Lung cancer is the leading cause of cancer deaths worldwide, with an estimated 1.8 million new cases and 1.3 million deaths in 2012 . Tobacco smoking is responsible for most cases of lung cancer (approximately 90 percent for men and 70 to 85 percent for women).
Smoking cessation is the only proven means to decrease the risk of death from lung cancer. Former smokers continue to have an elevated risk of developing lung cancer for at least 30 years after stopping smoking, making these individuals an important target group for further efforts at mortality reduction [2,3]. (See "Overview of smoking cessation management in adults" and "Screening for lung cancer".)
Chemoprevention is the use of dietary or pharmacologic agents to prevent or slow the progression of cancer . Multiple agents have been studied to decrease the incidence of lung cancer, particularly in those at high risk for the development of this disease. The rationale for various approaches to chemoprevention beyond smoking cessation, observational data and its implications for epidemiologic studies, and results of chemoprevention trials that have been conducted are discussed in this topic.
Patient population — For chemoprevention to be feasible, a high-risk population must be identified and an effective chemopreventive agent with minimal side effects must be available. Current or former smokers with an annual risk of up to 2 percent are identifiable using a combination of clinically available risk factors including smoking history, age, gender, airflow obstruction or emphysema, environmental/occupational exposure, and family history of lung cancer [5,6].
Pathology — All the histologic cell types of lung cancer are genetically complex, with squamous cell demonstrating the highest frequency of mutations . No common mutation is shared across a majority of lung cancers, making a personalized approach to chemoprevention challenging. Common pathways for the early stages of premalignancy (airway inflammation, emphysema, tissue hypoxia) or distinct phenotypes susceptible to lung carcinogenesis may be definable and targeted for intervention [8-10].