Previous research has found that there may be a link between statin use and improved outcomes for prostate cancer.
Previous research has found that there may be a link between statin use and improved outcomes for prostate cancer. But researchers have not had much data on how outcome is affected by statins in combination with androgen deprivation therapy (ADT) - the "cornerstone" treatment for metastatic hormone-sensitive prostate cancer.
The researchers behind the study, from the Dana-Farber Cancer Institute in Boston, MA, investigated a transporter gene that allows various drugs and hormones to enter cells.
As well as being used by statins to enter cells, this gene - SLCO2B1 - is also used by the testosterone precursor dehydroepiandrosterone sulfate (DHEAS).
The Dana-Farber team wanted to find out whether statins would interfere with the ability of DHEAS to penetrate cells, and if so, whether this could delay resistance to ADT. To do this, the researchers analyzed statin use in 926 patients who initiated ADT for prostate cancer between 1996 and 2013.
Time to disease progression varied between statin users and non-users
They found that 31% of the participants were taking a statin when they began ADT. After 6 years, the disease progressed in 70% of the patients while they were receiving ADT.
The researchers then compared the median disease progression times of patients who had been taking statins with patients who had not been taking statins. They found that the median time to disease progression among statin users was longer at 27.5 months than it was for non-users at 17.4 months.
The authors write:
"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."
Jorge D. Ramos and Dr. Evan Y. Yu, of University of Washington School of Medicine in Seattle, write in a related editorial that the study is a "compelling argument for a biologic mechanism of action of statins in advanced prostate cancer through competitive inhibition of the uptake of DHEAS via SLCO2B1-encoded transporters."
However, Ramos and Yu point out that "randomized, prospective validation of the clinical benefits of statin use in advanced prostate cancer is necessary" to confirm the findings.
While the current study provides a framework for future evaluation, Ramos and Yu conclude that "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."