Institute for Tumor Biology and Experimental Therapy, Georg-Speyer-Haus, 60596 Frankfurt/Main, Germany; Frankfurt Cancer Institute, Goethe University Frankfurt, 60596 Frankfurt/Main, Germany; German Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany.
Cancer Prevention and Control Program, Fox Chase Cancer Center, Philadelphia, PA, 19111, USA.
Immunity. 2019 Jul 16;51(1):27-41. doi: 10.1016/j.immuni.2019.06.025.
Inflammation predisposes to the development of cancer and promotes all stages of tumorigenesis. Cancer cells, as well as surrounding stromal and inflammatory cells, engage in well-orchestrated reciprocal interactions to form an inflammatory tumor microenvironment (TME). Cells within the TME are highly plastic, continuously changing their phenotypic and functional characteristics. Here, we review the origins of inflammation in tumors, and the mechanisms whereby inflammation drives tumor initiation, growth, progression, and metastasis. We discuss how tumor-promoting inflammation closely resembles inflammatory processes typically found during development, immunity, maintenance of tissue homeostasis, or tissue repair and illuminate the distinctions between tissue-protective and pro-tumorigenic inflammation, including spatiotemporal considerations. Defining the cornerstone rules of engagement governing molecular and cellular mechanisms of tumor-promoting inflammation will be essential for further development of anti-cancer therapies.
炎症易导致癌症的发生，并促进肿瘤发生的各个阶段。癌细胞以及周围的基质和炎症细胞之间进行着精心协调的相互作用，形成了炎症肿瘤微环境（TME）。TME 中的细胞具有高度的可塑性，不断改变其表型和功能特征。在这里，我们回顾了肿瘤炎症的起源，以及炎症驱动肿瘤起始、生长、进展和转移的机制。我们讨论了促肿瘤炎症如何与通常在发育、免疫、组织稳态维持或组织修复过程中发现的炎症过程非常相似，并阐明了组织保护性炎症和促肿瘤性炎症之间的区别，包括时空考虑。定义控制促肿瘤炎症的分子和细胞机制的基石规则对于进一步开发抗癌疗法将是至关重要的。
