• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

通过打破白血病干细胞休眠来靶向它们。

Targeting leukemic stem cells by breaking their dormancy.

机构信息

HI-STEM (Heidelberg Institute for Stem Cell Technology and Experimental Medicine), Division of Stem Cells and Cancer, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 280, Heidelberg, Germany.

出版信息

Mol Oncol. 2010 Oct;4(5):443-50. doi: 10.1016/j.molonc.2010.06.001. Epub 2010 Jun 9.

DOI:10.1016/j.molonc.2010.06.001
PMID:20599449
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5527930/
Abstract

Transient or long-term quiescence, the latter referred to as dormancy are fundamental features of at least some adult stem cells. The status of dormancy is likely a critical mechanism for the observed resistance of normal HSCs and leukemic stem cells (LSCs) to anti-proliferative chemotherapy. Recent studies have revealed cytokines such as Interferon-alpha (IFNα) and G-CSF as well as arsenic trioxide (As(2)O(3)) to be efficient agents for promoting cycling of dormant HSCs and LSCs. Most interestingly, such cell cycle activated stem cells become exquisitely sensitive to killing by different chemotherapeutic agents, suggesting that dormant LSCs in patients may be targeted by a sequential two-step protocol involving an initial activation by IFNα, G-CSF or As(2)O(3), followed by targeted chemotherapy.

摘要

短暂或长期的静止,后者被称为休眠,是至少一些成人干细胞的基本特征。休眠状态可能是观察到正常造血干细胞和白血病干细胞(LSCs)对抗增殖化疗具有抗性的关键机制。最近的研究表明,干扰素-α(IFNα)和 G-CSF 等细胞因子以及三氧化二砷(As(2)O(3))是促进休眠 HSCs 和 LSCs 循环的有效药物。最有趣的是,这种细胞周期激活的干细胞对不同的化疗药物变得非常敏感,这表明患者体内的休眠 LSCs 可能是通过一个两步顺序方案来靶向,该方案包括先用 IFNα、G-CSF 或 As(2)O(3)进行初始激活,然后进行靶向化疗。

相似文献

1
Targeting leukemic stem cells by breaking their dormancy.通过打破白血病干细胞休眠来靶向它们。
Mol Oncol. 2010 Oct;4(5):443-50. doi: 10.1016/j.molonc.2010.06.001. Epub 2010 Jun 9.
2
Awakening dormant haematopoietic stem cells.唤醒休眠的造血干细胞。
Nat Rev Immunol. 2010 Mar;10(3):201-9. doi: 10.1038/nri2726.
3
Differential expression and response to arsenic stress of MRPs and ASAN1 determine sensitivity of classical multidrug-resistant leukemia cells to arsenic trioxide.多药耐药相关蛋白(MRPs)和ASAN1对砷应激的差异表达及反应决定了经典多药耐药白血病细胞对三氧化二砷的敏感性。
Leuk Res. 2016 Nov;50:116-122. doi: 10.1016/j.leukres.2016.10.003. Epub 2016 Oct 3.
4
Regulatory effects of mammalian target of rapamycin-mediated signals in the generation of arsenic trioxide responses.雷帕霉素哺乳动物靶标介导的信号在三氧化二砷反应产生中的调节作用。
J Biol Chem. 2008 Jan 25;283(4):1992-2001. doi: 10.1074/jbc.M705227200. Epub 2007 Nov 29.
5
Arsenic but not all-trans retinoic acid overcomes the aberrant stem cell capacity of PML/RARalpha-positive leukemic stem cells.砷而非全反式维甲酸可克服PML/RARα阳性白血病干细胞的异常干细胞能力。
Haematologica. 2007 Mar;92(3):323-31. doi: 10.3324/haematol.10541.
6
Arsenic trioxide (As2O3)-induced apoptosis and differentiation in retinoic acid-resistant acute promyelocytic leukemia model in hGM-CSF-producing transgenic SCID mice.三氧化二砷(As2O3)诱导人粒细胞巨噬细胞集落刺激因子(hGM-CSF)转基因SCID小鼠中耐维甲酸急性早幼粒细胞白血病模型的细胞凋亡和分化。
Leukemia. 2000 Mar;14(3):431-8. doi: 10.1038/sj.leu.2401646.
7
Docosahexaenoic acid enhances arsenic trioxide-mediated apoptosis in arsenic trioxide-resistant HL-60 cells.二十二碳六烯酸增强三氧化二砷对三氧化二砷耐药的HL-60细胞的介导凋亡作用。
Blood. 2003 Jun 15;101(12):4990-7. doi: 10.1182/blood-2002-08-2391. Epub 2003 Feb 27.
8
Arsenic trioxide plus cisplatin/interferon α-2b/doxorubicin/capecitabine combination chemotherapy for unresectable hepatocellular carcinoma.三氧化二砷联合顺铂/干扰素α-2b/阿霉素/卡培他滨治疗不可切除肝细胞癌的联合化疗
Hematol Oncol Stem Cell Ther. 2011;4(2):60-6. doi: 10.5144/1658-3876.2011.60.
9
A novel differentiation-inducing therapy for acute promyelocytic leukemia with a combination of arsenic trioxide and GM-CSF.一种采用三氧化二砷与粒细胞巨噬细胞集落刺激因子联合治疗急性早幼粒细胞白血病的新型分化诱导疗法。
Leukemia. 2001 Aug;15(8):1176-84. doi: 10.1038/sj.leu.2402162.
10
Application of heavy metal and cytokine for differentiation-inducing therapy in acute promyelocytic leukemia.重金属和细胞因子在急性早幼粒细胞白血病分化诱导治疗中的应用。
J Natl Cancer Inst. 1998 Dec 16;90(24):1906-7. doi: 10.1093/jnci/90.24.1906.

