In particular, the study showed that the affected class of prostate cancer cells, characterized by mutated receptors for androgens, the male hormone, can proliferate in response to BPA.
"The results may have implications for men who develop BPA-susceptible mutations in their androgen receptor genes during the course of prostate cancer treatment, although these concepts will need to be verified in animal systems," according to Dr. Knudsen, assistant professor in the Department of Cell Biology, Neurobiology and Anatomy and UC's Center for Environmental Genetics.
Scientists estimate that anywhere from 8 to 25 percent of all prostate cancer patients may fall into this category.
In the U.S. alone this year, almost 220,000 men will be diagnosed with prostate cancer. The disease is the second most common type of cancer found in American men, and approximately 29,000 men will die from prostate cancer this year.
Many cases of prostate cancer depend on androgens like testosterone for tumor growth and cancer cell proliferation, says Dr. Knudsen. A common treatment for prostate cancer includes limiting testosterone synthesis. Patients with mutated androgen receptors may not respond to this therapy and according to this new study, exposure to BPA among these patients could potentially put them at higher risk for increased cancer cell growth.
"The results we see in cell culture in response to BPA are ready to be moved to appropriate animal models next," says Dr. Knudsen.
The effect of the environmental non-steroidal BPA on human prostate cancer tumor implants in laboratory models will shed additional light on whether the synthetic pseudo-estrogen encourages tumor growth in whole systems.
The safety of BPA has been under intense debate for several years. Some argue that exposure to the chemical among humans is safe; others contend that it may promote the growth of human tumor cells and alter the growth and development of animals.
Also participating in the study were Yelena Wetherill, PhD, Nicola Fisher and Ann Staubach, all with the Univer-sity of Cincinnati; Mark Danielsen, PhD, Georgetown University, Washington, D.C.; and Ralph De Vere White, MD, the University of California, Davis.
