HMG CoA reductase inhibitors, NSAIDs and risk of glioma

Authors

  • Jennifer S. Ferris,

    1. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY
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  • Lucie McCoy,

    1. Department of Neurological Surgery, University of California San Francisco, San Francisco, CA
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  • Alfred I Neugut,

    1. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY
    2. Department of Medicine, Division of Medical Oncology, Columbia University Medical Center, New York, NY
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  • Margaret Wrensch,

    1. Department of Neurological Surgery, University of California San Francisco, San Francisco, CA
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  • Rose Lai

    Corresponding author
    1. Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY
    2. The Neurological Institute, Columbia University, New York, NY
    • The University of Southern California, Keck School of Medicine, 1441 Eastlake Avenue, Norris Topping Tower Suite 3407, Los Angeles, CA 90089-9173
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    • Tel.: +323-865-3980, Fax: +323-865-0061


  • This article was published online on 04 April 2012. An error was subsequently identified. This notice is included to indicate that it was corrected 20 July 2012.

Abstract

3-Hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins) have shown inverse associations with cancer risks, but the results have been inconsistent. As there are no previous published data in brain tumors, we conducted a case–control study to investigate statin therapy and risk of glioma. We further evaluated the use of nonsteriodal anti-inflammatory drugs (NSAIDs) and risk of these tumors. We recruited newly diagnosed glioma cases and frequency matched controls at Columbia University and the University of California San Francisco. Standardized questions on statins and NSAIDs were used at both institutions. Intakes of these drugs were defined as >6 months of at least twice weekly use versus less than this amount or never use. From July 2007 to January 2010, we recruited a total of 517 cases and 400 controls. Simvastatin and lovastatin showed significant inverse associations with glioma (odds ratio [OR] = 0.49, 95% confidence interval [CI] 0.30, 0.81 and OR = 0.47, 95% CI 0.24, 0.93, respectively). For NSAIDs, aspirin use was also inversely related to glioma risk (OR = 0.68, 95% CI 0.49, 0.96). Both statins and NSAIDs showed significant inverse trends between the duration of drug use and glioma risk (trend tests p = 0.03 and p = 0.02, respectively), and drug intake for >120 months demonstrated the most significant associations for both types of medication. The inverse association between statin therapy and risk of glioma supports the roles of Ras/Rho GTPases or inflammatory cytokines in gliomagenesis, and a similar relationship between NSAIDs and glioma highlights the importance of cyclo-oxygenase 2 in glioma pathogenesis.

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