Glasgow Royal Infirmary, Glasgow, UK.
Respiration. 2011;81(2):89-104. doi: 10.1159/000323946. Epub 2011 Feb 10.
Chronic obstructive pulmonary disease (COPD) and lung cancer currently form the basis for an enormous disease burden in the developed world. As a result of changing smoking trends and tobacco use, regrettably, a similar picture is arising rapidly within the developing world. COPD is a recognised risk factor for lung cancer, and a significant proportion of patients diagnosed with lung cancer have COPD. An association between both conditions has long been suspected but has proven difficult to demonstrate thus far. However, the common factors between both conditions are now becoming apparent thanks to recent clinical and molecular advances. Abnormal regulation of the immune system and the establishment of chronic inflammation appear to be key events in this process. In addition, the complex interplay between genes and environment and the possibility of a genetic basis to lung cancer susceptibility in the context of COPD are becoming clearer concepts. As we begin to unravel the common pathways and molecules in the pathogenesis of both conditions, we may be able to not only identify novel strategies to prevent and treat COPD and lung cancer, but also recognise molecular markers to identify patients at high risk of developing lung cancer.
慢性阻塞性肺疾病(COPD)和肺癌目前是发达国家巨大疾病负担的基础。由于吸烟趋势和烟草使用的变化,令人遗憾的是,发展中国家也迅速出现了类似的情况。COPD 是肺癌的一个公认危险因素,相当一部分被诊断患有肺癌的患者同时患有 COPD。这两种疾病之间的关联早已被怀疑,但迄今为止一直难以证明。然而,由于最近的临床和分子进展,这两种疾病之间的共同因素现在变得明显了。免疫系统的异常调节和慢性炎症的建立似乎是这一过程中的关键事件。此外,基因和环境之间的复杂相互作用以及 COPD 背景下肺癌易感性的遗传基础的可能性正在成为更清晰的概念。随着我们开始揭示这两种疾病发病机制中的共同途径和分子,我们不仅能够确定预防和治疗 COPD 和肺癌的新策略,还能够识别出高风险患肺癌的分子标志物。