For years, researchers have suspected a close causal relationship between stress and the development of cancer. We know that stress causes hormonal reactions that can potentially affect the development of malignant cells, but no direct cause and affect link has been proven. Now new research proves that once cancer is developing inside the body, stress biochemically helps it grow.
The study, headed by Dr. George Kulik, associate professor of cancer biology at Wake Forest University, Baptist Medical Center, observed the effects of stress on prostate cancer in two mouse models. It found that stress reduces the effectiveness of the anti-cancer drugs used to treat prostate cancer, and accelerated the development of the cancer.
In the first model, mice were implanted with human prostate cancer cells, then treated with a drug currently in clinical trials. When the mice were kept calm and not subjected to stress, the drug successfully destroyed the prostate cancer cells and inhibited new tumor growth. When the mice were stressed, the drug did not kill the cancer cells, nor did it inhibit tumor growth.
In the second model, the mice used had been genetically modified to develop prostate cancer. Under repeated stress, the size of the prostate tumors increased. When the mice received a drug currently in use to treat prostate cancer, the tumors shrank. But in mice that were repeatedly stressed, the prostate tumors were much less responsive to the drug therapy.
Through analysis of the date, the researchers identified the cell signaling pathway by which the hormone epinephrine, sometimes known as adrenaline, initiates the cellular chain reaction that controls cell death. Kulik writes:
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.
Mice in both study models then received a beta-blocker, which inhibits the release of adrenaline and slows down the heart rate, blood pressure and other bodily processes. Administration of the beta-blocker drug prevented stress from accelerating the growth of tumors. Kulik concluded,
Providing beta-blockers to prostate cancer patients who had increased epinephrine levels could improve the effectiveness of anti-cancer therapies. Our findings could be used to identify prostate cancer patients who will benefit from stress reduction or from pharmacological inhibition of stress-inducing signaling.
Kulik says the researchers will not test the signaling mechanism observed in the mice to find out if it operates similarly in human prostates. He added,
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. 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.