慢性阻塞性肺疾病(COPD)及其与肺癌的关系:分子机制和治疗靶点

S. G, Rakshit S, S. K.
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引用次数: 0

摘要

慢性阻塞性肺疾病(COPD)和肺癌是全球肺部疾病相关死亡的主要原因。慢性炎症是慢性阻塞性肺病的一个关键特征,也是肺癌发生的潜在驱动因素。在各种环境危险因素中,吸烟在COPD和肺癌的发生和发展中起着至关重要的作用。几项流行病学研究表明,慢性阻塞性肺病患者患肺癌的风险更大,与吸烟无关,这表明遗传易感性在疾病发展中的作用。由于这两种疾病的异质性,揭示这两种疾病之间的机制联系受到阻碍:每种疾病都具有几种亚表型的特征。这篇综述的重点是两种疾病之间联系的本质和在COPD和肺癌中发生的特定机制,目前使用的一些治疗靶点,以及基因编辑技术在对抗这些使人衰弱的肺部炎症性疾病中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Chronic Obstructive Pulmonary Disease (COPD) and Its Association with Lung Cancer: Molecular Mechanism and Therapeutic Targets
Chronic Obstructive Pulmonary Disease (COPD) and Lung cancer are the major reasons for lung disease-related mortality worldwide. Chronic inflammation is a key attribute of COPD and a potential driver of lung carcinogenesis. Among various environmental risk factors, cigarette smoke plays a crucial role in the development and progression of COPD and lung cancer. Several epidemiological studies show that COPD patients are at a greater risk of developing lung cancer independently of cigarette smoking which suggests the role of genetic predisposition in the disease development. Uncovering the mechanistic link between these two diseases is hampered due to their heterogeneous nature: each is characterized by several sub-phenotypes of diseases. This review focuses on the nature of the link between the two diseases and specific mechanisms that occur in both COPD and lung cancer, some of the therapeutic targets which are currently employed, and the role of gene-editing technology to combat these debilitating lung-inflammatory disorders.
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