文献

J-GLOBAL ID：202202266436348328   整理番号：22A0621633

Spred1欠損は慢性期CMLの治療抵抗性と形質転換を促進する【JST・京大機械翻訳】

Spred1 deficit promotes treatment resistance and transformation of chronic phase CML

著者 (24件)： Qiao Junjing (Department of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, P. R. China) ,  Qiao Junjing (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Qiao Junjing (Phase I Clinical Research Center, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, Henan, P. R. China) ,  Liang Chen (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Liang Chen (State Key Laboratory of Experimental Hematology, National Clinical Research Center for Blood Diseases, Institute of Hematology & Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, P. R. China) ,  Zhao Dandan (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Nguyen Le Xuan Truong (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Chen Fang (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Suo Shanshan (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Suo Shanshan (Department of Hematology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, P. R. China) ,  Hoang Dinh Hoa (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Pellicano Francesca (Paul O’ Gorman Leukemia Research Centre, College of Medical, Veterinary and Life Sciences, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK) ,  Rodriguez Ivan Rodriguez (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Elhajmoussa Yasmin (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Ghoda Lucy (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Yoshimura Akihiko (Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan) ,  Stein Anthony S. (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Ali Haris (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Koller Paul (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Perrotti Danilo (University of Maryland, Baltimore, MD, USA) ,  Copland Mhairi (Paul O’ Gorman Leukemia Research Centre, College of Medical, Veterinary and Life Sciences, Institute of Cancer Sciences, University of Glasgow, Glasgow, UK) ,  Han Anjia (Department of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, P. R. China) ,  Zhang Bin (Amber) (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA) ,  Marcucci Guido (Department of Hematological Malignancies Translational Science, Gehr Family Center for Leukemia Research, City of Hope Medical Center and Beckman Research Institute, Duarte, CA, USA)
資料名： Leukemia  (Leukemia)
巻： 36  号： 2  ページ： 492-506  発行年： 2022年 
JST資料番号： W4691A  ISSN： 0887-6924  資料種別： 逐次刊行物 (A)
記事区分： 原著論文  発行国： ドイツ (DEU)  言語： 英語 (EN)

抄録/ポイント： Spred1は正常な造血幹細胞(HSC)で高度に発現する。Spred1機能の欠如は,異常な造血および急性白血病と関係する。慢性骨髄性白血病(CML)において,Spred1は,加速期(AP)または爆風発症(BC)CMLの患者において減少し,それによって,この蛋白質の欠損が疾患形質転換に寄与する可能性があることを示唆する。実際,SCLtTA/BCR-ABL CMLマウスにおけるSpred1ノックアウト(KO)は,グローバルに,または造血細胞(すなわち,HSC)または内皮細胞(EC)に制限され,慢性期(CP)CMLのAP/BC CMLへの変換につながった。BCR-ABL誘導により,3つのSpred1 KO CMLモデルはAP/BC特徴を示した。しかし,全体的Spred1KOと比較して,HSC-Spred1KOとEC-Spred1KO CMLモデルのAP/BC表現型は減弱し,CML形質転換に対する白血病骨髄ニッチの多重区画におけるSpred1欠損の同時寄与を示唆した。Spred1 KOは,HSCまたはECにおいて発生するかどうかにかかわらず,白血病幹細胞(LSCs)に富む集団であるLSKs(Lin-Sca-1+c-Kit+)においてmiR-126を増加させ,Bcl-2発現および安定性を増強するMAPK/ERK経路の過活性化を介して,LSCの拡大をもたらした。これは最終的に,LSCのホメオスタシス,生存及び活性を支持し,AP/BC形質転換を駆動するBcl-2依存性酸化的リン酸化の増強をもたらした。Copyright The Author(s), under exclusive licence to Springer Nature Limited 2021 Translated from English into Japanese by JST.【JST・京大機械翻訳】

シソーラス用語： 骨髄 ,  白血病 ,  表現型 ,  マウス ,  多重化 ,  ホメオスタシス ,  爆風 ,  造血幹細胞 ,  内皮細胞 ,  幹細胞 ,  MAPキナーゼ ,  *急性白血病 ,  慢性骨髄性白血病
準シソーラス用語： *治療抵抗性 ,  造血細胞 ,  白血病幹細胞 , 【Automatic Indexing@JST】

分類 (1件)： 血液の腫よう  (GK04000M)

タイトルに関連する用語 (6件)： 欠損 ,  慢性期 ,  CML ,  治療抵抗性 ,  形質転換 ,  促進