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抗血管生成导致动脉高血压的机制。

Mechanisms of antiangiogenic-induced arterial hypertension.

机构信息

Department of Internal Medicine and Arterial Hypertension, Avicenne Hospital, 125 Rue de Stalingrad, 93000 Bobigny, France.

出版信息

Curr Hypertens Rep. 2011 Aug;13(4):289-93. doi: 10.1007/s11906-011-0206-y.

DOI:10.1007/s11906-011-0206-y
PMID:21479992
Abstract

Antiangiogenic therapy has emerged as an important concept in the treatment of solid tumors. Vascular endothelial growth factor (VEGF) represents an important therapeutic target, as it is the primary mediator of angiogenesis and is induced by multiple tumor-relevant stimuli. Arterial hypertension has been commonly reported in all clinical trials testing inhibitors of angiogenesis (especially inhibitors of VEGF/VEGFR-2 signalling), with incidence ranging from 11% to 43% in all studies. The mechanism of elevated blood pressure in patients treated with antiangiogenic agents is not fully understood, but it is probably multifactorial, involving endothelial dysfunction and capillary rarefaction. Recently, several studies have suggested that early blood pressure rise was associated with better antitumoral efficacy and improved prognosis, making this commonly observed effect a promising marker of efficacy.

摘要

抗血管生成治疗已成为治疗实体瘤的一个重要概念。血管内皮生长因子 (VEGF) 是一个重要的治疗靶点,因为它是血管生成的主要介质,并且受到多种与肿瘤相关的刺激诱导。在所有测试抗血管生成抑制剂(特别是 VEGF/VEGFR-2 信号抑制剂)的临床试验中,均常报告有动脉高血压,所有研究中的发生率为 11%至 43%。在接受抗血管生成药物治疗的患者中,血压升高的机制尚未完全清楚,但可能是多因素的,涉及内皮功能障碍和毛细血管稀疏。最近,一些研究表明,早期血压升高与更好的抗肿瘤疗效和改善预后相关,使这种常见的观察到的效应成为一种有前途的疗效标志物。

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Br J Cancer. 2011 Feb 15;104(4):599-604. doi: 10.1038/bjc.2011.2. Epub 2011 Feb 8.
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Reversibility of capillary density after discontinuation of bevacizumab treatment.贝伐珠单抗治疗停药后毛细血管密度的可恢复性。
Ann Oncol. 2010 May;21(5):1100-5. doi: 10.1093/annonc/mdp417. Epub 2009 Oct 23.
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Effect of the multitargeted receptor tyrosine kinase inhibitor, ABT-869 [N-(4-(3-amino-1H-indazol-4-yl)phenyl)-N'-(2-fluoro-5-methylphenyl)urea], on blood pressure in conscious rats and mice: reversal with antihypertensive agents and effect on tumor growth inhibition.
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