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Activation of Src signaling mediates acquired resistance to ALK inhibition in lung cancer
https://asahikawa-med.repo.nii.ac.jp/records/5839
https://asahikawa-med.repo.nii.ac.jp/records/5839457e5b82-bc4c-425c-915c-b777dfbec124
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
6916.pdf (573.4 kB)
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| Item type | 学位論文 / Thesis or Dissertation_02(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2017-12-28 | |||||
| タイトル | ||||||
| タイトル | Activation of Src signaling mediates acquired resistance to ALK inhibition in lung cancer | |||||
| 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_db06 | |||||
| 資源タイプ | doctoral thesis | |||||
| アクセス権 | ||||||
| アクセス権 | open access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||
| その他（別言語等）のタイトル | ||||||
| その他のタイトル | ALK融合遺伝子陽性肺癌におけるALK阻害薬の耐性機序としてのSrcシグナル活性化の役割 | |||||
| 著者 |
吉田, 遼平
× 吉田, 遼平 |
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| 著者 ローマ字 | ||||||
| 値 | Yoshida, Ryohei | |||||
| 書誌情報 |
International journal of oncology 巻 51, 号 5, p. 1533-1540, 発行日 2017-11-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1019-6439 | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.3892/ijo.2017.4140. | |||||
| 識別番号 その他 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | PMID:29048652 | |||||
| 学位授与番号 | ||||||
| 学位授与番号 | 甲521 | |||||
| 学位授与年月日 | ||||||
| 学位授与年月日 | 2017-12-26 | |||||
| 学位名 | ||||||
| 学位名 | 博士（医学） | |||||
| 学位授与機関 | ||||||
| 学位授与機関識別子Scheme | kakenhi | |||||
| 学位授与機関識別子 | 10107 | |||||
| 学位授与機関名 | 旭川医科大学 | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Anaplastic lymphoma kinase (ALK) fusion oncogenes occur in approximately 3-5% of non-small cell lung cancer (NSCLC) cases. Various ALK inhibitors are in clinical use for the treatment of ALK-NSCLC, including the first generation ALK inhibitor, crizotinib, and recently the more highly potent alectinib and ceritinib. However, most tumors eventually become resistant to ALK specific inhibitors. To address the mechanisms underlying the development of ALK inhibitor resistance, we used iTRAQ quantitative mass spectrometry and phosphor-receptor tyrosine kinase arrays to investigate intracellular signaling alterations in ALK inhibitor resistant NSCLC cell lines. Src signaling was identified as an alectinib resistance mechanism, and combination treatment with ALK and Src inhibitors was highly effective for inhibiting the growth of ALK inhibitor resistant cells in vitro and in mouse xenograft models. Furthermore, phospho-receptor tyrosine kinase activation and downstream PI3K/AKT signaling was effectively blocked by inhibiting Src in alectinib resistant cells. Finally, we showed that the combined use of ALK and Src inhibitors inhibited the growth of other ALK-NSCLC cell lines, including those that were ceritinib or lorlatinib resistant. Our data suggest that targeting Src signaling may be an effective approach to the treatment of ALK-NSCLC with acquired resistance to ALK inhibitors. | |||||
| 資源タイプ | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | application/pdf | |||||
| 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 | |||||
| フォーマット | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | application/pdf | |||||
