WEKO3
インデックスリンク
アイテム
Hepatocyte growth factor reduces susceptibility to an irreversible epidermal growth factor receptor inhibitor in EGFR-T790M mutant lung cancer
https://doi.org/10.24517/00027058
https://doi.org/10.24517/0002705899992e8a-4b4b-461d-8066-3e6dc0548e2b
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
HO-PR-YAMADA-T-174.pdf (677.3 kB)
|
.png)
|
| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 公開日 | 2017-10-05 | |||||||||||||||
| タイトル | ||||||||||||||||
| タイトル | Hepatocyte growth factor reduces susceptibility to an irreversible epidermal growth factor receptor inhibitor in EGFR-T790M mutant lung cancer | |||||||||||||||
| 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 | 10.24517/00027058 | |||||||||||||||
| ID登録タイプ | JaLC | |||||||||||||||
| 著者 |
Yamada, Tadaaki
× Yamada, Tadaaki× 松本, 邦夫× Wang, Wei× Li, Qi× Nishioka, Yasuhiko× Sekido, Yoshitaka× Sone, Saburo× Yano, Seiji |
|||||||||||||||
| 著者別表示 |
山田, 忠明
× 山田, 忠明
× 松本, 邦夫
× 西岡, 安彦
× 曽根, 三郎
× 矢野, 聖二
|
|||||||||||||||
| 提供者所属 | ||||||||||||||||
| 内容記述タイプ | Other | |||||||||||||||
| 内容記述 | 金沢大学附属病院がん高度先進治療センター | |||||||||||||||
| 書誌情報 |
Clinical Cancer Research 巻 16, 号 1, p. 174-183, 発行日 2010-01-01 |
|||||||||||||||
| ISSN | ||||||||||||||||
| 収録物識別子タイプ | ISSN | |||||||||||||||
| 収録物識別子 | 1078-0432 | |||||||||||||||
| NCID | ||||||||||||||||
| 収録物識別子タイプ | NCID | |||||||||||||||
| 収録物識別子 | AA11029881 | |||||||||||||||
| DOI | ||||||||||||||||
| 関連タイプ | isVersionOf | |||||||||||||||
| 識別子タイプ | DOI | |||||||||||||||
| 関連識別子 | 10.1158/1078-0432.CCR-09-1204 | |||||||||||||||
| 出版者 | ||||||||||||||||
| 出版者 | American Association for Cancer Research | |||||||||||||||
| 抄録 | ||||||||||||||||
| 内容記述タイプ | Abstract | |||||||||||||||
| 内容記述 | Purpose: The secondary T790M mutation in epidermal growth factor receptor (EGFR) is the most frequent cause of acquired resistance to the reversible EGFR tyrosine kinase inhibitors (EGFR-TKI), gefitinib and erlotinib, in lung cancer. Irreversible EGFR-TKIs are expected to overcome the reversible EGFR-TKI resistance of lung cancer harboring T790M mutation in EGFR. However, it is clear that resistance may also develop to this class of inhibitors. We showed previously that hepatocyte growth factor (HGF) induced gefitinib resistance of lung cancer harboring EGFR-activating mutations. Here, we investigated whether HGF induced resistance to the irreversible EGFR-TKI, CL-387,785, in lung cancer cells (H1975) harboring both L858R activating mutation and T790M secondary mutation in EGFR. Experimental Design: CL-387,785 sensitivity and signal transduction in H1975 cells were examined in the presence or absence of HGF or HGF-producing fibroblasts with or without HGF-MET inhibitors. Results: HGF reduced susceptibility to CL-387,785 in H1975 cells. Western blotting and small interfering RNA analyses indicated that HGF-induced hyposensitivity was mediated by the MET/phosphoinositide 3-kinase/Akt signaling pathway independent of EGFR, ErbB2, ErbB3, and ErbB4. Hyposensitivity of H1975 cells to CL-387,785 was also induced by coculture with high-level HGF-producing lung fibroblasts. The hyposensitivity was abrogated by treatment with anti-HGF neutralizing antibody, HGF antagonist NK4, or MET-TKI. Conclusions: We showed HGF-mediated hyposensitivity as a novel mechanism of resistance to irreversible EGFR-TKIs. It will be clinically valuable to investigate the involvement of HGF-MET-mediated signaling in de novo and acquired resistance to irreversible EGFR-TKIs in lung cancer harboring T790M mutation in EGFR. ©2010 AACR. | |||||||||||||||
| 著者版フラグ | ||||||||||||||||
| 出版タイプ | AM | |||||||||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||||||||
