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High efficacy of third generation EGFR inhibitor AZD9291 in a leptomeningeal carcinomatosis model with EGFR-mutant lung cancer cells
https://doi.org/10.24517/00027513
https://doi.org/10.24517/00027513b8f84f64-6832-4ff6-9cd4-9654a9a49e1e
名前 / ファイル | ライセンス | アクション |
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CA-PR-YANO-S-3847.pdf (3.6 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 | High efficacy of third generation EGFR inhibitor AZD9291 in a leptomeningeal carcinomatosis model with EGFR-mutant 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 | 10.24517/00027513 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Nanjo, Shigeki
× Nanjo, Shigeki× Ebi, Hiromichi× Arai, Sachiko× Takeuchi, Shinji× Yamada, Tadaaki× Mochizuki, Satsuki× Okada, Yasunori× Nakada, Mitsutoshi× Murakami, Takashi× Yano, Seiji |
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著者別表示 |
南條, 成輝
× 南條, 成輝× 衣斐, 寛倫× 新井, 祥子× 竹内, 伸司× 山田, 忠明× 望月, 早月× 岡田, 保典× 中田, 光俊× 村上, 孝× 矢野, 聖二 |
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書誌情報 |
Oncotarget 巻 7, 号 4, p. 3847-3856, 発行日 2016-01-01 |
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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 | 10.18632/oncotarget.6758 | |||||
出版者 | ||||||
出版者 | Impact Journals LLC | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Leptomeningeal carcinomatosis (LMC) remarkably decreases the quality of life of EGFR-mutant lung cancer patients. In contrast to the lesions outside the central nervous system (CNS), molecular mechanisms of EGFR tyrosine kinase inhibitor (TKI) resistance in CNS lesions including LMC are largely unknown. In this study, we established an in vivo imaging model for LMC with EGFR mutant lung cancer cell lines harboring an exon 19 deletion in EGFR and evaluated the effect of first generation EGFR-TKIs, erlotinib, second generation afatinib, and third generation AZD9291. In PC-9/ffluc model, erlotinib treatment slowed the development of LMC. Importantly, treatment with afatinib or AZD9291 apparently delayed the development of LMC. Moreover, treatment with a higher dose of AZD9291, also associated with inhibited phosphorylation of EGFR downstream molecule S6, regressed LMC refractory to the aforementioned EGFR-TKI treatments. These observations suggest that the third generation EGFR-TKI AZD9291 may be an effective treatment for first or second generation EGFR-TKI resistant LMC caused by EGFR-mutant lung cancer. | |||||
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 |