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Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation
https://doi.org/10.24517/00049523
https://doi.org/10.24517/00049523e5142b0c-74e5-4164-9922-b58a322a69b4
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
CA-PR-TAKAHASHI-C-1726.pdf (686.4 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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| 公開日 | 2017-12-22 | |||||||||
| タイトル | ||||||||||
| タイトル | Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation | |||||||||
| 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 | 10.24517/00049523 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Kitajima, Shunsuke
× Kitajima, Shunsuke× Takahashi, Chiaki |
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| 著者別表示 |
北嶋, 俊輔
× 北嶋, 俊輔
× 髙橋, 智聡
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| 提供者所属 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 金沢大学がん進展制御研究所 | |||||||||
| 書誌情報 |
Cancer Science 巻 108, 号 2017, p. 1726-1731, 発行日 2017-09 |
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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.13312 | |||||||||
| 出版者 | ||||||||||
| 出版者 | Japanese Cancer Association / Blackwell Publishing Ltd | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | The Retinoblastoma (RB) tumor suppressor regulates G1/S transition during cell cycle progression by modulating the activity of E2F transcription factors. The RB pathway plays a central role in the suppression of most cancers, and RB mutation was initially discovered by virtue of its role in tumor initiation. However, as cancer genome sequencing has evolved to profile more advanced and treatment-resistant cancers, it has become increasingly clear that, in the majority of cancers, somatic RB inactivation occurs during tumor progression. Furthermore, despite the presence of deregulation of cell cycle control due to an INK4A deletion, additional CCND amplification and/or other mutations in the RB pathway, mutation or deletion of the RB gene is often observed during cancer progression. Of note, RB inactivation during cancer progression not only facilitates G1/S transition but also enhances some characteristics of malignancy, including altered drug sensitivity and a return to the undifferentiated state. Recently, we reported that RB inactivation enhances pro-inflammatory signaling through stimulation of the interleukin-6/STAT3 pathway, which directly promotes various malignant features of cancer cells. In this review, we highlight the consequences of RB inactivation during cancer progression, and discuss the biological and pathological significance of the interaction between RB and pro-inflammatory signaling. © 2017 Japanese Cancer Association. | |||||||||
| 権利 | ||||||||||
| 権利情報 | Copyright © 2017 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/ | |||||||||
| 関連名称 | http://www.jca.gr.jp/ | |||||||||
