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Suppression of Tumor Angiogenesis by Nonsteroidal Anti-Inflammatory Drugs: A New Function for Old Drugs

机译:非甾体抗炎药对肿瘤血管生成的抑制作用:旧药的新功能

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摘要

There is solid epidemiological evidence demonstrating that the regular use of nonsteroidal anti-inflammatory drugs (NSAIDs) reduces the risk of developing colorectal cancer, and to a lesser extent gastric and esophageal cancers[1]. Importantly, NSAIDs suppress colon polyp formation and progression in patients diagnosed with familial adenomatous polyposis coli (APC)[2]. In many animal studies, NSAIDs have been shown to prevent tumor formation and slow tumor progression, thus confirming and extending the clinical observations[3,4,5]. Recent findings have demonstrated that NSAIDs inhibit angiogenesis, suggesting that the tumor suppressive activity of these drugs may be due, at least in part, to their ability to inhibit tumor angiogenesis[6]. The study of the mechanism by which NSAIDs suppress tumor angiogenesis, is matter of intense research.
机译:有可靠的流行病学证据表明,定期使用非甾体类抗炎药(NSAID)可以降低患结直肠癌的风险,并在较小程度上降低胃癌和食道癌的发生率[1]。重要的是,NSAIDs可抑制诊断为家族性腺瘤性息肉病大肠杆菌(APC)的患者的结肠息肉形成和进展[2]。在许多动物研究中,NSAIDs可以防止肿瘤形成并减缓肿瘤进展,从而证实并扩展了临床观察[3,4,5]。最近的发现表明,NSAIDs抑制血管生成,提示这些药物的抑癌活性可能至少部分是由于其抑制肿瘤血管生成的能力[6]。 NSAIDs抑制肿瘤血管生成的机制的研究是一项深入的研究。

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