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Chunk #18 — RESULTS — Abstinence outcomes

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Influence of a dopamine pathway additive genetic efficacy score on smoking cessation: results from two randomized clinical trials of bupropion.
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Results of Cox proportional hazards models evaluating time to first lapse using maximum likelihood estimation and logistic regression models evaluating PPA are summarized in Table 2. Proportional hazards assumptions for the model were supported by evaluation of Schoenfeld residuals (X2 = 13.86, p<0.13). We first confirmed the pharmacological and behavioral treatment effects of the trials, independent of participants’ genetic status. In both samples we confirmed a similarly strong effect of bupropion in reducing the risk for smoking lapse and PPA at the end of treatment (p < 0.001). The main effect of AGES on risk for smoking lapse during treatment was statistically significant (hazard ratios (22) of 1.10, 95% CI = 1.06 – 1.14) but, on PPA-EOT, it was not statistically significant (odds ratio = 1.00, 95% CI = 0.94 – 1.05) (Table 2). We also report the performance of individual genotypes on risk of lapse or PPA-EOT using the additive modeling – counting risk alleles (0,1,2). The only main effect of any single marker genotype was DRD4 in increasing risk for smoking lapse (HR = 1.29; 95% CI = 1.17 – 1.41; p<0.008).