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炎症与癌症之间的分子途径。

Molecular pathways linking inflammation and cancer.

机构信息

Istituto Clinico Humanitas IRCCS, via Manzoni 56, 20089 Rozzano, Milan, Italy.

出版信息

Curr Mol Med. 2010 Jun;10(4):369-73. doi: 10.2174/156652410791316968.


DOI:10.2174/156652410791316968
PMID:20455855
Abstract

Inflammatory conditions in selected organs increase the risk of cancer. An inflammatory component is present also in the microenvironment of tumours that are not epidemiologically related to inflammation. Compounds of the inflammatory tumor microenvironment include leukocytes, cytokines, complement components, and are orchestrated by transcription factors, such as NFkB and Stat3. Recent studies have begun to unravel molecular pathways linking inflammation and cancer. An intrinsic (driven by genetic events that cause neoplasia) and an extrinsic (driven by inflammatory conditions which predispose to cancer) pathway link inflammation and cancer. Smouldering inflammation in the tumour microenvironment promotes proliferation and survival of malignant cells, angiogenesis, metastasis, subversion of adaptive immunity, response to hormones and chemotherapeutic agents. Cancer-related inflammation represents a target for innovative diagnostic and therapeutic strategies.

摘要

某些器官的炎症状态会增加癌症的风险。肿瘤的微环境中也存在炎症成分,而这些肿瘤与炎症在流行病学上并无关联。炎症肿瘤微环境的组成包括白细胞、细胞因子、补体成分,并受转录因子(如 NFkB 和 Stat3)的调控。最近的研究开始揭示炎症与癌症之间的分子途径。内在途径(由导致肿瘤发生的遗传事件驱动)和外在途径(由导致癌症易感性的炎症条件驱动)将炎症与癌症联系起来。肿瘤微环境中的慢性炎症促进恶性细胞的增殖和存活、血管生成、转移、适应性免疫逃避、对激素和化疗药物的反应。与癌症相关的炎症是创新的诊断和治疗策略的靶点。

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