Cancer researchers have identified a link between a cellular signaling protein and the hormone androgen that could play a role in hormone-resistant prostate cancer.
According to researchers at Thomas Jefferson University’s Kimmel Cancer Center in Philadelphia, the protein Stat5 is turned on in almost all recurrent prostate cancers that are resistant to hormone therapy.
Writing in the January issue of Cancer Research, the researchers also reported that Stat5 could work with cellular receptors for the hormone androgen in cases of recurrent prostate cancer.
“These findings validate Stat5 as a potential drug target in prostate cancer, and in particular, in a form of prostate cancer for which there are no effective therapies,” Dr. Marja Nevalainen, associate professor of cancer biology, said in a prepared statement.
Prostate cancer is the most common cancer in men in the United States. About 219,000 men are diagnosed with the disease every year, according to the U.S. National Cancer Institute. The majority are over the age of 65. About 27,000 men die from the cancer annually.
Men with prostate cancer are often first treated with either surgery or radiation. Hormone therapy is used for subsequent disease. However, when prostate cancer returns years later, it is often more aggressive and tends to resist hormone treatment.
The researchers have previously shown that when Stat5 is turned on, men have a significantly increased risk of recurring cancer.
The research team analyzed prostate cancer cells from 198 patients with prostate cancer recurrence. Stat5 was active in three out of four (74 percent) of the recurrent prostate cancers, they found, and, of those patients, 127 had been treated with androgen deprivation therapy, a hormone therapy. Stat5 was active in 95 percent of the hormone-resistant tumors.
According to the researchers, Stat5 is more likely to be active if patients are treated with androgen deprivation therapy. The protein interacts with the hormone receptors and keeps them active.
The researchers plan to test the dynamic between Stat5 and androgen receptors using animal models to find out if the relationship produces androgen-independent prostate tumor growth.