a tumor xenograft model},
 year = {2010}
}