18.5 Chemoprevention of tobacco–related disease

Last updated: August 2016 

Suggested citation: Greenhalgh, EM, & Scollo, MM 18.5 Chemoprevention of tobacco–related disease. In Scollo, MM and Winstanley, MH [editors]. Tobacco in Australia: Facts and issues. Melbourne: Cancer Council Victoria; 2016. Available from: http://www.tobaccoinaustralia.org.au/chapter-18-harm-reduction/18-5-chemoprevention

The global incidence of cancer has been steadily increasing over time, and with its high personal, social, and healthcare costs, researchers have increasingly focused their efforts on prevention.1 The identification of risk factors including tobacco, obesity, family history, sedentary lifestyle, viruses, and sun exposure have prompted the development of strategies that might hinder the carcinogenic pathway.2 One such approach is chemoprevention, which is the use of natural, synthetic (made in a laboratory), or biologic (from a living source) substances to reverse, suppress, prevent, or delay the development of cancer.1 An improved understanding of the biology of carcinogenesis along with the identification of potential molecular targets that can disrupt this process has led to a marked increase in attention to this approach.1 Chemoprevention may target a variety of steps in tumour initiation, promotion and progression. Compounds that prevent cancer initiation are traditionally termed ‘blocking agents’. Once initiation has happened, chemopreventive agents that may hinder the promotion and progression of initiated cells are often called ‘suppressing agents’.1

Positive outcomes have been shown for the chemoprevention of a number of cancers, such as breast, prostate and colon cancer, and as at 2011 in the US there were 10 FDA-approved agents for the treatment of precancerous lesions or cancer risk reduction. For example, the HPV vaccine has been approved to reduce the risk of cervical cancer, cervical precancerous lesions, vulvovaginal cancer, and anal cancer and its precursor lesions. There are also many more published clinical trials in the literature that have reported positive results, but most have not received regulatory approvals.2 

The vast majority of lung cancers are caused by smoking, with current smokers and even those who have successfully quit being at high risk. In light of the high mortality and suffering caused by lung cancer, chemoprevention of lung carcinogenesis has been suggested as a way forward.3 To date, no agent has been identified as effective in those at high risk for lung cancer. Two large chemoprevention trials have evaluated the effects of beta-carotene on the prevention of lung cancer, but both resulted in higher rates of lung cancer and lung cancer mortality in participants treated.2 Some researchers have suggested that the target for chemoprevention should be tobacco smoke carcinogens and toxicants, the cause of lung cancer in smokers and ex-smokers.3 Others have suggested focusing on former smokers in chemoprevention trials, due to current smokers’ great risk of many other tobacco-related diseases that may mask any potential benefits of the approach.4 

Recent news and research

For recent news items and research on this topic, click here (Last updated March 2018) 



1. Steward W and Brown K. Cancer chemoprevention: a rapidly evolving field. British Journal of Cancer, 2013; 109(1):1–7. Available from: http://www.nature.com/bjc/journal/v109/n1/abs/bjc2013280a.html

2. Wu X, Patterson S, and Hawk E. Chemoprevention–history and general principles. Best Practice & Research Clinical Gastroenterology, 2011; 25(4):445–59. Available from: http://www.bpgastro.com/article/S1521-6918(11)00100-4/abstract

3. Hecht SS, Kassie F, and Hatsukami DK. Chemoprevention of lung carcinogenesis in addicted smokers and ex-smokers. Nature Reviews Cancer, 2009; 9(7):476–88. Available from: http://www.nature.com/nrc/journal/v9/n7/abs/nrc2674.html

4. Clamon G. Chemoprevention and screening for lung cancer: changing our focus to former smokers. Clinical Lung Cancer, 2015; 16(1):1–5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/25454006


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