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衰老、炎症与癌症。

Aging, inflammation and cancer.

机构信息

Humanitas Clinical and Research Center, via Manzoni 56, 20089, Rozzano, Milan, Italy.

Humanitas University, via Rita Levi Montalcini, 20090, Pieve Emanuele, Milan, Italy; School of Public Health, Imperial College London, London, UK.

出版信息

Semin Immunol. 2018 Dec;40:74-82. doi: 10.1016/j.smim.2018.10.011. Epub 2018 Nov 6.

DOI:10.1016/j.smim.2018.10.011
PMID:30409538
Abstract

Aging is a key aspect of neoplasia at the level of cells, individuals and populations. Unrestrained expression and production of inflammatory mediators is a key feature of aging at the cellular and organism level. Inflammatory cells and mediators are a key component of the tumor microenvironment and drive tumor progression. Non-resolving smoldering inflammation increases the risk of cancer (the extrinsic pathway connecting inflammation and cancer). In the intrinsic pathway, genetic events that cause neoplasia (oncogenes and oncosupressor genes) orchestrate the construction of cancer-related inflammation. We argue that uncontrolled smoldering inflammation drives carcinogenesis in aging and acts as a common denominator linking aging and cancer.

摘要

衰老是细胞、个体和群体水平上新生物形成的一个关键方面。在细胞和机体水平上,炎症介质不受控制的表达和产生是衰老的一个关键特征。炎症细胞和介质是肿瘤微环境的一个关键组成部分,并推动肿瘤进展。未解决的慢性炎症增加了癌症的风险(连接炎症和癌症的外在途径)。在内在途径中,导致新生物形成的遗传事件(癌基因和抑癌基因)协调构建与癌症相关的炎症。我们认为,失控的慢性炎症驱动衰老中的致癌作用,并作为连接衰老和癌症的共同因素。

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