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肿瘤坏死因子相关凋亡诱导配体(TRAIL)作为血液系统恶性肿瘤的潜在治疗靶点。

TNF-related apoptosis-inducing ligand (TRAIL) as the potential therapeutic target in hematological malignancies.

机构信息

Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran; Student Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.

Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

Biomed Pharmacother. 2018 Feb;98:566-576. doi: 10.1016/j.biopha.2017.12.082. Epub 2017 Dec 27.

DOI:10.1016/j.biopha.2017.12.082
PMID:29288972
Abstract

Despite numerous attempts to find the treatment strategies that can selectively target the cancer cells, cancer still remains a major public health problem. Conventional cancer treatments such as chemo- and radio-therapies are associated with systemic toxicity and the risk of recurrence. Additionally, acquired or pre-existing resistance is the main problem of most therapies. TNF-related apoptosis-inducing ligand (TRAIL), a member of TNF superfamily, has significantly attracted the researchers to use it as an effective treatment strategy for cancer since it can preferentially induce apoptosis in a variety of primary tumor cells without affecting the adjacent normal cells. Recently, recombinant forms of TRAIL and the multiple agonists of its receptor have been evaluated in many cell lines and phase II clinical trials. Hence, we have tried to summarize the TRAIL-related therapies as a potential therapeutic option in hematological malignancies.

摘要

尽管人们已经尝试了许多方法来寻找能够选择性靶向癌细胞的治疗策略,但癌症仍然是一个主要的公共卫生问题。传统的癌症治疗方法,如化疗和放疗,与全身毒性和复发风险有关。此外,获得性或预先存在的耐药性是大多数治疗方法的主要问题。TNF 相关凋亡诱导配体(TRAIL)是 TNF 超家族的一员,由于它可以优先诱导多种原发性肿瘤细胞凋亡,而不影响相邻的正常细胞,因此引起了研究人员的极大兴趣,将其作为癌症的有效治疗策略。最近,TRAIL 的重组形式及其受体的多种激动剂已经在许多细胞系和 II 期临床试验中进行了评估。因此,我们试图总结 TRAIL 相关的治疗方法作为血液系统恶性肿瘤的一种潜在治疗选择。

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TNF-related apoptosis-inducing ligand (TRAIL) as the potential therapeutic target in hematological malignancies.肿瘤坏死因子相关凋亡诱导配体(TRAIL)作为血液系统恶性肿瘤的潜在治疗靶点。
Biomed Pharmacother. 2018 Feb;98:566-576. doi: 10.1016/j.biopha.2017.12.082. Epub 2017 Dec 27.
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