| Item type |
文献 / Documents(1) |
| 公開日 |
2017-11-15 |
| アクセス権 |
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|
アクセス権 |
open access |
| 資源タイプ |
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|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_1843 |
|
資源タイプ |
other |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
ヒト肺癌細胞による癌性胸水形成におけるVEGF（Vascular Endothelial Growth Factor）の意義 |
|
言語 |
ja |
| タイトル |
|
|
タイトル |
ヒト ハイガン サイボウ ニヨル ガンセイ キョウスイ ケイセイ ニオケル VEGF Vascular Endothelial Growth Factor ノ イギ |
|
言語 |
ja-Kana |
| タイトル別表記 |
|
|
その他のタイトル |
Role of vascular endothelial growth factor in the formation of malignant pleural effusion |
|
言語 |
en |
| 著者 |
矢野, 聖二
軒原, 浩
三木, 豊和
西岡, 安彦
Fidler, Isaiah J.
曽根, 三郎
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| 抄録 |
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内容記述タイプ |
Abstract |
|
内容記述 |
The purpose of this study was to determine the molecular mechanisms that regulate the pathogenesis of malignant pleural effusion (PE) associated with advanced stage human non-small cell lung cancer. Intravenous injection of human PC14PE6 (adenocarcinoma) or H226 (squamous cell carcinoma) cells into nude mice yielded numerous lung lesions. PC14 PE6 lung lesions invaded the pleura and produced PE containing a high level of vascular endothelial growth factor (VEGF)/vascular permeability factor (VPF), resulting in vascular hyperpermeability in the thoracic cavity. Lung lesions produced by H226 cells were confined to the lung parenchyma and did not induce PE. The expression of VEGF/VPF mRNA and protein by the cell lines directly correlated with PE formation. Transfection of H226 cells with either sense-VEGF 165 or sense-VEGF 121 genes did not increase cell invasion into the pleura nor induce formation of PE. However, the injection of the VEGF/ VPF-transfected H226 cells into the pleural space resulted in induction of vascular hyperpermeability and PE, indicating that the production of malignant PE requires tumor cells to invade the pleura and express high levels of VEGF/VPF. Therefore, targeting these steps may control malignant PE in lung cancer patients. PTK787, an inhibitor of VEGF/VPF receptor tyrosine kinase phosphorylation, does not affect the in vitro proliferation of PC14PE6 cells. Oral feeding with PTK787 significantly reduced the formation of PE, but not the number of lung lesions of PC14PE6 cells. Furthermore, treatment with PTK787 significantly suppressed vascular hyperpermeability of PE-bearing mice, suggesting that PTK787 reduced PE formation mainly by inhibition of vascular permeability. Therefore, the VEGF/VPF receptor tyrosine kinase inhibitor PTK787 could be useful clinically for the control of malignant PE in lung cancer patients. |
|
言語 |
en |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
VEGF |
| キーワード |
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|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
pleural effusion |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
angiogenesis |
| 書誌情報 |
ja : 四国医学雑誌
巻 56,
号 3,
p. 109-110,
発行日 2000-06-25
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| 収録物ID |
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|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
00373699 |
| 収録物ID |
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|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AN00102041 |
| 出版者 |
|
|
出版者 |
徳島医学会 |
|
言語 |
ja |
| 言語 |
|
|
言語 |
jpn |
sam_56_3_109.pdf (16.8 KB)
