Prostate cancer micrograph, image via Wikpedia
For years we’ve heard that there’s a connection between stress and cancer. The claim is anecdotal, but has a certain horse sense that appeals to reason — stress is hard on the body, causing hormonal reactions that can potentially influence the development of cancerous cells.
New research doesn’t quite prove the claim, but does indicate that once cancer has taken hold, stress biochemically feeds its growth. The study, by researchers at Wake Forest Baptist Medical Center, focused on the effects of stress on prostate cancer, and found that stress can both reduce the effectiveness of prostate cancer drugs and accelerate the development of the cancer.
The study team, headed by George Kulik, D.V.M., Ph.D., associate professor of cancer biology, 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 trial 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 withbicalutamide, a drug currently used to treat prostate cancer, their prostate tumors decreased in size. However, if mice were subjected to repeated stress, the prostate tumors didn’t respond as well to the drug.
After analyzing the data, the Wake Forest Baptist researchers identified the cell signaling pathway by which epinephrine, a hormone also known as adrenaline, 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,” Kulik said.
In both study models, the mice were then given a beta-blocker–a drug that inhibits the body’s release of adrenaline, with the effect of slowing down heart rate, blood pressure and other bodily functions. The results showed that administering a beta-blocker prevented stress from accelerating tumor growth.
“Providing beta-blockers to prostate cancer patients who had increased epinephrine levels could improve the effectiveness of anti-cancer therapies,” Kulik said. “Our findings could be used to identify prostate cancer patients who will benefit from stress reduction or from pharmacological inhibition of stress-inducing signaling.”
The researchers now plan to test the same signaling mechanism that was identified in mice to determine if it also works in the same way in human prostates, Kulik said.
“We are at the very beginning of understanding complex stress-cancer interactions with multifaceted responses to stress that affect cancer cells, tumor microenvironment, and the organism overall,” he said. “We hope that components of this signaling pathway could be used as biomarkers to predict whether and how a given tumor will respond to stress and anti-stress therapies.”
The findings are published in the February issue of the Journal of Clinical Investigation.
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