REVIEW ARTICLE
Year : 2013  |  Volume : 12  |  Issue : 1  |  Page : 1

Nicotine and lung cancer


1 Department of Radiation Oncology; Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, SC, USA and Roswell Park Cancer Institute, Buffalo, NY, USA
2 Department of Radiation Medicine, Medical University of South Carolina, Charleston, SC, USA and Roswell Park Cancer Institute, Buffalo, NY, USA

Correspondence Address:
Graham W Warren
Department of Radiation Oncology; Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, SC, USA and Roswell Park Cancer Institute, Buffalo, NY
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1477-3163.106680

Tobacco use in cancer patients is associated with increased cancer treatment failure and decreased survival. Nicotine is one of over 7,000 compounds in tobacco smoke and nicotine is the principal chemical associated with addiction. The purpose of this article is to review the tumor promoting activities of nicotine. Nicotine and its metabolites can promote tumor growth through increased proliferation, angiogenesis, migration, invasion, epithelial to mesenchymal transition, and stimulation of autocrine loops associated with tumor growth. Furthermore, nicotine can decrease the biologic effectiveness of conventional cancer treatments such as chemotherapy and radiotherapy. Common mechanisms appear to involve activation of nicotinic acetylcholine receptors and beta-adrenergic receptors leading to downstream activation of parallel signal transduction pathways that facilitate tumor progression and resistance to treatment. Data suggest that nicotine may be an important mechanism by which tobacco promotes tumor development, progression, and resistance to cancer treatment.


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