炎症作为癌症预防目标的过去和未来。

Laura Antonucci, Michael Karin
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引用次数: 0

摘要

炎症是一种重要的防御机制,先天性免疫细胞在遇到有害刺激(包括病原体、组织损伤、有毒化合物和代谢物)时被协调激活,以中和并消除煽动者,启动愈合和再生。适当终止炎症对健康至关重要,但失控的慢性炎症会引发各种炎症和代谢疾病,并增加癌症风险。慢性炎症会使受损组织表现为 "无法愈合的伤口",并使以组织愈合为生理功能的生长因子持续产生,从而加速癌症从恶性病变中萌发。1863 年,德国著名病理学家鲁道夫-维尔肖(Rudolf Virchow)提出了炎症与肿瘤形成之间可能存在的联系,但人们又花了 140 年的时间才充分阐明和认识到炎症的致癌作用。主要发现概述了炎症级联中促进癌症发生和发展的分子事件,并使人们能够更好地理解何时何地应该抑制炎症。这些努力引发了目前的研究工作,以发现和开发减少炎症的化学预防策略,降低癌症风险和发病率。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Past and Future of Inflammation as a Target to Cancer Prevention.

Inflammation is an essential defense mechanism in which innate immune cells are coordinately activated on encounter of harmful stimuli, including pathogens, tissue injury, and toxic compounds and metabolites to neutralize and eliminate the instigator and initiate healing and regeneration. Properly terminated inflammation is vital to health, but uncontrolled runaway inflammation that becomes chronic begets a variety of inflammatory and metabolic diseases and increases cancer risk. Making damaged tissues behave as "wounds that do not heal" and sustaining the production of growth factors whose physiologic function is tissue healing, chronic inflammation accelerates cancer emergence from premalignant lesions. In 1863, Rudolf Virchow, a leading German pathologist, suggested a possible association between inflammation and tumor formation, but it took another 140 years to fully elucidate and appreciate the tumorigenic role of inflammation. Key findings outlined molecular events in the inflammatory cascade that promote cancer onset and progression and enabled a better appreciation of when and where inflammation should be inhibited. These efforts triggered ongoing research work to discover and develop inflammation-reducing chemopreventive strategies for decreasing cancer risk and incidence.

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