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HIV vaccine development is a critical path in developing a long-term strategy to control the worldwide HIV epidemic. (1) The evaluation of candidate preventive HIV vaccines is a priority for […]

Sometimes the simplest SAS® task can become unnecessarily complex. Often the complexity of SAS®, itself, is the cause. Crucial details are easily hidden among the thousands of pages of SAS® documentation, technical notes, release updates, etc. The authors demonstrate a collection of SAS® features and techniques that are not well known, somewhat counterintuitive or undocumented, but all are surprisingly useful once learned and mastered. Mysterious SAS® behavior that might have inspired ‘work-arounds’ should now become transparent. Topics include environment settings; system options; and operators, functions and statements from SAS Language®, Macro Language®, SCL® and SAS/Graph®. The authors intend, through this selective review of uncommon techniques, to inspire a general interest in leveraging the power and maximizing the efficiency of programming tools. [ABSTRACT FROM AUTHOR]

To examine whether endogenous androgens influence the occurrence of prostate cancer, we conducted a nested case-control study among participants enrolled in the Carotene and Retinol Efficacy Trial. We analyzed serum samples of 300 cases diagnosed between 1987 and 1998, and 300 matched controls. Higher concentrations of testosterone (T) were not associated with increased prostate cancer risk. Relative to men with levels in the lowest fourth of the distribution, men in the upper fourth of total T had a risk of 0.82 [95% confidence interval (CI), 0.52-1.29]. The corresponding relative risks for free T (0.72; 95% CI, 0.45-1.14), percentage of free T (0.74; 95% CI, 0.46-1.19), and total T:sex hormone binding globulin ratio (0.52; 95% CI, 0.32-0.83) similarly were not elevated. Higher concentrations of androstenedione, dehydroepiandrosterone sulfate, and 3 alpha-androstanediol glucuronide were weakly associated with risk. Relative risks associated with being in the highest fourth for androstenedione, dehydroepiandrosterone sulfate, and 3 alpha-androstanediol glucuronide were 1.20 (95% CI, 0.76-1.89), 1.38 (95% CI, 0.86-2.21), and 1.27 (95% CI, 0.80-2.00), respectively. Men in the upper fourth of total estradiol (E2), free E2 and percentage of free E2 had relative risks of 0.71 (95% CI, 0.42-1.13), 0.52 (95% CI, 0.33-0.82), and 0.65 (95% CI, 0.40-1.05), respectively. The inverse association between E2 and prostate cancer risk was largely restricted to men with blood collection within 3 years of diagnosis. Our results add to the evidence that serum testosterone is unrelated to prostate cancer incidence. The suggestions that intraprostatic androgen activity may increase risk and that serum estrogens may decrease risk, warrant additional study.

The human androgen receptor gene contains polymorphic CAG and GGC repeats in exon 1. We investigated whether the number of CAG and/or GGC repeats is related to prostate cancer risk in a case-control study nested within the beta Carotene and Retinol Efficacy Trial. Among 300 cases and 300 controls, we did not observe any increase in risk associated with fewer CAG or GGC repeats. We observed a nonsignificant decrease in risk associated with each unit of decrease in CAG length [odds ratio (OR), 0.98; 95% confidence interval (CI), 0.93-1.03). Men with CAG <22 had a relative risk of prostate cancer of 0.89 (95% CI, 0.65-1.23) compared with men with CAG > or =22. There was no appreciable difference in the mean number of GGC repeats between cases and controls; the estimated change in the risk of prostate cancer associated with one fewer GGC repeat was 0.97 (95% CI, 0.88-1.06). The risk in men at or below the mean number of GGC repeats (17) was 0.80 (95% CI, 0.57-1.12). In contrast to prior reports, men with both short CAG (<22) and short GGC (< or =17) repeats were not at increased risk of prostate cancer (OR, 0.56; 95% CI, 0.32-0.98), compared with men with > or =22 CAG repeats and >17 GGC repeats. Our results do not support the hypothesis that a small number of CAG or GGC repeats in the androgen receptor gene increases a man's risk of prostate cancer.