Commentary on Chen etal. (2014): Another step on the road to clinical utility of pharmacogenetics for smoking cessation?

摘要

Tobacco smoking continues to be the leading cause of preventable death in the world [1], and yet the most efficacious behavioral and pharmacological treatments are ineffective in the majority of treatment-seeking smokers. While social and other environmental determinants are major contributors to tobacco use, twin and family studies over decades confirm that additive genetic factors contribute substantially to smoking behavior and smoking-attributable disease [2]. Converging research on the molecular genetics of smoking has pointed to at least two biologically plausible genetic loci contributing to nicotine dependence: cigarette consumption and smoking cessation. The alpha5-alpha3-beta4 (CHRNA5-CHRNA3-CHRNB4) nicotinic acetylcholine receptor gene cluster on chromosome 15q24-25.1 has been associated with cigarette consumption [3], lung cancer and chronic obstructive pulmonary disease [4,5] and smoking cessation [6-9].