Experimental Drug Limits Growth of Prostate Cancer

Agent found to stop growth and spread of prostate cancer with a common chromosomal abnormality.

Agent found to stop growth and spread of prostate cancer with a common chromosomal abnormality.

An investigational treatment for prostate cancer exhibited promising results in slowing the spread of the disease during animal testing.

In laboratory testing, researchers at the Georgetown Lombardi Comprehensive Cancer Center found that the agent, dubbed YK-4-279, prevented the growth and spread of tumors in mice with prostate cancer that carried a common chromosomal abnormality. The study, published online December 5, 2014 in PLOS ONE, examined the potential of YK-4-279, which is the first drug to target the chromosomal translocations found in approximately half of prostate cancer cells.

"Having a compound that works in mouse models brings us closer to early phase human clinical trials," said study lead investigator, Aykut Üren, MD, in a press release. "However, we are only mid-way through that process. We need to establish the potential side effects and figure out the best way to administer this compound in a human clinical study."

The chromosomal translocations occur when 2 normal genes break away from a chromosome and join together in a new location as part of a process called ETS fusion. As a result, this fusion generates new genes that subsequently manufacture proteins that cause prostate cancer cells to become more aggressive and spread.

The researchers tested YK-4-279 using 2 prostate cancer lines that were growing in immunocompromised mice. The agent exhibited strong efficacy when the fusion occurred in mice.

YK-4-279 was found to limit both the growth of the primary tumor and the spread of cancer to the lungs. The drug was also tolerated by mice for long term treatment of 6 to 12 weeks.

"YK-4-279 was very effective against the mice with ETS fusion and was not effective against the mice without it," Üren said. "That demonstrated to us the specificity with which the drug works, and gave us a good reason to expect a similar response in patients with ETS fusion-positive prostate cancer in future clinical trials."