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Novel therapeutic approach to eradicate tyrosine kinase inhibitor resistant chronic myeloid leukemia stem cells
https://doi.org/10.24517/00027512
https://doi.org/10.24517/00027512100c5efa-cbe6-4069-a408-1222c083e662
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
CA-PR-HIRAO-A-1577.pdf (336.4 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||||
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| 公開日 | 2017-10-05 | |||||||||||
| タイトル | ||||||||||||
| タイトル | Novel therapeutic approach to eradicate tyrosine kinase inhibitor resistant chronic myeloid leukemia stem cells | |||||||||||
| 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 | 10.24517/00027512 | |||||||||||
| ID登録タイプ | JaLC | |||||||||||
| 著者 |
Naka, Kazuhito
× Naka, Kazuhito× Hoshii, Takayuki× Hirao, Atsushi |
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| 著者別表示 |
仲, 一仁
× 仲, 一仁
× 星居, 孝之
× 平尾, 敦
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| 提供者所属 | ||||||||||||
| 内容記述タイプ | Other | |||||||||||
| 内容記述 | がん進展制御研究所 | |||||||||||
| 書誌情報 |
Cancer Science 巻 101, 号 7, p. 1577-1581, 発行日 2010-07-01 |
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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/j.1349-7006.2010.01584.x | |||||||||||
| 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 | Although discovery of the tyrosine kinase inhibitor (TKI) imatinib mesylate has significantly improved the prognosis of chronic myeloid leukemia (CML) patients, a rare population of CML stem cells is known to be resistant to TKI therapy, causing recurrence of CML. However, recent progress in CML stem cell biology may present a novel therapeutic avenue for CML patients. In this review, we focus on mechanisms used by CML stem cells to maintain TKI-resistance. Comprehensive approaches including mouse genetics, prospective identification of CML stem cells, and syngenic transplantation techniques have identified several key molecules or signaling pathways, including hedgehog (Hh)/Smo, promyelocytic leukemia (PML), 5-lipoxygenase (5-LO), and forkhead box class O (FOXO), that function in CML stem cell maintenance. Inhibiting some of these factors in combination with TKI administration successfully antagonized resistance of CML stem cells to TKI therapy, resulting in efficient eradication of leukemia cells in vivo. Thus, development of methods that sensitize CML stem cells to TKI therapy may lead to novel therapies to treat CML patients. © 2010 Japanese Cancer Association. | |||||||||||
| 権利 | ||||||||||||
| 権利情報 | © Japanese Cancer Association 日本癌学会 | |||||||||||
| 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/ | |||||||||||
