Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology, University of California San Diego School of Medicine, La Jolla, California.
Cancer Prev Res (Phila). 2024 Apr 2;17(4):141-155. doi: 10.1158/1940-6207.CAPR-23-0423.
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.
炎症是一种重要的防御机制,当遇到有害刺激物(包括病原体、组织损伤、有毒化合物和代谢物)时,固有免疫细胞会协同激活,以中和和消除引发炎症的物质,并启动愈合和再生过程。适当终止的炎症对健康至关重要,但失控的、持续存在的炎症如果变成慢性炎症,就会导致各种炎症和代谢性疾病,并增加癌症风险。慢性炎症使受损组织表现为“无法愈合的伤口”,并持续产生生长因子,这些生长因子的生理功能是组织愈合,但慢性炎症会加速癌前病变向癌症的发展。1863 年,德国著名病理学家鲁道夫·菲尔绍(Rudolf Virchow)提出炎症与肿瘤形成之间可能存在关联,但直到 140 年后,人们才充分阐明并认识到炎症在肿瘤发生中的作用。关键发现概述了炎症级联反应中的分子事件,这些事件促进了癌症的发生和进展,并使人们更好地理解了何时以及何地应该抑制炎症。这些努力引发了正在进行的研究工作,以发现和开发减少炎症的化学预防策略,从而降低癌症风险和发病率。
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