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In this issue of JAMA Oncology, Harshman et al1 report longer time to progression (TTP) while receiving androgen deprivation therapy (ADT) for patients with prostate cancer who are using statins compared with nonusers (median TTP, 27.5 vs 17.4 months, respectively). The authors1 propose a mechanism through statin-induced competitive inhibition of the androgen precursor, dehydroepiandrosterone-sulfate (DHEAS), uptake via an organic anionic transporting polypeptide (OATP) encoded by SLCO2B1. Preclinical mechanistic data support DHEAS uptake dependence on SLCO2B1 expression, and DHEAS uptake and cell proliferation are decreased at physiologic statin concentrations. As the authors1 point out, the main challenges to the clinical findings of this study are potential inherent confounders and bias associated with any retrospective analysis, of which all cannot be accounted for in a multivariate analysis. For example, patients prescribed statin therapy had generally better prognostic features and likely represent a group more apt to seek early medical care and health maintenance, such as prostate-specific antigen (PSA) screening. Nevertheless, we are provided with intriguing evidence for a mechanism of how statins may exert an antitumor effect in patients being treated for prostate cancer.
Ramos JD, Yu EY. Progress in Understanding What Is Being Statin(ed) in Prostate Cancer. JAMA Oncol. 2015;1(4):428–430. doi:10.1001/jamaoncol.2015.0833
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