In animal model, Emotional stress reduces effectiveness of prostate cancer therapies
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| Credit:ScienceDaily.com |
Not
surprisingly, a cancer diagnosis creates stress. And patients with prostate
cancer show higher levels of anxiety compared to other cancer patients. A new
study by researchers at Wake Forest Baptist Medical Center indicates that
stress is not just an emotional side effect of the diagnosis; it also can
reduce the effectiveness of prostate cancer drugs and accelerate the
development of prostate cancer.
The findings are published in the February issue of the Journal of Clinical Investigation.
The
Wake Forest Baptist 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 with bicalutamide, 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.
Yet in
both models in which the mice were given beta-blocker, stress did not promote
prostate tumor growth. Beta-blocker is a drug that inhibits the activation of
anti-death signaling by epinephrine.
"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."
Source: Wake
Forest Baptist Medical Center
Posted by Unknown
on Monday, January 28, 2013.
Filed under
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