引用本文的文献

1
Phosphatidic acid phosphatase LPIN1 in phospholipid metabolism and stemness in hematopoiesis and AML.磷脂酸磷酸酶LPIN1在磷脂代谢以及造血和急性髓系白血病的干性维持中的作用
Hemasphere. 2025 Apr 22;9(4):e70118. doi: 10.1002/hem3.70118. eCollection 2025 Apr.
2
The role of YTHDF2 in anti-tumor immunity.YTHDF2在抗肿瘤免疫中的作用。
Cell Investig. 2025 Mar;1(1). doi: 10.1016/j.clnves.2025.100008. Epub 2025 Feb 26.
3
Targeting pivotal amino acids metabolism for treatment of leukemia.靶向关键氨基酸代谢用于白血病治疗。
Heliyon. 2024 Nov 16;10(23):e40492. doi: 10.1016/j.heliyon.2024.e40492. eCollection 2024 Dec 15.
4
PU.1 eviction at lymphocyte-specific chromatin domains mediates glucocorticoid response in acute lymphoblastic leukemia.PU.1 在淋巴细胞特异性染色质结构域中的驱逐介导了急性淋巴细胞白血病中的糖皮质激素反应。
Nat Commun. 2024 Nov 8;15(1):9697. doi: 10.1038/s41467-024-54096-2.
5
Inhibition of mitochondrial folate metabolism drives differentiation through mTORC1 mediated purine sensing.线粒体叶酸代谢的抑制通过mTORC1介导的嘌呤感知驱动分化。
Nat Commun. 2024 Mar 2;15(1):1931. doi: 10.1038/s41467-024-46114-0.
6
Minimal Residual Disease in Acute Myeloid Leukemia: Old and New Concepts.急性髓细胞白血病中的微小残留病:旧概念与新概念。
Int J Mol Sci. 2024 Feb 10;25(4):2150. doi: 10.3390/ijms25042150.
7
FBXW7 and human tumors: mechanisms of drug resistance and potential therapeutic strategies.FBXW7与人类肿瘤:耐药机制及潜在治疗策略
Front Pharmacol. 2023 Nov 13;14:1278056. doi: 10.3389/fphar.2023.1278056. eCollection 2023.
8
Cancer cell cycle heterogeneity as a critical determinant of therapeutic resistance.癌细胞周期异质性作为治疗耐药性的关键决定因素。
Genes Dis. 2023 Jan 14;11(1):189-204. doi: 10.1016/j.gendis.2022.11.025. eCollection 2024 Jan.
9
Acute Myeloid Leukemia Stem Cells in Minimal/Measurable Residual Disease Detection.微小/可测量残留病检测中的急性髓系白血病干细胞
Cancers (Basel). 2023 May 22;15(10):2866. doi: 10.3390/cancers15102866.
10
Radiated tumor cell-derived microparticles effectively kill stem-like tumor cells by increasing reactive oxygen species.辐射肿瘤细胞衍生的微粒通过增加活性氧有效地杀死肿瘤干细胞样细胞。
Front Bioeng Biotechnol. 2023 Jun 5;11:1156951. doi: 10.3389/fbioe.2023.1156951. eCollection 2023.

