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Hepatocyte growth factor/MET in cancer progression and biomarker discovery
https://doi.org/10.24517/00027500
https://doi.org/10.24517/0002750014ac1b74-1054-48a6-b476-ade24e14a6f8
名前 / ファイル | ライセンス | アクション |
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CA-PR-MATSUMOTO-K-296.pdf (967.2 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2017-10-05 | |||||
タイトル | ||||||
タイトル | Hepatocyte growth factor/MET in cancer progression and biomarker discovery | |||||
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 | 10.24517/00027500 | |||||
ID登録タイプ | JaLC | |||||
著者 |
Matsumoto, Kunio
× Matsumoto, Kunio× Umitsu, Masataka× Silva, Dinuka M. De× Roy, Arpita× Bottaro, Donald P. |
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著者別表示 |
松本, 邦夫
× 松本, 邦夫 |
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提供者所属 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 金沢大学ナノ生命科学研究所 / 金沢大学がん進展制御研究所 | |||||
書誌情報 |
Cancer Science 巻 108, 号 3, p. 296-307, 発行日 2017-03-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1347-9032 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA11808050 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.1111/cas.13156 | |||||
出版者 | ||||||
出版者 | Japanese Cancer Association = 日本癌学会 / John Wiley & Sons | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Signaling driven by hepatocyte growth factor (HGF) and MET receptor facilitates conspicuous biological responses such as epithelial cell migration, 3-D morphogenesis, and survival. The dynamic migration and promotion of cell survival induced by MET activation are bases for invasion–metastasis and resistance, respectively, against targeted drugs in cancers. Recent studies indicated that MET in tumor-derived exosomes facilitates metastatic niche formation and metastasis in malignant melanoma. In lung cancer, gene amplification-induced MET activation and ligand-dependent MET activation in an autocrine/paracrine manner are causes for resistance to epidermal growth factor receptor tyrosine kinase inhibitors and anaplastic lymphoma kinase inhibitors. Hepatocyte growth factor secreted in the tumor microenvironment contributes to the innate and acquired resistance to RAF inhibitors. Changes in serum/plasma HGF, soluble MET (sMET), and phospho-MET have been confirmed to be associated with disease progression, metastasis, therapy response, and survival. Higher serum/plasma HGF levels are associated with therapy resistance and/or metastasis, while lower HGF levels are associated with progression-free survival and overall survival after treatment with targeted drugs in lung cancer, gastric cancer, colon cancer, and malignant melanoma. Urinary sMET levels in patients with bladder cancer are higher than those in patients without bladder cancer and associated with disease progression. Some of the multi-kinase inhibitors that target MET have received regulatory approval, whereas none of the selective HGF-MET inhibitors have shown efficacy in phase III clinical trials. Validation of the HGF-MET pathway as a critical driver in cancer development/progression and utilization of appropriate biomarkers are key to development and approval of HGF-MET inhibitors for clinical use. © 2017 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. | |||||
権利 | ||||||
権利情報 | Copyright © 2017 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. | |||||
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 | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.jca.gr.jp/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://onlinelibrary.wiley.com/journal/10.1111/%28ISSN%291349-7006 |