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Statins may slow prostate cancer progression in advanced disease

They may ward off resistance to hormone therapy by interfering with testosterone pathway

Caroline White

Friday, 08 May 2015

Statins may help slow prostate cancer progression in men with advanced disease taking hormone suppressants, suggests research* published online in JAMA Oncology.

Previous research has suggested an association between statin use and improved clinical outcomes for prostate cancer, possibly because these drugs use the same transporter gene (SLCO2B1) to enter cells as many other drugs and hormones.

But it has not been clear if statins have any impact on the disease in men on androgen deprivation therapy, the cornerstone of treatment for advanced hormone-sensitive prostate cancer.

The researchers used prostate cancer cell lines to see whether statins interfered with uptake of dehydroepiandrosterone sulfate (DHEAS), a precursor of testosterone which uses SLCO2B1 to gain entry into cells.

These laboratory studies showed that statins block DHEAS uptake by competitively binding to SLCO2B1.

They then analysed statin use in 926 patients taking hormone suppressants for prostate cancer between 1996 and 2013. Some 283 (31%) were taking a statin when they started hormone suppressant therapy.

After an average monitoring period of nearly six years, the disease progressed in 644 patients (70%). The average time to progression was 20.3 months, but in men taking statins the average time to progression was longer, at 27.5 months compared with 17.4 months among those not taking statins.

“Our in vitro finding that statins competitively reduce DHEAS uptake, thus effectively decreasing the available intratumoral androgen pool, affords a plausible mechanism to support the clinical observation of prolonged TTP [time to progression] in statin users,” write the authors from the Dana-Farber Cancer Institute in Boston, Massachusetts.

It’s possible that the explanation for this may lie in the ability of statins to delay resistance to hormone suppressants by interfering with the ability of DHEAS to get into cells.  

In a linked editorial**, Drs Jorge Ramos and Evan Yu, of University of Washington School of Medicine, Seattle, say that the authors make a compelling case for the biological action of statins.

But they caution that the findings would need to be replicated in randomised, clinical trials before any firm conclusions could be drawn.

“In all, [the authors] have conducted an interesting analysis linking in vitro preclinical data with retrospective patient outcomes, providing a framework for future evaluation. Nonetheless, the current data are not sufficient to support incorporation of statin use into clinical oncology practice for patients with prostate cancer and additional studies are required,” they write.

* Lauren C. Harshman, et al. Statin Use at the Time of Initiation of Androgen Deprivation Therapy and Time to Progression in Patients With Hormone-Sensitive Prostate Cancer. JAMA Oncol. Published online May 07, 2015. doi:10.1001/jamaoncol.2015.0829

** Jorge D. Ramos, et al. Progress in Understanding What Is Being Statin(ed) in Prostate Cancer. JAMA Oncol. Published online May 07, 2015. doi:10.1001/jamaoncol.2015.0833

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