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本文引用的文献

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VEGFA-VEGFR pathway blockade inhibits tumor-induced regulatory T-cell proliferation in colorectal cancer.VEGFA-VEGFR 通路阻断抑制结直肠癌中的肿瘤诱导调节性 T 细胞增殖。
Cancer Res. 2013 Jan 15;73(2):539-49. doi: 10.1158/0008-5472.CAN-12-2325. Epub 2012 Oct 29.
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Vascular normalizing doses of antiangiogenic treatment reprogram the immunosuppressive tumor microenvironment and enhance immunotherapy.抗血管生成治疗的血管正常化剂量可重新编程免疫抑制性肿瘤微环境并增强免疫治疗。
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Comprehensive analysis of current approaches to inhibit regulatory T cells in cancer.全面分析抑制癌症中调节性 T 细胞的现有方法。
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Sorafenib prevents escape from host immunity in liver cirrhosis patients with advanced hepatocellular carcinoma.索拉非尼可防止晚期肝细胞癌肝硬化患者逃避宿主免疫。
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Tumor-expressed inducible nitric oxide synthase controls induction of functional myeloid-derived suppressor cells through modulation of vascular endothelial growth factor release.肿瘤诱导型一氧化氮合酶通过调节血管内皮生长因子的释放控制功能性髓源抑制细胞的诱导。
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Anti-angiogenesis therapy in cancer: current challenges and future perspectives.癌症的抗血管生成治疗:当前的挑战与未来展望。
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Targeting MET in cancer: rationale and progress.靶向 MET 治疗癌症:原理与进展。
Nat Rev Cancer. 2012 Jan 24;12(2):89-103. doi: 10.1038/nrc3205.
8
Vascular endothelial growth factor-induced skin carcinogenesis depends on recruitment and alternative activation of macrophages.血管内皮生长因子诱导的皮肤癌发生依赖于巨噬细胞的募集和替代激活。
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10
A CCR4 antagonist combined with vaccines induces antigen-specific CD8+ T cells and tumor immunity against self antigens.一种 CCR4 拮抗剂与疫苗联合使用可诱导针对自身抗原的抗原特异性 CD8+ T 细胞和肿瘤免疫。
Blood. 2011 Nov 3;118(18):4853-62. doi: 10.1182/blood-2011-01-329656. Epub 2011 Sep 9.

癌症中抗血管生成分子对免疫的调节作用

Modulation of immunity by antiangiogenic molecules in cancer.

作者信息

Terme Magali, Colussi Orianne, Marcheteau Elie, Tanchot Corinne, Tartour Eric, Taieb Julien

机构信息

INSERM U970, Paris Cardiovascular Research Center, Université Paris-Descartes, Sorbonne Paris Cité, 56 rue Leblanc, 75015 Paris, France.

出版信息

Clin Dev Immunol. 2012;2012:492920. doi: 10.1155/2012/492920. Epub 2012 Dec 24.

DOI:10.1155/2012/492920
PMID:23320019
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3540780/
Abstract

In the last decades a new class of therapeutic drugs have been developed that block tumor angiogenesis. These antiangiogenic molecules, which target VEGF or VEGFR, PDGFR, and c-kit, can act not only on endothelial cells but also on immune cells. Some antiangiogenic molecules inhibit the development of immunosuppressive mechanisms developed by the tumors to escape the immune system (such as regulatory T cells, myeloid-derived suppressor cells, and immunosuppressive cytokines). These immunomodulatory effects must be characterized in detail to enable a better prescription of these treatments. In this paper we will focus on the impact of anti-angiogenic drugs on immunosuppression and their potential combination with immunotherapeutic strategies. Interestingly, immune parameters or their modulation during treatment could serve as potential biomarkers of response or resistance to anti-angiogenic therapies.

摘要

在过去几十年中,已开发出一类新的治疗药物,可阻断肿瘤血管生成。这些抗血管生成分子靶向血管内皮生长因子(VEGF)或血管内皮生长因子受体(VEGFR)、血小板衍生生长因子受体(PDGFR)和原癌基因c-kit,不仅可作用于内皮细胞,还可作用于免疫细胞。一些抗血管生成分子可抑制肿瘤为逃避免疫系统而形成的免疫抑制机制(如调节性T细胞、髓源性抑制细胞和免疫抑制细胞因子)。必须详细表征这些免疫调节作用,以便更好地开具这些治疗药物的处方。在本文中,我们将重点关注抗血管生成药物对免疫抑制的影响及其与免疫治疗策略的潜在联合应用。有趣的是,治疗期间的免疫参数或其调节可作为抗血管生成治疗反应或耐药性的潜在生物标志物。