Cardiac drug, digoxin, could lower risk for prostate cancer

April 4th, 2011 - 4:20 pm ICT by ANI  

Washington, Apr 4 (ANI): Scientists have found that heart drug, digoxin, could be a possible therapy for prostate cancer after using a combination of laboratory science and epidemiology.

The scientists found that men using the cardiac drug had a 24 percent lower risk for prostate cancer, and said that further research may lead to use of the drug, or new ones that work the same way, to treat the cancer.

“Epidemiologists and basic scientists often do not understand each other, as we often are only clear on our own strengths and the other’s weaknesses,” Elizabeth Platz, Sc.D., M.P.H, professor of epidemiology and Martin D. Abeloff, M.D., scholar in cancer prevention at Johns Hopkins University, said.

Digoxin, made from the foxglove plant, has been used for centuries in folk medicine and for decades to treat congestive heart failure and heart rhythm abnormalities.

It also emerged as a leading candidate among 3,000 drugs screened by the Johns Hopkins team for the drugs’ ability to curb prostate cancer cell growth.

The scientists cautioned, however, that their work does not prove digoxin prevents prostate cancer nor are they suggesting the drug be used to prevent the disease.

“This is not a drug you’d give to healthy people,” Platz said.

Platz shares authorship with Srinivasan Yegnasubramanian, M.D., Ph.D., and assistant professor of oncology at Johns Hopkins.

Platz said the multidisciplinary team of scientists had come together to identify existing drugs that could be used to treat prostate cancer in a process called drug repositioning.

“If you use drugs that are already available then you have a long history of safety research that does not necessarily need to be redone, and we can move more quickly to testing whether the drug will actually work in a new setting,” Platz said.

The idea of drug repositioning has been offered before, but each branch of scientific inquiry had enough flaws that it had not previously gained substantial traction.

“When we combined the basic science and the epidemiology approaches, the flaws were not the same and were covered by their respective strengths,” she said.

Platz, Yegnasubramanian and colleagues from Johns Hopkins and Harvard combined a high-throughput laboratory-based screen and a large, prospective cohort study.

In the first stage, the laboratory scientists conducted an in vitro prostate cancer cell toxicity screen of 3,187 compounds, and digoxin, a known heart failure drug emerged as a leading candidate due to its potency in inhibiting cell proliferation in vitro.

In the second stage, the epidemiology team observed the drug’s use in a cohort of 47,884 men who were followed from 1986 to 2006.

Regular digoxin users had a 24 percent lower risk of prostate cancer, while those who had used the drug for more than 10 years had a 46 percent reduced risk.

Platz said this multidisciplinary team is now working toward identifying the pathways digoxin targets in prostate cancer.

Knowing the targets will help inform the design of a trial that will confirm whether digoxin or molecules acting on the same targets has utility as a prostate cancer treatment.

The findings have been published in the April 3 issue of Cancer Discovery. (ANI)

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