• William Cs Cho, Chung K Kwan, Stephen Yau, Peter Pf So, Patricia Cm Poon, and Joseph Sk Au.
• Queen Elizabeth Hospital, Department of Clinical Oncology, Kowloon, Hong Kong. chocs@ha.org.hk
• Expert Opin. Ther. Targets. 2011 Sep 1; 15 (9): 1127-37.

IntroductionIt 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.Areas CoveredThe 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.Expert OpinionAdvances 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.

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