The Prince Charles Hospital, Department of Thoracic Medicine, Thoracic Research Laboratory, Brisbane, Australia.
Expert Opin Ther Targets. 2011 Apr;15(4):439-56. doi: 10.1517/14728222.2011.555400. Epub 2011 Feb 2.
Lung cancer and COPD commonly coexist in smokers, and the presence of COPD increases the risk of developing lung cancer. In addition to smoking cessation and preventing smoking initiation, understanding the shared mechanisms of these smoking-related lung diseases is critical, in order to develop new methods of prevention, diagnosis and treatment of lung cancer and COPD.
This review discusses the common mechanisms for susceptibility to lung cancer and COPD, which in addition to cigarette smoke, may involve inflammation, epithelial-mesenchymal transition, abnormal repair, oxidative stress, and cell proliferation. Furthermore, we discuss the underlying genomic and epigenomic changes (single nucleotide polymorphisms (SNPs), copy number variation, promoter hypermethylation and microRNAs) that are likely to alter biological pathways, leading to susceptibility to lung cancer and COPD (e.g., altered nicotine receptor biology).
Strategies to study genomics, epigenomics and gene-environment interaction will yield greater insight into the shared pathogenesis of lung cancer and COPD, leading to new diagnostic and therapeutic modalities.
肺癌和 COPD 在吸烟者中通常同时存在，而 COPD 的存在会增加患肺癌的风险。除了戒烟和预防吸烟的开始，了解这些与吸烟相关的肺部疾病的共同机制至关重要，以便为肺癌和 COPD 的预防、诊断和治疗开发新方法。
这篇综述讨论了肺癌和 COPD 易感性的共同机制，除了香烟烟雾外，还可能涉及炎症、上皮-间充质转化、异常修复、氧化应激和细胞增殖。此外，我们还讨论了潜在的基因组和表观基因组变化（单核苷酸多态性 (SNP)、拷贝数变异、启动子过度甲基化和 microRNAs），这些变化可能改变生物途径，导致肺癌和 COPD 的易感性（例如，尼古丁受体生物学的改变）。
研究基因组学、表观基因组学和基因-环境相互作用的策略将更深入地了解肺癌和 COPD 的共同发病机制，从而为新的诊断和治疗方式提供依据。
