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三氧化二砷抗癌模式的新机制见解

Novel Mechanistic Insights into the Anti-cancer Mode of Arsenic Trioxide.

作者信息

Wahiduzzaman Md, Ota Akinobu, Hosokawa Yoshitaka

机构信息

Department of Biochemistry, School of Medicine, Aichi Medical University, Nagakute, Aichi 480-1195, Japan.

出版信息

Curr Cancer Drug Targets. 2020;20(2):115-129. doi: 10.2174/1568009619666191021122006.

DOI:10.2174/1568009619666191021122006
PMID:31736446
Abstract

Arsenic, a naturally-occurring toxic element, and a traditionally-used drug, has received a great deal of attention worldwide due to its curative anti-cancer properties in patients with acute promyelocytic leukemia. Among the arsenicals, arsenic trioxide has been most widely used as an anti-cancer drug. Recent advances in cancer therapeutics have led to a paradigm shift away from traditional cytotoxic drugs towards the targeting of proteins closely associated with driving the cancer phenotype. Due to the diverse anti-cancer effects of ATO on different types of malignancies, numerous studies have made efforts to uncover the mechanisms of ATO-induced tumor suppression. From in vitro cellular models to studies in clinical settings, ATO has been extensively studied. The outcomes of these studies have opened doors to establishing improved molecular-targeted therapies for cancer treatment. The efficacy of ATO has been augmented by combination with other drugs. In this review, we discuss recent arsenic-based cancer therapies and summarize the novel underlying molecular mechanisms of the anti-cancer effects of ATO.

摘要

砷是一种天然存在的有毒元素,也是一种传统使用的药物,因其对急性早幼粒细胞白血病患者具有抗癌治疗特性而在全球受到广泛关注。在各种砷化合物中,三氧化二砷作为抗癌药物应用最为广泛。癌症治疗领域的最新进展已导致一种范式转变,即从传统的细胞毒性药物转向针对与驱动癌症表型密切相关的蛋白质。由于三氧化二砷对不同类型恶性肿瘤具有多种抗癌作用,众多研究致力于揭示其诱导肿瘤抑制的机制。从体外细胞模型到临床研究,三氧化二砷都得到了广泛研究。这些研究成果为建立改进的癌症分子靶向治疗方法打开了大门。三氧化二砷与其他药物联合使用可增强其疗效。在本综述中,我们讨论了近期基于砷的癌症治疗方法,并总结了三氧化二砷抗癌作用的新潜在分子机制。

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PeerJ. 2024 Jun 4;12:e17559. doi: 10.7717/peerj.17559. eCollection 2024.
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Effect of arsenic trioxide plus etoposide, solumedrol, high‑dose cytarabine and cisplatin chemotherapy on the treatment of relapsed or ref7ractory ALK+ anaplastic large cell lymphoma.
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