Abstract

Abstract Background: HMG-CoA reductase inhibitors (“statins”) have shown broad-spectrum anti-cancer properties in laboratory studies. In epidemiologic studies, statin use has been linked to reduced risk of advanced prostate cancer (PCa). We investigated whether statin use is associated with reduced risk of recurrence in PCa patients who received radical prostatectomy. Methods: All men with incident PCa diagnosed between 2004-2005 who subsequently underwent radical prostatectomy in Kaiser Permanente Southern California (KPSC) health plan were identified using KPSC's accredited cancer registry. Exclusion criteria included <24 months prior KPSC membership, use of neoadjuvant therapy, and stage 4 disease. Subjects were followed for 5 years after prostatectomy for: (1) Biochemical recurrence, defined as a single PSA measurement >0.2 ng/ml; and (2) clinical disease progression, defined as diagnosis of metastatic disease (identified using ICD-9 codes) or PCa-related death (i.e., PCa as primary cause of death). Information on statin use, demographics, co-morbid conditions, pathoclinical prognostic factors, e.g., stage and Gleason score, and outcomes were obtained from cancer registry and electronic medical records. The effects of statin use prior to and after prostatectomy were both examined using bivariate and multivariable Cox models, adjusting for known prognostic factors. For post-operative statin exposure, a time-dependent Cox model was used. Results: A total of 1192 men were included; 38% had pre-operative and 55% had post-operative statin use. Neither pre- nor post-operative statin use was associated with risk of any outcome, as there was no evidence of a clear dose-response relationship (Table). Conclusion: These data suggest that despite statin's protective effect in developing PCa, statin use may not prevent PCa progression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 647. doi:1538-7445.AM2012-647

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