Queen Elizabeth Hospital, Department of Clinical Oncology, Kowloon, Hong Kong.
Expert Opin Ther Targets. 2011 Sep;15(9):1127-37. doi: 10.1517/14728222.2011.599801. Epub 2011 Jul 13.
It is reported that cancer may arise in chronically inflamed tissue. There is mounting evidence suggesting that the connection between inflammation and lung cancer is not coincidental but may indeed be causal. The inflammatory molecules may be responsible for augmented macrophage recruitment, delayed neutrophil clearance and an increase in reactive oxygen species. The cytokines and growth factors unusually produced in chronic pulmonary disorders have been found to have harmful properties that pave the way for epithelial-to-mesenchymal transition and tumor microenvironment. However, the role of inflammation in lung cancer is not yet fully understood.
The role of chronic inflammation in the pathogenesis of lung cancer and some of the possible mechanisms involved, with particular focus on inflammatory mediators, genetic and epigenetic alterations, inflammatory markers, tumor microenvironment and anti-inflammatory drugs are discussed. A framework for understanding the connection between inflammation and lung cancer is provided, which may afford the opportunity to intercede in specific inflammatory damage mediating lung carcinogenesis and therapeutic resistance.
Advances in tumor immunology support the clinical implementation of immunotherapies for lung cancer. Along with therapeutic benefits, immunotherapy presents the challenges of drug-related toxicities. Gene modification of immunocytokine may lower the associated toxic effects.
据报道，癌症可能发生在慢性炎症组织中。越来越多的证据表明，炎症与肺癌之间的联系并非偶然，而是确实存在因果关系。炎症分子可能导致巨噬细胞募集增加、中性粒细胞清除延迟和活性氧增加。在慢性肺部疾病中异常产生的细胞因子和生长因子被发现具有有害特性，为上皮-间充质转化和肿瘤微环境铺平了道路。然而，炎症在肺癌中的作用尚未完全阐明。
讨论了慢性炎症在肺癌发病机制中的作用以及一些可能涉及的机制，特别关注炎症介质、遗传和表观遗传改变、炎症标志物、肿瘤微环境和抗炎药物。提供了一个理解炎症与肺癌之间联系的框架，这可能为干预特定的炎症损伤介导的肺癌发生和治疗耐药性提供机会。
肿瘤免疫学的进展支持肺癌免疫疗法的临床应用。免疫疗法除了带来治疗益处外，还带来了与药物相关的毒性挑战。免疫细胞因子的基因修饰可能降低相关的毒副作用。
