Heart drug may fight prostate cancer

Digitalis users less likely to develop the malignancy

ORLANDO, Fla. — A long-standing drug for heart failure might find new utility as a treatment for prostate cancer, a new study finds.

Digitalis, also called digoxin, is derived from the foxglove plant and has a lengthy medical history. Its role as a treatment for heart failure and heart arrhythmia has declined in recent years with the advent of newer drugs, but it remains an option for patients.

The drug’s potential new use arose after researchers screened more than 3,100 compounds, more than half of them existing drugs, looking for an effect on prostate cancer cells. Digitalis stood out by inhibiting proliferation of the cells in vitro.

Using a two-pronged strategy reported in the April Cancer Discovery, the researchers then tested this apparent biological effect by evaluating the medical histories of more than 47,000 men who had taken part in a medical study between 1986 and 2006.

That database showed that digitalis users were 6 to 28 percent less likely to develop prostate cancer than were men who had never used the heart drug. And men who took the drug for at least 10 years were 37 to 79 percent less likely to develop the cancer, the scientists report.

Digitalis works by binding to an enzyme in the membrane of heart muscle cells, starting a chain reaction that boosts the cells’ ability to contract. This slows the heart rate while improving pumping action.

The researchers now plan to study how the drug influences cancer, says study coauthor Elizabeth Platz, an epidemiologist at the Johns Hopkins Medical Institutions in Baltimore. “If we can figure out the mechanisms, maybe new drugs can be developed that specifically target that mechanism,” she says. “Or maybe digoxin itself can be modified so that it homes to the prostate.”

Digitalis has side effects, so it’s unlikely that doctors would use it in men with early-stage prostate cancer. The drug might find use in men who have more severe cancer and few good treatment options, Platz says. “But we still need to know the mechanisms of action.”

The new study deploys “an interesting strategy that illustrates a growing trend toward coupling massively parallel screening [of compounds] with large patient-population datasets in order to understand the relationship between, in this case, medication use and the risk of developing disease,” says Louis Weiner, a medical oncologist and director of the Lombardi Comprehensive Cancer Center at Georgetown University in Washington, D.C. “This is a retrospective analysis that creates a very attractive hypothesis that now needs to be validated in a prospective study.”

Cancer Discovery is a new scientific journal designed to provide an outlet for such studies. Its inaugural issue, which includes this paper, was unveiled April 3 at the American Association for Cancer Research’s annual meeting in Orlando, Fla.

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