Sears Catherine R
Division of Pulmonary, Critical Care, Sleep and Occupational Medicine, Department of Medicine, Indiana University, Indianapolis, Indiana; The Richard L. Roudebush Veterans Affairs Medical Center; 980W, Walnut Street, Walther Hall, C400, Indianapolis, IN, 46202, USA.
Respir Investig. 2019 Mar;57(2):111-121. doi: 10.1016/j.resinv.2018.11.005. Epub 2019 Jan 7.
Cigarette smoking is the leading cause of lung cancer and chronic obstructive pulmonary disease (COPD). Many of the detrimental effects of cigarette smoke have been attributed to the development of DNA damage, either directly from chemicals contained in cigarette smoke or as a product of cigarette smoke-induced inflammation and oxidative stress. In this review, we discuss the environmental, epidemiological, and physiological links between COPD and lung cancer and the likely role of DNA damage and repair in COPD and lung cancer development. We explore alterations in DNA damage repair by DNA repair proteins and pathways. We discuss emerging data supporting a key role for the DNA repair protein, xeroderma pigmentosum group C (XPC), in cigarette smoke-induced COPD and early lung cancer development. Understanding the interplay between cigarette smoke, DNA damage repair, COPD, and lung cancer may lead to prognostic tools and new, potentially targetable, pathways for lung cancer prevention and treatment.
吸烟是肺癌和慢性阻塞性肺疾病(COPD)的主要病因。香烟烟雾的许多有害影响都归因于DNA损伤的发生,这要么直接源于香烟烟雾中所含的化学物质,要么是香烟烟雾诱导的炎症和氧化应激的产物。在本综述中,我们讨论了COPD与肺癌之间的环境、流行病学和生理联系,以及DNA损伤和修复在COPD和肺癌发展中可能发挥的作用。我们探讨了DNA修复蛋白和途径对DNA损伤修复的改变。我们讨论了新出现的数据,这些数据支持DNA修复蛋白——着色性干皮病C组(XPC)在香烟烟雾诱导的COPD和早期肺癌发展中起关键作用。了解香烟烟雾、DNA损伤修复、COPD和肺癌之间的相互作用,可能会带来预后工具以及肺癌预防和治疗的新的、可能可靶向的途径。