New research from Dana-Farber Cancer Institute in Boston suggests that statins may help slow the growth of prostate cancer in patients receiving hormone therapy. Statins are normally used to lower cholesterol levels in people with high cholesterol. There has been previous research which has shown a link between statins and prostate cancer, however, there has not been much evidence to show how statins work in combination with androgen deprivation therapy.
What is ADT for Prostate Cancer?
Androgen deprivation therapy (ADT) is a hormone therapy used to treat prostate cancer that has spread beyond the prostate gland or when a patient experiences a recurrence of prostate cancer. Androgen hormones, such as testosterone, are hormones that fuel the growth of prostate cancer. Androgen deprivation therapy works by depriving the body of testosterone since they help prostate cancer cells grow. Unfortunately, androgen deprivation therapy does not work forever; it becomes less effective after having been on it for a while in which case the cancer begins to grow again.
Researchers at the Dana-Farber Cancer Institute decided to investigate a transporter gene called SLCO2B1 which allows certain drugs and hormones to enter cells. SLCO2B1 is used by statins to enter cells, as well as the testosterone precursor dehydroepiandrosterone sulfate (DHEAS).
Statins and Prostate Cancer
The researchers wanted to investigate whether statins intervene with DHEAS’s ability to enter cells and if they do, whether this could defer resistance to androgen deprivation therapy. In order to test this, the researchers gathered 926 patients who started androgen deprivation therapy for prostate cancer between 1996 and 2013, and analyzed their statin use.
The results showed that the length of time of the progression of prostate cancer varied between patients who used statins and patients who did not. They found that 31 percent of the patients were taking a statin when they started androgen deprivation therapy. After following the patients for six years, they found that the disease progressed in 70 percent of the patients while they were receiving androgen deprivation therapy.
The researchers 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 patients who used statins was longer at 27.5 months than it was for patients who did not use statins at 17.4 months.
"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," said the study’s authors.
In the study, the statins kept testosterone from entering prostate cancer cells. They blocked DHEAS which prevented cancer cell growth. The study also showed that statins use up the amount of SLCO2B1, which is what kept DHEAS from the cancer cells and made androgen deprivation therapy more effective.
Before statins can be used for prostate cancer, more research is needed to verify the study’s findings. "We have a strong hypothesis, but it is by no means proof that statins prolong the time to relapse. But the data is strongly suggestive that that's the fact," said senior author Dr. Philip Kantoff. Dr. Kantoff is the chief of solid tumor oncology at the Dana-Farber Cancer Institute.
The study was published this month in the online journal JAMA Oncology.