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三氧化二砷与神经母细胞瘤细胞毒性

Arsenic trioxide and neuroblastoma cytotoxicity.

作者信息

Pettersson Helen M, Karlsson Jenny, Pietras Alexander, Øra Ingrid, Påhlman Sven

机构信息

Department of Laboratory Medicine, Division of Molecular Medicine, Lund University, University Hospital MAS, Malmö, Sweden.

出版信息

J Bioenerg Biomembr. 2007 Feb;39(1):35-41. doi: 10.1007/s10863-006-9058-6.

DOI:10.1007/s10863-006-9058-6
PMID:17549641
Abstract

The majority of aggressive forms of the childhood tumor neuroblastoma can with current treatment protocols not be cured and possess a major challenge in pediatric oncology. After initial rounds of chemotherapy, surgery and irradiation, which in most cases result in tumor regression, these aggressive neuroblastomas relapse and frequently develop drug resistance. As approximately 50% of the children with neuroblastoma have an aggressive form, there is a compelling demand for new treatment strategies. Arsenic trioxide has the capacity to kill multidrug-resistant neuro-blastoma cells in vitro and in vivo and the drug is currently being evaluated in clinical trials. In this report we discuss the background to the use of arsenic trioxide in cancer therapy and the currently known mechanisms by which arsenic trioxide kills human neuroblastoma cells.

摘要

大多数侵袭性儿童肿瘤神经母细胞瘤,按照目前的治疗方案无法治愈,这是儿科肿瘤学面临的一项重大挑战。在首轮化疗、手术和放疗之后(多数情况下会导致肿瘤消退),这些侵袭性神经母细胞瘤会复发,并常常产生耐药性。由于约50%的神经母细胞瘤患儿患的是侵袭性类型,因此迫切需要新的治疗策略。三氧化二砷有能力在体外和体内杀死多药耐药神经母细胞瘤细胞,目前该药物正在进行临床试验评估。在本报告中,我们讨论了三氧化二砷用于癌症治疗的背景,以及目前已知的三氧化二砷杀死人类神经母细胞瘤细胞的机制。

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Arsenic trioxide and neuroblastoma cytotoxicity.三氧化二砷与神经母细胞瘤细胞毒性
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Novel Combination of Arsenic Trioxide (AsO) Plus Resveratrol in Inducing Programmed Cell Death of Human Neuroblastoma SK-N-SH Cells.三氧化二砷(AsO)联合白藜芦醇诱导人神经母细胞瘤SK-N-SH细胞程序性细胞死亡的新组合
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本文引用的文献

1
Multidrug-resistant neuroblastoma cells are responsive to arsenic trioxide at both normoxia and hypoxia.多药耐药神经母细胞瘤细胞在常氧和缺氧条件下均对三氧化二砷有反应。
Mol Cancer Ther. 2005 Jul;4(7):1128-35. doi: 10.1158/1535-7163.MCT-05-0047.
2
Use of arsenic trioxide in haematological malignancies: insight into the clinical development of a novel agent.三氧化二砷在血液系统恶性肿瘤中的应用:对一种新型药物临床开发的洞察
Curr Med Res Opin. 2005 Mar;21(3):403-11. doi: 10.1185/030079904X20349.
3
Arsenic trioxide therapy in acute promyelocytic leukemia and beyond: from bench to bedside.
砷、镉和铅的优化混合物通过星形胶质细胞活化、炎症和P38丝裂原活化蛋白激酶诱导C6胶质瘤细胞发生线粒体介导的凋亡。
Am J Cancer Res. 2015 Jul 15;5(8):2396-408. eCollection 2015.
4
Sodium arsenite exposure inhibits AKT and Stat3 activation, suppresses self-renewal and induces apoptotic death of embryonic stem cells.亚砷酸钠暴露会抑制 AKT 和 Stat3 的激活,抑制胚胎干细胞的自我更新并诱导其凋亡死亡。
Apoptosis. 2013 Feb;18(2):188-200. doi: 10.1007/s10495-012-0779-1.
5
Regulation of apoptosis in human melanoma and neuroblastoma cells by statins, sodium arsenite and TRAIL: a role of combined treatment versus monotherapy.他汀类药物、亚砷酸钠和 TRAIL 对人黑色素瘤和神经母细胞瘤细胞凋亡的调节:联合治疗与单药治疗的作用。
Apoptosis. 2011 Dec;16(12):1268-84. doi: 10.1007/s10495-011-0649-2.
6
New approaches to pharmacotherapy of tumors of the nervous system during childhood and adolescence.儿童和青少年期神经系统肿瘤药物治疗的新方法。
Pharmacol Ther. 2009 Apr;122(1):44-55. doi: 10.1016/j.pharmthera.2009.01.001. Epub 2009 Jan 23.
7
Neuroblastoma cell death is induced by inorganic arsenic trioxide (As(2)O(3)) and inhibited by a normal human bone marrow cell-derived factor.神经母细胞瘤细胞死亡由无机三氧化二砷(As₂O₃)诱导,并受到一种源自正常人骨髓细胞的因子抑制。
Cancer Microenviron. 2008 Dec;1(1):153-7. doi: 10.1007/s12307-008-0015-2. Epub 2008 Aug 27.
三氧化二砷在急性早幼粒细胞白血病及其他疾病中的治疗:从实验室到临床应用
Leuk Lymphoma. 2004 Dec;45(12):2387-401. doi: 10.1080/10428190412331272686.
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Arsenic trioxide-induced death of neuroblastoma cells involves activation of Bax and does not require p53.三氧化二砷诱导神经母细胞瘤细胞死亡涉及Bax激活且无需p53参与。
Clin Cancer Res. 2004 May 1;10(9):3179-88. doi: 10.1158/1078-0432.ccr-03-0309.
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All-trans retinoic acid/As2O3 combination yields a high quality remission and survival in newly diagnosed acute promyelocytic leukemia.全反式维甲酸/三氧化二砷联合用药可使新诊断的急性早幼粒细胞白血病患者获得高质量的缓解和生存。
Proc Natl Acad Sci U S A. 2004 Apr 13;101(15):5328-35. doi: 10.1073/pnas.0400053101. Epub 2004 Mar 24.
6
The p18 truncated form of Bax behaves like a Bcl-2 homology domain 3-only protein.Bax的p18截短形式表现得像一种仅含Bcl-2同源结构域3的蛋白。
J Biol Chem. 2004 Mar 19;279(12):11503-12. doi: 10.1074/jbc.M311922200. Epub 2003 Dec 17.
7
Essential role of the voltage-dependent anion channel (VDAC) in mitochondrial permeability transition pore opening and cytochrome c release induced by arsenic trioxide.电压依赖性阴离子通道(VDAC)在三氧化二砷诱导的线粒体通透性转换孔开放和细胞色素c释放中的重要作用。
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Arsenic trioxide uses caspase-dependent and caspase-independent death pathways in myeloma cells.三氧化二砷在骨髓瘤细胞中利用半胱天冬酶依赖性和非依赖性死亡途径。
Mol Cancer Ther. 2003 Nov;2(11):1155-64.
9
Tumour hypoxia, chemotherapeutic resistance and hypoxia-related therapies.肿瘤缺氧、化疗耐药性与缺氧相关治疗
Cancer Treat Rev. 2003 Aug;29(4):297-307. doi: 10.1016/s0305-7372(03)00003-3.
10
Acute and chronic arsenic toxicity.急性和慢性砷中毒。
Postgrad Med J. 2003 Jul;79(933):391-6. doi: 10.1136/pmj.79.933.391.