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Receptor ligand-triggered resistance to alectinib and its circumvention by Hsp90 inhibition in EML4-ALK lung cancer cells
https://doi.org/10.24517/00027514
https://doi.org/10.24517/0002751451315c84-0ba8-4dd3-af97-34d2346b404c
名前 / ファイル | ライセンス | アクション |
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CA-PR-TANIMOTO-A-4920.pdf (937.0 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-05 | |||||
タイトル | ||||||
タイトル | Receptor ligand-triggered resistance to alectinib and its circumvention by Hsp90 inhibition in EML4-ALK lung cancer cells | |||||
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_6501 | |||||
資源タイプ | journal article | |||||
ID登録 | ||||||
ID登録 | 10.24517/00027514 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Tanimoto, Azusa
× Tanimoto, Azusa× Yamada, Tadaaki× Nanjo, Shigeki× Takeuchi, Shinji× Ebi, Hiromichi× Kita, Kenji× Matsumoto, Kunio× Yano, Seiji |
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著者別表示 |
谷本, 梓
× 谷本, 梓× 山田, 忠明× 南條, 成輝× 竹内, 伸司× 衣斐, 寛倫× 北, 賢二× 松本, 邦夫× 矢野, 聖二 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学がん進展制御研究所 | |||||
書誌情報 |
Oncotarget 巻 5, 号 13, p. 4920-4928, 発行日 2014-01-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1949-2553 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.18632/oncotarget.2055 | |||||
出版者 | ||||||
出版者 | Impact Journals LLC | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Alectinib is a new generation ALK inhibitor with activity against the gatekeeper L1196M mutation that showed remarkable activity in a phase I/II study with echinoderm microtubule associated protein-like 4 (EML4) - anaplastic lymphoma kinase (ALK) non-small cell lung cancer (NSCLC) patients. However, alectinib resistance may eventually develop. Here, we found that EGFR ligands and HGF, a ligand of the MET receptor, activate EGFR and MET, respectively, as alternative pathways, and thereby induce resistance to alectinib. Additionally, the heat shock protein 90 (Hsp90) inhibitor suppressed protein expression of ALK, MET, EGFR, and AKT, and thereby induced apoptosis in EML4-ALK NSCLC cells, even in the presence of EGFR ligands or HGF. These results suggest that Hsp90 inhibitors may overcome ligand-triggered resistance to new generation ALK inhibitors and may result in more successful treatment of NSCLC patients with EML4-ALK. | |||||
権利 | ||||||
権利情報 | Copyright © 2016 Impact Journals, LLC | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |