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慢性骨髄性白血病とケモカイン
http://hdl.handle.net/2297/45899
http://hdl.handle.net/2297/45899e6462ad2-b508-4e91-ba40-10b10e6c133b
名前 / ファイル | ライセンス | アクション |
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CA-PR-MUKAIDA-N-129.pdf (1.0 MB)
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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 | 慢性骨髄性白血病とケモカイン | |||||
言語 | ||||||
言語 | jpn | |||||
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 | |||||
その他のタイトル | ||||||
Chemokines in chronic myeloid leukemia | ||||||
その他のタイトル | ||||||
Feature Articles: Update in clinical hematology 2016 (Myeloid diseases) | ||||||
著者 |
向田, 直史
× 向田, 直史× 馬場, 智久 |
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書誌情報 |
臨床血液 = The Japanese journal of clinical hematology 巻 57, 号 2, p. 129-136, 発行日 2016-02-01 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 0485-1439 | |||||
NCID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AN00252940 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.11406/rinketsu.57.129 | |||||
出版者 | ||||||
出版者 | 日本血液学会 = The Japanese Society of Hematology | |||||
抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 慢性骨髄性白血病(CML)に特徴的に認められるBCR-ABL遺伝子を標的とした,チロシン・キナーゼ阻害剤が開発され,著明な治療成績の改善を見ている。BCR-ABL遺伝子発現CML細胞は,正常造血細胞と,骨髄内の限られた空間を巡って競合しながら増殖する。さらに,CML細胞は骨髄内微小環境を利用することで,チロシン・キナーゼ阻害剤に対して耐性を獲得する可能性も指摘されている。したがって,CMLの新たな治療戦略の開発には,骨髄微小環境内でのCMLと正常造血細胞との相互作用の細胞・分子基盤を解明する必要がある。本論文では,CML細胞による骨髄内微小環境の再構築過程において,ケモカイン,なかでもCXCL12・CCL3が果たしている役割について解説を加えるとともに,これらのケモカインを標的とした新たなCML治療法の可能性についても論じる。Several tyrosine kinase inhibitors have been developed to target the BCR-ABL fusion gene, a pathognomonic genetic change in chronic myeloid leukemia (CML), and have dramatically improved the outcomes of CML patients. BCR-ABL-expressing CML cells compete with normal hematopoietic cells over the limited space in the bone marrow to proliferate. Moreover, CML cells can gain resistance to tyrosine kinase inhibitors by utilizing bone marrow microenvironments. Thus, in order to develop a novel treatment strategy for CML, it is necessary to elucidate the cellular and molecular basis underlying the interactions between CML and normal hematopoietic cells. Herein, we discuss the roles of chemokines, particularly CXCL12 and CCL3, in reconstruction processes of bone marrow microenvironments by CML cells and the possibility of novel treatment modalities against CML, based on targeting these chemokines. | |||||
権利 | ||||||
権利情報 | Copyright © 2016 The Japanese Society of Hematology 日本血液学会 | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | http://www.jshem.or.jp/ | |||||
関連URI | ||||||
識別子タイプ | URI | |||||
関連識別子 | https://www.jstage.jst.go.jp/browse/rinketsu/-char/ja/ |