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Articles by P. A Decker
Total Records ( 2 ) for P. A Decker
  J. A Schwartzbaum , Y Xiao , Y Liu , S Tsavachidis , M. S Berger , M. L Bondy , J. S Chang , S. M Chang , P. A Decker , B Ding , S. J Hepworth , R. S Houlston , F. J Hosking , R. B Jenkins , M. L Kosel , L. S McCoy , P. A McKinney , K Muir , J. S Patoka , M Prados , T Rice , L. B Robertson , M. J Schoemaker , S Shete , A. J Swerdlow , J. L Wiemels , J. K Wiencke , P Yang and M. R. Wrensch

To determine whether inherited variations in immune function single-nucleotide polymorphisms (SNPs), genes or pathways affect glioblastoma risk, we analyzed data from recent genome-wide association studies in conjunction with predefined immune function genes and pathways. Gene and pathway analyses were conducted on two independent data sets using 6629 SNPs in 911 genes on 17 immune pathways from 525 glioblastoma cases and 602 controls from the University of California, San Francisco (UCSF) and a subset of 6029 SNPs in 893 genes from 531 cases and 1782 controls from MD Anderson (MDA). To further assess consistency of SNP-level associations, we also compared data from the UK (266 cases and 2482 controls) and the Mayo Clinic (114 cases and 111 controls). Although three correlated epidermal growth factor receptor (EGFR) SNPs were consistently associated with glioblastoma in all four data sets (Mantel–Haenzel P values = 1 x 10–5 to 4 x 10–3), independent replication is required as genome-wide significance was not attained. In gene-level analyses, eight immune function genes were significantly (minP < 0.05) associated with glioblastoma; the IL-2RA (CD25) cytokine gene had the smallest minP values in both UCSF (minP = 0.01) and MDA (minP = 0.001) data sets. The IL-2RA receptor is found on the surface of regulatory T cells potentially contributing to immunosuppression characteristic of the glioblastoma microenvironment. In pathway correlation analyses, cytokine signaling and adhesion–extravasation–migration pathways showed similar associations with glioblastoma risk in both MDA and UCSF data sets. Our findings represent the first systematic description of immune genes and pathways that characterize glioblastoma risk.

  J. T Hays , R. D Hurt , P. A Decker , I. T Croghan , K. P Offord and C. A. Patten

Studies examining the efficacy of tobacco dependence treatment among recovering alcoholic smokers have produced mixed findings. We set out to investigate this issue further by conducting a randomized, double-blind, placebo-controlled trial of bupropion sustained-release (SR) for smoking relapse prevention among abstinent alcoholic smokers.


Participants (N = 195) met DSM-IV criteria for a history of alcohol abuse or dependence and had at least 1 year of continuous abstinence from alcohol and drugs. Open-label treatment with nicotine patch therapy was provided to all subjects for 8 weeks. The initial nicotine patch dose was determined by the subject's baseline serum cotinine concentration with an aim to achieve 100% cotinine replacement. All subjects who were confirmed abstinent from smoking throughout the final week of nicotine patch therapy (Week 8) were randomly assigned to receive bupropion SR 300 mg/day or placebo through Week 52.


A total of 110 participants were randomized to the double-blind treatment. No significant difference was observed between the bupropion and placebo groups for rates of continuous smoking abstinence, 41.1% (95% CI = 28.1%–55.0%) versus 40.7% (95% CI = 27.6%–55.0%), respectively, p = 1.0, or point prevalence abstinence, 39.3% (95% CI = 26.5%–53.3%) versus 40.7% (95% CI = 27.6%–55.0%), respectively, p = 1.0, at the end of the treatment (Week 52). Relapse to alcohol occurred in 4% of subjects (n = 4) during the study.


Treatment with bupropion SR among abstinent alcoholic smokers did not delay relapse or result in improved long-term smoking abstinence.

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