| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2017-10-05 |
| タイトル |
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タイトル |
In vivo imaging models of bone and brain metastases and pleural carcinomatosis with a novel human EML4-ALK lung cancer cell line |
| 言語 |
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|
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 |
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|
ID登録 |
10.24517/00027483 |
|
ID登録タイプ |
JaLC |
| 著者 |
Nanjo, Shigeki
Nakagawa, Takayuki
Takeuchi, Shinji
Kita, Kenji
Fukuda, Koji
Nakada, Mitsutoshi
Uehara, Hisanori
Nishihara, Hiroshi
Hara, Eiji
Uramoto, Hidetaka
Tanaka, Fumihiro
Yano, Seiji
|
| 著者別表示 |
南條, 成輝
竹内, 伸司
北, 賢二
福田, 康二
中田, 光俊
上原, 久典
原, 英二
矢野, 聖二
|
| 提供者所属 |
|
|
内容記述タイプ |
Other |
|
内容記述 |
がん進展制御研究所 |
| 書誌情報 |
Cancer Science
巻 106,
号 3,
p. 244-252,
発行日 2015-03-01
|
| ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
1347-9032 |
| NCID |
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|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA11808050 |
| DOI |
|
|
関連タイプ |
isIdenticalTo |
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識別子タイプ |
DOI |
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関連識別子 |
10.1111/cas.12600 |
| 出版者 |
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出版者 |
Japanese Cancer Association / Blackwell Publishing Ltd |
| 抄録 |
|
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内容記述タイプ |
Abstract |
|
内容記述 |
EML4-ALK lung cancer accounts for approximately 3-7% of non-small-cell lung cancer cases. To investigate the molecular mechanism underlying tumor progression and targeted drug sensitivity/resistance in EML4-ALK lung cancer, clinically relevant animal models are indispensable. In this study, we found that the lung adenocarcinoma cell line A925L expresses an EML4-ALK gene fusion (variant 5a, E2:A20) and is sensitive to the ALK inhibitors crizotinib and alectinib. We further established highly tumorigenic A925LPE3 cells, which also have the EML4-ALK gene fusion (variant 5a) and are sensitive to ALK inhibitors. By using A925LPE3 cells with luciferase gene transfection, we established in vivo imaging models for pleural carcinomatosis, bone metastasis, and brain metastasis, all of which are significant clinical concerns of advanced EML4-ALK lung cancer. Interestingly, crizotinib caused tumors to shrink in the pleural carcinomatosis model, but not in bone and brain metastasis models, whereas alectinib showed remarkable efficacy in all three models, indicative of the clinical efficacy of these ALK inhibitors. Our in vivo imaging models of multiple organ sites may provide useful resources to analyze further the pathogenesis of EML4-ALK lung cancer and its response and resistance to ALK inhibitors in various organ microenvironments. © 2015 The Authors. |
| 権利 |
|
|
権利情報 |
© Japanese Cancer Association 日本癌学会 |
| 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 |
| 関連URI |
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|
識別子タイプ |
URI |
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関連識別子 |
http://www.jca.gr.jp/ |
CA-PR-YANO-S-244.pdf (2.2 MB)
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