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Genomics of Smoking Exposure and Cessation: Lessons for Cancer Prevention and Treatment

Authors' Affiliations: ¹ Center of Excellence in Environmental Toxicology, Transdisciplinary Tobacco Use Research Center, Abramson Cancer Center, and Departments of ² Pharmacology and ³ Psychiatry, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania

Requests for reprints: Trevor M. Penning, University of Pennsylvania, 3620 Hamilton Walk, Philadelphia, PA 19104-6084. Phone: 215-898-9445; Fax: 215-573-2236; E-mail: penning{at}pharm.med.upenn.edu.

Abstract

Tobacco use is the greatest preventable cause of cancer in the United States, accounting for almost one third of all cancer-related deaths and 90% of deaths from lung cancer. Despite widespread knowledge of these risks, tobacco use prevalence rates are 20% in the United States and up to 30% to 50% in the developing world (1, 2). Nicotine, the addictive chemical in tobacco, produces a biological dependence (3), and therefore, even with the most efficacious medications available, only one in four smokers is able to maintain long-term abstinence (4). Persistent tobacco use is common even following a diagnosis of tobacco-related cancer and is associated with poorer outcomes of radiation therapy and chemotherapy and with increased risk of second primary malignancies (5). Although smoking cessation is optimal, it may not be realistic for all patients. Therefore, it is essential to gain a better understanding of the cellular and molecular mechanisms through which tobacco exposure contributes to cancer pathogenesis and outcomes, and to develop targeted prevention and therapeutic approaches.

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