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Chemokines as a conductor of bone marrow microenvironment in chronic myeloid leukemia
https://doi.org/10.24517/00049628
https://doi.org/10.24517/00049628b65fe088-564a-4a68-a930-67dc3fd988ef
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
CA-PR-MUKAIDA-N-01824.pdf (1.4 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||||||
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| 公開日 | 2017-12-28 | |||||||||
| タイトル | ||||||||||
| タイトル | Chemokines as a conductor of bone marrow microenvironment in chronic myeloid leukemia | |||||||||
| 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 | 10.24517/00049628 | |||||||||
| ID登録タイプ | JaLC | |||||||||
| 著者 |
Mukaida, Naofumi
× Mukaida, Naofumi× Tanabe, Yamato× Baba, Tomohisa |
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| 著者別表示 |
向田, 直史
× 向田, 直史
× 馬場, 智久
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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 |
International Journal of Molecular Sciences 巻 18, 号 8, p. 01824, 発行日 2017-08-22 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | ISSN | |||||||||
| 収録物識別子 | 1661-6596 | |||||||||
| DOI | ||||||||||
| 関連タイプ | isIdenticalTo | |||||||||
| 識別子タイプ | DOI | |||||||||
| 関連識別子 | 10.3390/ijms18081824 | |||||||||
| 出版者 | ||||||||||
| 出版者 | MDPI AG | |||||||||
| 抄録 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | All blood lineage cells are generated from hematopoietic stem cells (HSCs), which reside in bone marrow after birth. HSCs self-renew, proliferate, and differentiate into mature progeny under the control of local microenvironments including hematopoietic niche, which can deliver regulatory signals in the form of bound or secreted molecules and from physical cues such as oxygen tension and shear stress. Among these mediators, accumulating evidence indicates the potential involvement of several chemokines, particularly CXCL12, in the interaction between HSCs and bone marrow microenvironments. Fusion between breakpoint cluster region (BCR) and Abelson murine leukemia viral oncogene homolog (ABL)-1 gene gives rise to BCR-ABL protein with a constitutive tyrosine kinase activity and transforms HSCs and/or hematopoietic progenitor cells (HPCs) into disease-propagating leukemia stem cells (LSCs) in chronic myeloid leukemia (CML). LSCs can self-renew, proliferate, and differentiate under the influence of the signals delivered by bone marrow microenvironments including niche, as HSCs can. Thus, the interaction with bone marrow microenvironments is indispensable for the initiation, maintenance, and progression of CML. Moreover, the crosstalk between LSCs and bone marrow microenvironments can contribute to some instances of therapeutic resistance. Furthermore, evidence is accumulating to indicate the important roles of bone marrow microenvironment-derived chemokines. Hence, we will herein discuss the roles of chemokines in CML with a focus on bone marrow microenvironments. © 2017 by the authors. Licensee MDPI, Basel, Switzerland. | |||||||||
| 権利 | ||||||||||
| 権利情報 | Copyright © MDPI AG | |||||||||
| 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 | |||||||||
