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Ability of the Met kinase inhibitor crizotinib and new generation EGFR inhibitors to overcome resistance to EGFR inhibitors
https://doi.org/10.24517/00027430
https://doi.org/10.24517/00027430b091978c-0700-4893-963d-ab5e01c1c9a9
名前 / ファイル | ライセンス | アクション |
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CA-PR-NANJO-S-84700.pdf (1.9 MB)
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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 | Ability of the Met kinase inhibitor crizotinib and new generation EGFR inhibitors to overcome resistance to EGFR inhibitors | |||||
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 | 10.24517/00027430 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Nanjo, Shigeki
× Nanjo, Shigeki× Yamada, Tadaaki× Nishihara, Hiroshi× Takeuchi, Shinji× Sano, Takako× Nakagawa, Takayuki× Ishikawa, Daisuke× Zhao, Lu× Ebi, Hiromichi× Yasumoto, Kazuo× Matsumoto, Kunio× Yano, Seiji |
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著者別表示 |
南條, 成輝
× 南條, 成輝× 山田, 忠明× 竹内, 伸司× 衣斐, 寛倫× 安本, 和生× 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 |
PLoS ONE 巻 8, 号 12, p. 84700, 発行日 2013-12-26 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1932-6203 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1371/journal.pone.0084700 | |||||
出版者 | ||||||
出版者 | Public Library of Science | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Purpose: Although EGF receptor tyrosine kinase inhibitors (EGFR-TKI) have shown dramatic effects against EGFR mutant lung cancer, patients ultimately develop resistance by multiple mechanisms. We therefore assessed the ability of combined treatment with the Met inhibitor crizotinib and new generation EGFR-TKIs to overcome resistance to first-generation EGFR-TKIs. Experimental Design: Lung cancer cell lines made resistant to EGFR-TKIs by the gatekeeper EGFR-T790M mutation, Met amplification, and HGF overexpression and mice with tumors induced by these cells were treated with crizotinib and a new generation EGFR-TKI. Results: The new generation EGFR-TKI inhibited the growth of lung cancer cells containing the gatekeeper EGFRT790M mutation, but did not inhibit the growth of cells with Met amplification or HGF overexpression. In contrast, combined therapy with crizotinib plus afatinib or WZ4002 was effective against all three types of cells, inhibiting EGFR and Met phosphorylation and their downstream molecules. Crizotinib combined with afatinib or WZ4002 potently inhibited the growth of mouse tumors induced by these lung cancer cell lines. However, the combination of high dose crizotinib and afatinib, but not WZ4002, triggered severe adverse events. Conclusions: Our results suggest that the dual blockade of mutant EGFR and Met by crizotinib and a new generation EGFR-TKI may be promising for overcoming resistance to reversible EGFR-TKIs but careful assessment is warranted clinically. © 2013 Nanjo et al. | |||||
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 |