Statins delay PCa progression in patients on ADT

June 1, 2015

Despite the benefit shown in this research, a study author says it’s too early to change practice.

A new study suggests statins delay prostate cancer progression by a median of 10 months in patients receiving androgen deprivation therapy (ADT).

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“This median 10-month benefit in delaying disease progression suggests that statins could be a valuable addition to our current therapies for prostate cancer,” said the study’s first author, Lauren C. Harshman, MD, of Harvard Medical School and Dana-Farber Cancer Institute, Boston.

But while the association sounds promising, it’s too early to change practice, senior author Philip Kantoff, MD, of Dana-Farber Cancer Institute, told Urology Times.

“Statins might be beneficial to men being treated with initial androgen deprivation therapy, but prospectively collected data is required to change practice,” Dr. Kantoff said.

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For the study, which was published online in JAMA Oncology (May 7, 2015), the authors studied statin use in 926 patients who received ADT for biochemical, metastatic recurrence, or de novo metastatic prostate cancer. They performed in vitro studies to determine statins’ impact on dehydroepiandrosterone sulfate (DHEAS) uptake and then assessed an institutional database for an association between statin use and time to progression during ADT.

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Longer TTP in statin cohort

They found that 283 (31%) of the patients were taking statins at the start of ADT. Seventy percent of the total patient population, or 644 patients, experienced disease progression after a median follow-up of 5.8 years. Median time to progression during ADT was 20.3 months, the authors reported. However, men taking statins had a median time to progression of 27.5 months, compared to non-statin users’ median time to progression of 17.4 months.

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This positive effect with statins occurred in patients with and without metastases.

Laboratory studies have long suggested that statins might delay prostate cancer growth in patients receiving ADT because the therapy reduces androgen in the body, therefore preventing prostate cancer cells from using it to fuel their growth.

In lab-grown prostate cancer cell lines, Dr. Harshman and colleagues demonstrated that statins block DHEAS uptake by competitively binding to a protein called SLCO2B1. DHEAS and statins are substrates for SLCO2B1.

“We present a plausible mechanism by which statins may work in prostate cancer by decreasing the tumor’s available androgen pool and thus improving patient outcomes," Dr. Kantoff said.

 

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