A monoclonal antibody targeting a well known cell surface protein inhibited prostate cancer growth and metastasis in an aggressive form of the disease that did not respond to hormone therapy, according to a study by researchers with the UCLA Department of Urology and UCLA's Jonsson Comprehensive Cancer Center.
The researchers also found that the protein, N-cadherin, is up regulated or turned on in prostate cancer that does not respond to hormone therapy, known as castration resistant disease. The results of the study, done in cell lines and mouse models, were confirmed in humans after researchers examined tissue from dozens of men who died from prostate cancer, said Dr. Robert Reiter, a professor of urology, a Jonsson Cancer Center scientist and senior author of the study.
"This therapy may be particularly useful in men who are failing the newest forms of treatment that target the androgen receptor, which regulates testosterone," said Reiter, who is director of the cancer center's Specialized Program of Research Excellence (SPORE) in prostate cancer. "This could potentially offer an effective alternative or addition to those hormone therapies."
The study appears Nov. 7, 2010 in the early online edition of the peer-reviewed journal Nature Medicine.
The study represents a translational effort by Reiter and his team to take their basic science observations and transform them into new therapies for this aggressive form of prostate cancer to be tested in clinical trials. Observations made in those future clinical trials also could be used in the laboratory to refine potential therapies.
Reiter and his team first found that the N-cadherin gene was up regulated in castration resistant prostate cancer, presenting a potential target for therapy. The findings in cell lines and mouse models were confirmed by studying tissue from men who died from their castration resistant disease. Researchers then found that the up
|Contact: Kim Irwin|
University of California - Los Angeles