WEKO3
アイテム
At-211放射性薬剤の現状と将来
https://repo.qst.go.jp/records/2002326
https://repo.qst.go.jp/records/2002326771626b4-97b7-45ef-9bc7-6727a69b8d11
| アイテムタイプ | 会議発表用資料 / Presentation(1) | |||||||
|---|---|---|---|---|---|---|---|---|
| 公開日 | 2025-08-25 | |||||||
| タイトル | ||||||||
| タイトル | At-211放射性薬剤の現状と将来 | |||||||
| 言語 | en | |||||||
| 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 presentation | |||||||
| 著者 |
Zhang Ming-Rong
× Zhang Ming-Rong
|
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| 抄録 | ||||||||
| 内容記述 | Metabotropic glutamate receptor 1 (mGluR1), a key mediator of glutamatergic signaling, is frequently overexpressedin tumor cells and is an attractive drug target for most cancers. Here, we present a targeted radiopharmaceuticaltherapy strategy that antagonistically recognizes mGluR1 and eradicates mGluR1+ humantumors by harnessing a small-molecule alpha (a)-emitting radiopharmaceutical, 211At-AITM. A single doseof 211At-AITM (2.96 MBq) in mGluR1+ cancers exhibits long-lasting in vivo antitumor efficacy across sevensubtypes of four of the most common tumors, namely, breast cancer, pancreatic cancer, melanoma, and coloncancers, with little toxicity. Moreover, complete regression of mGluR1+ breast cancer and pancreatic canceris observed in approximate 50% of tumor-bearing mice. Mechanistically, the functions of 211At-AITM areuncovered in downregulating mGluR1 oncoprotein and inducing senescence of tumor cells with a reprogrammedsenescence-associated secretory phenotype. Our findings suggest a-radiopharmaceutical therapywith 211At-AITM can be a useful strategy for mGluR1+ pan-cancers, regardless of their tissue of origin. | |||||||
| 会議概要（会議名, 開催地, 会期, 主催者等） | ||||||||
| 内容記述 | 2025 International Forum on Theranostics in Nuclear Medicine | |||||||
| 発表年月日 | ||||||||
| 日付 | 2025-09-07 | |||||||
