FRIDAY, May 31 (HealthDay News) -- Researchers have identified a new class of drugs that show promise for treating advanced prostate cancer. The drugs, known as peptidomimetics, interfere with the signaling necessary for prostate cancer cells to grow, according to a new study.
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Prostate cancer depends upon the actions of androgens, such as the "male" hormone testosterone. Androgens activate androgen receptors, resulting in a signal that causes prostate cancer cells to grow.
To stop tumor growth, men with prostate cancer have been treated with drugs to block the production of androgens or block the receptor where androgens bind. However, tumors can grow despite this treatment because of mutations in androgens or receptors.
In the latest study, published online May 28 in Nature Communications, a team of researchers led by Dr. Ganesh Raj, associate professor of urology at UT Southwestern Medical Center at Dallas, found the nontoxic peptidomimetic agents could disrupt androgen-receptor signaling and prevent tumor growth.
When tested in mouse and human tissue models, the drugs blocked the activity of androgens by attacking the protein in a different spot from where the androgen binds, the researchers explained. As a result, prostate cancer cells do not receive the signal to grow -- even when the androgen receptor is activated.
"We are hopeful that this novel class of drugs will shut down androgen-receptor signaling and lead to added options and increased longevity for men with advanced prostate cancer," Raj, the study's senior author, noted in a university news release.
The researchers noted more testing is needed before the drugs could progress to clinical trials involving humans. Results obtained in laboratory experiments are not always replicated in humans.
"Most drugs now available to treat advanced prostate cancer improve survival rates by three or four months," Raj added. "Our new agents may offer hope for men who fail with the current drugs."
-- Mary Elizabeth Dallas
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SOURCE: UT Southwestern, news release, May 28, 2013
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