本文引用的文献

1
Comparison of human cord blood engraftment between immunocompromised mouse strains.人脐血在免疫抑制小鼠品系中的植入比较。
Blood. 2010 Jul 15;116(2):193-200. doi: 10.1182/blood-2010-02-271841. Epub 2010 Apr 19.
2
Arsenic trioxide controls the fate of the PML-RARalpha oncoprotein by directly binding PML.三氧化二砷通过直接结合 PML 来控制 PML-RARα 癌蛋白的命运。
Science. 2010 Apr 9;328(5975):240-3. doi: 10.1126/science.1183424.
3
Awakening dormant haematopoietic stem cells.唤醒休眠的造血干细胞。
Nat Rev Immunol. 2010 Mar;10(3):201-9. doi: 10.1038/nri2726.
4
Induction of cell cycle entry eliminates human leukemia stem cells in a mouse model of AML.诱导细胞周期进入可消除 AML 小鼠模型中的人类白血病干细胞。
Nat Biotechnol. 2010 Mar;28(3):275-80. doi: 10.1038/nbt.1607. Epub 2010 Feb 14.
5
Treatment strategies for CML.CML 的治疗策略。
Best Pract Res Clin Haematol. 2009 Sep;22(3):303-13. doi: 10.1016/j.beha.2009.08.001.
6
Balancing dormant and self-renewing hematopoietic stem cells.平衡休眠和自我更新的造血干细胞。
Curr Opin Genet Dev. 2009 Oct;19(5):461-8. doi: 10.1016/j.gde.2009.08.005. Epub 2009 Oct 5.
7
Therapy-induced PML/RARA proteolysis and acute promyelocytic leukemia cure.治疗诱导的早幼粒细胞白血病融合蛋白降解和急性早幼粒细胞白血病的治愈。
Clin Cancer Res. 2009 Oct 15;15(20):6321-6. doi: 10.1158/1078-0432.CCR-09-0209. Epub 2009 Oct 6.
8
Tumour-initiating cells: challenges and opportunities for anticancer drug discovery.肿瘤起始细胞:抗癌药物研发面临的挑战与机遇
Nat Rev Drug Discov. 2009 Oct;8(10):806-23. doi: 10.1038/nrd2137.
9
Estimating dormant and active hematopoietic stem cell kinetics through extensive modeling of bromodeoxyuridine label-retaining cell dynamics.通过广泛建模溴脱氧尿苷标记保留细胞动力学来估计休眠和活跃造血干细胞动力学。
PLoS One. 2009 Sep 22;4(9):e6972. doi: 10.1371/journal.pone.0006972.
10
Stem cell in the adult Drosophila hindgut: just a sleeping beauty.成年果蝇后肠中的干细胞:只是一个沉睡的美人。
Cell Stem Cell. 2009 Sep 4;5(3):227-8. doi: 10.1016/j.stem.2009.08.013.