studies, and potential relation with cessation likelihood. In the smoking cessation trial, haplotype interacted with treatment in affecting success of cessation, in that active treatment was strongly associated with a lower risk of relapse in individuals with haplotype 3 (relative hazard = 0.48, p-value = 9.7×10−7) and haplotype 2 (relative hazard = 0.48, p-value = 2.7×10−8), but not haplotype 1 (relative hazard ratios = 0.83, p-value = 0.36). No significant differences were found in the effect of haplotype on abstinence/relapse between bupropion only, nicotine replacement therapy only, and combined therapies treatment groups (34). Exposure to environmental smoking-related cues may also play an important role in promoting relapse, as individual differences in response to the sight or smell of a lit cigarette may be mediated by the DRD4 VNTR polymorphism. Participants who were homozygous or heterozygous for the seven repeat or longer allele demonstrated significantly higher craving, more arousal, less positive affect, and more attention to the smoking cues than participants for whom this polymorphism was absent (104). The integration of genetic testing into standard clinical practice would be premature at this time, but pharmacologic studies of treatments for nicotine dependence eventually may guide individualized smoking-cessation treatments.
