Winston-Salem, N.C. -- New findings about how prostate cancer cells are able to resist hormone treatment and defy death may lead to more effective drug treatments, according to researchers from Wake Forest University School of Medicine and colleagues.

"We hope this will lead to new treatments or ways to monitor treatment to make sure it's having its intended effect," said George Kulik, Ph.D., D.V.M., assistant professor of cancer biology and senior researcher.

The goal of the research was to uncover how prostate cancer cells become resistant to treatment that lowers levels of male hormones such as testosterone, which the cells normally need to survive. They found that a protein known as BAD is involved in three different survival strategies used by the cancer cells. Their results are published in the July 28th issue of the Journal of Biological Chemistry.

"The normal response of prostate cells when male hormones are blocked is cell death," said Kulik. "The cancer cells find a way to resist the treatment and we wanted to discover the mechanism."

Treatments for prostate cancer include surgery, radiation therapy and hormone therapy, also known as androgen ablation therapy because it reduces levels of the male hormones that can stimulate the growth certain types of prostate cancer. Lowering hormone levels makes prostate cancer shrink or grow more slowly. It is considered the most efficient systemic therapy for prostate cancer. However, nearly all prostate cancers become resistant to this treatment over time.

The researchers evaluated three different pathways involved in cell signaling, the complex system of communication that governs cell actions. It had previously been shown that three pathways (activated by vasoactive intestinal peptide, epidermal growth factor or phosphoinositide 3-kinase) are known to be involved in cell survival. The goal of the researchers was to learn how these pathways are involved in the can
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Contact: Karen Richardson
krchrdsn@wfubmc.edu
336-716-4453
Wake Forest University Baptist Medical Center
27-Jul-2006