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短寿命PET核種による標識技術の開発
https://repo.qst.go.jp/records/2002503
https://repo.qst.go.jp/records/2002503897bc8a7-eca7-4b78-a410-56bb0c40a33e
| アイテムタイプ | 会議発表用資料 / Presentation(1) | |||||||
|---|---|---|---|---|---|---|---|---|
| 公開日 | 2025-11-05 | |||||||
| タイトル | ||||||||
| タイトル | 短寿命PET核種による標識技術の開発 | |||||||
| 言語 | ja | |||||||
| 言語 | ||||||||
| 言語 | jpn | |||||||
| 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 |
張 明栄
× 張 明栄
|
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| 抄録 | ||||||||
| 内容記述 | Metabotropic glutamate receptor 1 (mGluR1), a key mediator of glutamatergic signaling, is frequently overexpressed in tumor cells and is an attractive drug target for most cancers. Here, we present a targeted radiopharmaceutical therapy strategy that antagonistically recognizes mGluR1 and eradicates mGluR1+ human tumors by harnessing a small-molecule alpha (a)-emitting radiopharmaceutical, 211At-AITM. A single dose of 211At-AITM (2.96 MBq) in mGluR1+ cancers exhibits long-lasting in vivo antitumor efficacy across seven subtypes of four of the most common tumors, namely, breast cancer, pancreatic cancer, melanoma, and colon cancers, with little toxicity. Moreover, complete regression of mGluR1+ breast cancer and pancreatic cancer is observed in approximate 50% of tumor-bearing mice. Mechanistically, the functions of 211At-AITM are uncovered in downregulating mGluR1 oncoprotein and inducing senescence of tumor cells with a reprogrammed senescence-associated secretory phenotype. Our findings suggest a-radiopharmaceutical therapy with 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 | 第3回短寿命RI利用研究シンポジウム | |||||||
| 発表年月日 | ||||||||
| 日付 | 2025-11-28 | |||||||
