肺癌
慢性阻塞性肺病
医学
癌症
表观遗传学
肺
免疫学
遗传倾向
炎症
生物信息学
肿瘤科
生物
病理
内科学
疾病
遗传学
基因
作者
Gaetano Caramori,Paolo Ruggeri,Sharon Mumby,Antonio Ieni,Federica Lo Bello,Vrushali Chimankar,Chantal Donovan,Filippo Andò,Francesco Nucera,Irene Coppolino,Giovanni Tuccari,Philip M. Hansbro,Ian M. Adcock
标识
DOI:10.1080/14728222.2019.1615884
摘要
Introduction: COPD and lung cancer are leading causes of morbidity and mortality worldwide, and they share a common environmental risk factor in cigarette smoke exposure and a genetic predisposition represented by their incidence in only a fraction of smokers. This reflects the ability of cigarette smoke to induce an inflammatory response in the airways of susceptible smokers. Moreover, COPD could be a driving factor in lung cancer, by increasing oxidative stress and the resulting DNA damage and repression of the DNA repair mechanisms, chronic exposure to pro-inflammatory cytokines, repression of innate immunity and increased cellular proliferation.Areas covered: We have focused our review on the potential pathogenic molecular links between tobacco smoking-related COPD and lung cancer and the potential molecular targets for new drug development by understanding the common signaling pathways involved in COPD and lung cancer.Expert commentary: Research in this field is mostly limited to animal models or small clinical trials. Large clinical trials are needed but mostly combined models of COPD and lung cancer are necessary to investigate the processes caused by chronic inflammation, including genetic and epigenetic alteration, and the expression of inflammatory mediators that link COPD and lung cancer, to identify new molecular therapeutic targets.
科研通智能强力驱动
Strongly Powered by AbleSci AI