Statins and Prostate Cancer Risk: A Case-Control Study

Oregon Health and Science University, Portland, Oregon, United States
American Journal of Epidemiology (Impact Factor: 5.23). 09/2005; 162(4):318-25. DOI: 10.1093/aje/kwi203
Source: PubMed


Observational studies have shown that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) use may be associated with reduced cancer risk. The purpose of this case-control study was to elucidate the association between statin use and prostate cancer risk. Prostate cancer cases (n = 100), recruited upon referral for prostate biopsy, and frequency age-matched, prostate-specific antigen-normal clinic controls (n = 202) were recruited from the Portland, Oregon, Veterans Affairs Medical Center. Information on any use of statins from May 1997 through August 2004 was obtained from an electronic pharmacy database. Days of use, type of statin, dose, and prescription changes were recorded. Duration and intensity were calculated for each statin type on the basis of days of use and prescribed dose. Thirty-six percent of cases and 49 percent of controls had a record of any statin use. Following adjustment for other potential risk factors, statin use was associated with a significant reduction in prostate cancer risk (odds ratio = 0.38, 95% confidence interval: 0.21, 0.69). Furthermore, in analyses stratified by Gleason score, the inverse association with statin use was maintained only among men with Gleason scores of > or =7 (odds ratio = 0.24, 95% confidence interval: 0.11, 0.53). The results of this case-control study suggest that statins may reduce the risk of total prostate cancer and, specifically, more aggressive prostate cancer.

Download full-text


Available from: Paige E Farris, Oct 30, 2014
  • Source
    • "Changes of these processes in neoplastic cells may therefore result in the control of tumor initiation, growth, and metastasis by statins (Chan et al., 2003). Based on preclinical (Kubatka et al., 2011 a,b; Kubatka et al., 2012) and clinical (Poynter et al., 2005; Shannon et al., 2005; Fagherazzi et al., 2010; Kawata et al., 2001) evidence, statins demonstrated a risk reduction for several types of neoplasia. Although the favourable effects of statins in the prevention of cardiovascular diseases resulting from hypercholesterolemia are well established, the increasing evidence suggests that these drugs exert pleiotropic effects, independent of cholesterol reduction. "
    [Show abstract] [Hide abstract]
    ABSTRACT: From clinical practice, obvious positive effects of statins on plasma lipid metabolism are well known. On the other hand, there are several experimental rodent studies, where these beneficial effects were not confirmed. The effects of fluvastatin on selected serum lipid parameters in a rat model of experimental breast cancer were determined. The drug was dietary administered at two concentrations of 20 and 200 mg/kg. At the end of the study (experiment duration – 18 weeks) the blood from each animal was collected and serum lipid parameters were evaluated. Fluvastatin in both treated groups significantly increased parameters of serum lipids (mostly in a dose dependent manner). Fluvastatin in both treated groups of animals significantly increased serum levels of triacylglycerols, total cholesterol, and LDL-, HDL-, VLDL-cholesterol when compared to the control group. Our results pointed out to the apparent harmful effects of fluvastatin on plasma lipid metabolism in rat mammary carcinogenesis. Based on our previous results, it seems that rats commonly used in cancer model studies are generally unresponsive to the hypocholesterolemic effects of statins.
    Full-text · Article · Jun 2013 · Acta veterinaria
  • Source
    • "Until now, numbers of studies have been published and extensively reviewed [61]. Statin treatments do not seem to have any beneficial effect on the rate of appearance of prostate cancer conversely to the incidence of advanced PCa [62] [63] [64]. "
    [Show abstract] [Hide abstract]
    ABSTRACT: Cholesterol is a fundamental molecule for life. Located in the cell membrane, this sterol participates to the cell signaling of growth factors. Inside the cell it can be converted in hormones such as androgens or modulate the immune response. Such important functions could not be solely dependent of external supply by diet hence de novo synthesis could occur from acetate in almost all mammalian cells. If a deficiency in cholesterol sourcing leads to development troubles, overstocking has been associated to various diseases such as atherosclerosis and cancers. Cholesterol homeostasis should thus be tightly regulated at the uptake, de novo synthesis, storage and export processes. Various transcription factors have been described these last years as important to regulate cholesterol levels. Besides, synthetic molecules have been developed for many years to modulate cholesterol synthesis, such as statins. Many articles have associated prostate cancer, whose incidence is constantly increasing, to cholesterol disequilibrium. Targeting cholesterol could thus be a new pharmacological hit to counteract the initiation, development and/or progression of prostate cancer. Among the transcription factors regulating cholesterol homeostasis, the nuclear receptors Liver X Receptors (LXRs) control cholesterol uptake and export. Targeting the LXRs offers a new field of investigation to treat cancer. This review highlights the molecular relationships among LXRs, prostate cancer and cholesterol and why LXRs have good chance to be targeted one day in this tumor. LXRs, prostate cancer and cholesterol, more than a "Ménage à trois", The Good, the Bad and the Ugly.
    Full-text · Article · Jan 2013 · American Journal of Cancer Research
  • Source
    • "88 – 1994 ) 858 78 b NR 1 , 27 , 31 , 33 , 34 Graaf et al . , 2004 ( Netherlands ) [ 16 ] 1 3 ( 1995 – 1998 ) 9 , 785 186 c NR 1 , 3 , 5 , 11 – 13 , 27 , 29 – 31 Kaye and Jick , 2004 ( U . K . ) [ 12 ] 1 12 ( 1990 – 2002 ) 8 , 020 569 d B 1 , 4 , 19 , 32 Friis et al . , 2005 ( Denmark ) [ 9 ] { 13 ( 1989 – 2002 ) 168 , 133 1407 e C 1 , 5 , 28 , 29 Shannon et al . , 2005"
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Emerging evidence suggests that statins may decrease the risk of cancers. However, available evidence on prostate cancer (PCa) is conflicting. We therefore examined the association between statin use and risk of PCa by conducting a detailed meta-analysis of all observational studies published regarding this subject. Methods: Literature search in PubMed database was undertaken through February 2012 looking for observational studies evaluating the association between statin use and risk of PCa. Before meta-analysis, the studies were evaluated for publication bias and heterogeneity. Pooled relative risk (RR) estimates and 95% confidence intervals (CIs) were calculated using random-effects model (DerSimonian and Laird method). Subgroup analyses, sensitivity analysis and cumulative meta- analysis were also performed. Results: A total of 27 (15 cohort and 12 case-control) studies contributed to the analysis. There was heterogeneity among the studies but no publication bias. Statin use significantly reduced the risk of both total PCa by 7% (RR 0.93, 95% CI 0.87– 0.99, p = 0.03) and clinically important advanced PCa by 20% (RR 0.80, 95% CI 0.70–0.90, p,0.001). Long-term statin use did not significantly affect the risk of total PCa (RR 0.94, 95% CI 0.84–1.05, p = 0.31). Stratification by study design did not substantially influence the RR. Furthermore, sensitivity analysis confirmed the stability of results. Cumulative meta-analysis showed a change in trend of reporting risk from positive to negative in statin users between 1993 and 2011. Conclusions: Our meta-analysis provides evidence supporting the hypothesis that statins reduce the risk of both total PCa and clinically important advanced PCa. Further research is needed to confirm these findings and to identify the underlying biological mechanisms.
    Full-text · Article · Oct 2012 · PLoS ONE
Show more

We use cookies to give you the best possible experience on ResearchGate. Read our cookies policy to learn more.