@article{oai:repo.qst.go.jp:00045682,
 author = {Fujii, Yoshihiro and Kato, Takamitsu and Kubota, Nobuo and Fujimori, Akira and Niwa, Ohtsura and Okayasu, Ryuichi and 藤井 義大 and 加藤 宝光 and 窪田 宜夫 and 藤森 亮 and 丹羽 太貫 and 岡安 隆一},
 issue = {1},
 journal = {Oncology Reports},
 month = {Jan},
 note = {Inhibition of heat shock protein 90 (Hsp90) is an attractive modality for cancer therapy. Recent studies presented that an Hsp90 inhibitor, 17AAG (17-Allylamino-17-demethoxygeldanamycin), enhanced tumor radio-sensitivity, while this was not observed in normal cells. One of these studies reported that the effect of this drug was only observed in tumor cells carrying the wild type p53 gene, thus demonstrating the p53 dependent tumor radiosensitization by 17AAG.. We have now tested the effects of 17AAG on two human lymphoblastoid cell lines from the same donor, TK6 cells with the wild type p53 gene and WTK1 cells with the mutated p53 gene. The effects of 17AAG were tested at concentrations of 10nM and 100nM on various parameters, including growth inhibition of the cells, enhancement of radiosensitivity by colony formation assay, apoptosis and chromosomal radiosensitivity, and abrogation of radiation induced G2/M checkpoint. When 100nM 17AAG was applied, all of these parameters were enhanced in a similar fashion in both cell lines, indicating that the drug effect is p53 independent. Our results suggest that 17AAG is likely to be an effective sensitizer for radiotherapy, even on tumors with mutated p53},
 pages = {199--203},
 title = {p53 independent radio-sensitization of human lymphoblastoid cell lines by Hsp90 inhibitor 17-allylamino-17-demethoxygeldanamycin},
 volume = {23},
 year = {2010}
}