@misc{oai:repo.qst.go.jp:00066693,
 author = {大島, 康宏 and 渡辺, 茂樹 and 辻, 厚至 and 永津, 弘太郎 and 坂下, 哲哉 and 杉山, 僚 and 原田, 良信 and 脇, 厚生 and 吉永, 恵一郎 and 東, 達也 and 石岡, 典子 and 大島 康宏 and 渡辺 茂樹 and 辻 厚至 and 永津 弘太郎 and 坂下 哲哉 and 杉山 僚 and 原田 良信 and 脇 厚生 and 吉永 恵一郎 and 東 達也 and 石岡 典子},
 month = {Jun},
 note = {Beta-emitting meta-131I-iodo-benzylguanidine (MIBG) has been used in the treatment of malignant pheochromocytoma (PHEO). However the effects of MIBG and 5-year survival are limited. Alpha-emitters strongly suppress the growth of tumor cells. 211Astatine (211At) is an α-emitting halogen and has a suitable half-life for cancer therapy (t1/2=7.2 h). Therefore, meta-211At-astatobenzylguanidine (MABG) may potentially suppress the growth of malignant PHEO. In this study, we synthesized MABG and investigate the therapeutic effects of MABG in a rat PHEO model. 211At was produced via the 209Bi(α,2n)211At reaction and was isolated through dry distillation. MABG was synthesized by astatination of meta-trimethylsilylbenzylguanidine hemisulfate. MABG was highly taken up into a rat PHEO cell line, PC-12, through the norepinephrine transporter, and significantly suppressed clonogenic growth. DNA damage and cell cycle arrest at the G2/M phase were observed after MABG treatment. Biodistribution and therapeutic effects were examined using mice bearing PC-12. MABG was highly distributed and was retained in tumors. Furthermore, the tumor size was significantly reduced by the single administration of MABG (555 kBq/head) without an associated weight reduction. These results suggest that MABG might be an attractive therapeutic agent for the treatment of malignant PHEO., Society of Nuclear Medicine and Molecular Imaging 2016 Annual Meeting},
 title = {Therapeutic efficacy of α-emitter meta-211At-astato-benzylguanidine (MABG) in a pheochromocytoma model},
 year = {2016}
}