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Metabolic disorder, inflammation, and deregulated molecular pathways converging in pancreatic cancer development: Implications for new therapeutic strategies
http://hdl.handle.net/2297/27790
http://hdl.handle.net/2297/27790bfb8367a-69d5-4c0e-9007-d5b0e4348a6e
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-MOTOO-Y-446.pdf (390.2 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2017-10-03 | |||||
| タイトル | ||||||
| タイトル | Metabolic disorder, inflammation, and deregulated molecular pathways converging in pancreatic cancer development: Implications for new therapeutic strategies | |||||
| 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 | |||||
| 著者 |
Motoo, Yoshiharu
× Motoo, Yoshiharu× Shimasaki, Takeo× Ishigaki, Yasuhito× Nakajima, Hideo× Kawakami, Kazuyuki× Minamoto, Toshinari |
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| 提供者所属 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 金沢大学医薬保健研究域医学系 | |||||
| 書誌情報 |
Cancers 巻 3, 号 1, p. 446-460, 発行日 2011-03-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 2072-6694 | |||||
| DOI | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.3390/cancers3010446 | |||||
| 出版者 | ||||||
| 出版者 | MDPI Publishing | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Pancreatic cancer develops and progresses through complex, cumulative biological processes involving metabolic disorder, local inflammation, and deregulated molecular pathways. The resulting tumor aggressiveness hampers surgical intervention and renders pancreatic cancer resistant to standard chemotherapy and radiation therapy. Based on these pathologic properties, several therapeutic strategies are being developed to reverse refractory pancreatic cancer. Here, we outline molecular targeting therapies, which are primarily directed against growth factor receptor-type tyrosine kinases deregulated in tumors, but have failed to improve the survival of pancreatic cancer patients. Glycogen synthase kinase-3β (GSK3β) is a member of a serine/threonine protein kinase family that plays a critical role in various cellular pathways. GSK3β has also emerged as a mediator of pathological states, including glucose intolerance, inflammation, and various cancers (e.g., pancreatic cancer). We review recent studies that demonstrate the anti-tumor effects of GSK3β inhibition alone or in combination with chemotherapy and radiation. GSK3β inhibition may exert indirect anti-tumor actions in pancreatic cancer by modulating metabolic disorder and inflammation. © 2011 by the authors; licensee MDPI, Basel, Switzerland. | |||||
| 権利 | ||||||
| 権利情報 | Copyright © 2011, American Society for Microbiology. | |||||
| 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.mdpi.com/2072-6694/3/1/446/ | |||||
