Item type |
学術雑誌論文 / Journal Article_02(1) |
公開日 |
2010-11-01 |
タイトル |
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タイトル |
Vandetanib (ZD6474), an inhibitor of VEGFR and EGFR signalling, as a novel molecular-targeted therapy against cholangiocarcinoma |
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言語 |
en |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ |
journal article |
著者 |
吉川, 大太郎
Ojima, H
Kokubu, A
Ochiya, T
Kasai, S
Hirohashi, S
Shibata, T
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著者 ローマ字 |
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Yoshikawa, Daitaro |
著者 ローマ字 |
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en |
書誌情報 |
British Journal of Cancer
巻 100,
号 8,
p. 1257-1266,
発行日 2009-04-01
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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 |
0007-0920 |
DOI |
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識別子タイプ |
DOI |
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関連識別子 |
10.1038/sj.bjc.6604988 |
リンクURL |
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内容記述タイプ |
Other |
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内容記述 |
http://www.ncbi.nlm.nih.gov/pubmed?term=Vandetanib%20%28ZD6474%29%2C%20an%20inhibitor%20of%20VEGFR%20and%20EGFR%20signalling%2C%20as%20a%20novel%20molecular-targeted%20therapy%20against%20cholangiocarcinoma | http://www.ncbi.nlm.nih.gov/pubmed?term=Vandetanib%20%28ZD6474%29%2C%20an%20inhibitor%20of%20VEGFR%20and%20EGFR%20signalling%2C%20as%20a%20novel%20molecular-targeted%20therapy%20against%20cholangiocarcinoma |
抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Cholangiocarcinoma is an intractable cancer, with no effective therapy other than surgical resection. Elevated vascular endothelial growth factor (VEGF) and epidermal growth factor receptor (EGFR) expressions are associated with the progression of cholangiocarcinoma. We therefore examined whether inhibition of VEGFR and EGFR could be a potential therapeutic target for cholangiocarcinoma. Vandetanib (ZD6474, ZACTIMA), a VEGFR-2/EGFR inhibitor, was evaluated. Four human cholangiocarcinoma cell lines were molecularly characterised and investigated for their response to vandetanib. In vitro, two cell lines (OZ and HuCCT1), both of which harboured KRAS mutation, were refractory to vandetanib, one cell line (TGBC24TKB) was somewhat resistant, and another cell line (TKKK) was sensitive. The most sensitive cell line (TKKK) had EGFR amplification. Vandetanib significantly inhibited the growth of TKKK xenografts at doses >= 12.5 mg kg(-1) day(-1) (P<0.05), but higher doses (50 mg kg(-1) day(-1), P<0.05) of vandetanib were required to inhibit the growth of OZ xenografts. Vandetanib (25 mg kg(-1) day(-1)) also significantly (P = 0.006) prolonged the time to metastasis in an intravenous model of TKKK metastasis. Inhibiting both VEGFR and EGFR signalling appears a promising therapeutic approach for cholangiocarcinoma. The absence of KRAS mutation and the presence of EGFR amplification may be potential predictive molecular marker of sensitivity to EGFR-targeted therapy in cholangiocarcinoma. |
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言語 |
en |
注記 |
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内容記述タイプ |
Other |
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注記 |
http://creativecommons.org/licenses/by-nc-nd/3.0/ |
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言語 |
en |
資源タイプ |
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内容記述タイプ |
Other |
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資源タイプ |
text |
フォーマット |
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内容記述タイプ |
Other |
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内容記述 |
application/pdf |
ID(XooNIps) |
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19319137 |
閲覧数(XooNIps) |
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ダウンロード数(XooNIps) |
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1669 |