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Stress may reduce effectiveness of PCa therapies

Emotional stress may be more than a side effect of a prostate cancer diagnosis, according to a new study that found stress can also reduce the effectiveness of prostate cancer therapies and accelerate the development of the disease.

Emotional stress may be more than a side effect of a prostate cancer diagnosis, according to a new study that found stress can also reduce the effectiveness of prostate cancer therapies and accelerate the development of the disease.

The research findings, from Wake Forest Baptist Medical Center in Winston-Salem, NC, are published online in the Journal of Clinical Investigation (Jan. 25, 2013).

Researchers led by George Kulik, DVM, PhD, tested the effects of behavioral stress in two different mouse models of prostate cancer. One model used mice that were implanted with human prostate cancer cells and treated with a drug that is currently in clinical trials for prostate cancer treatment. When the mice were kept calm and free of stress, the drug destroyed prostate cancer cells and inhibited tumor growth. However, when the mice were stressed, the cancer cells didn’t die and the drug did not inhibit tumor growth.

In the second model, mice genetically modified to develop prostate cancer were used. When these mice were repeatedly stressed, the size of prostate tumors increased. When the mice were treated with bicalutamide (Casodex), their prostate tumors decreased in size. However, if mice were subjected to repeated stress, the prostate tumors didn’t respond as well to the agent.

After analyzing the data, researchers identified the cell signaling pathway by which epinephrine sets off the cellular chain reaction that controls cell death. Considering that prostate cancer diagnosis increases stress and anxiety levels, stress-induced activation of the signaling pathway that turns off the cell death process may lead to a vicious cycle of stress and cancer progression, Dr. Kulik said.

Yet in both models in which the mice were given a beta-blocker, which inhibits the activation of anti-death signaling by epinephrine, stress did not promote prostate tumor growth.

"Providing beta-blockers to prostate cancer patients who had increased epinephrine levels could improve the effectiveness of anti-cancer therapies," Dr. Kulik said. "Our findings could be used to indentify prostate cancer patients who will benefit from stress reduction or from pharmacological inhibition of stress-inducing signaling."

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