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癌症免疫治疗中的抗CD73:开启新机遇

Anti-CD73 in cancer immunotherapy: awakening new opportunities.

作者信息

Antonioli Luca, Yegutkin Gennady G, Pacher Pál, Blandizzi Corrado, Haskó György

机构信息

Department of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy; Department of Surgery and Center for Immunity and Inflammation, Rutgers-New Jersey Medical School, Newark, NJ 07103, USA.

Medicity Research Laboratory, Department of Medical Microbiology and Immunology, University of Turku, Finland.

出版信息

Trends Cancer. 2016 Feb 1;2(2):95-109. doi: 10.1016/j.trecan.2016.01.003.

Abstract

In recent years, cancer immunotherapy made significant advances due to a better understanding of the principles underlying tumor biology and immunology. In this context, CD73 is a key molecule, since via degradation of adenosine monophosphate into adenosine, endorses the generation of an immunosuppressed and pro-angiogenic niche within the tumor microenvironment that promotes the onset and progression of cancer. Targeting CD73 results in favorable antitumor effects in pre-clinical models and combined treatments of CD73 blockade with other immune-modulating agents (i.e. anti-CTLA-4 mAb or anti-PD1 mAb) is particularly attractive. Although there is still a long way to go, anti-CD73 therapy, through the development of CD73 monoclonal antibodies, can potentially constitute a new biologic therapy for cancer patients. In this review, we discuss the link between CD73 and the onset, development and spread of tumors, highlighting the potential value of this molecule as a target and as a novel biomarker in the context of personalized cancer therapy.

摘要

近年来,由于对肿瘤生物学和免疫学基本原理有了更深入的了解,癌症免疫疗法取得了重大进展。在这种背景下,CD73是一个关键分子,因为它通过将单磷酸腺苷降解为腺苷,促进在肿瘤微环境中产生免疫抑制和促血管生成的生态位,从而推动癌症的发生和发展。在临床前模型中,靶向CD73会产生良好的抗肿瘤效果,将CD73阻断与其他免疫调节药物(如抗CTLA-4单克隆抗体或抗PD1单克隆抗体)联合治疗尤其具有吸引力。尽管仍有很长的路要走,但通过开发CD73单克隆抗体,抗CD73疗法有可能成为癌症患者的一种新的生物疗法。在这篇综述中,我们讨论了CD73与肿瘤发生、发展和扩散之间的联系,强调了该分子作为个性化癌症治疗背景下的靶点和新型生物标志物的潜在价值。

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本文引用的文献

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Cancer Res. 2015 Nov 1;75(21):4494-503. doi: 10.1158/0008-5472.CAN-14-3569. Epub 2015 Sep 11.
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CD73 Activity is Dispensable for the Polarization of M2 Macrophages.CD73活性对于M2巨噬细胞的极化并非必需。
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Cancer Res. 2015 Jun 1;75(11):2139-45. doi: 10.1158/0008-5472.CAN-15-0255.

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