Component of plastic stimulates growth of certain prostate cancer cells

An estrogen-like chemical commonly used to synthesize plastic food containers has been shown to encourage the growth of a specific category of prostate cancer cell, potentially affecting the treatment efficacy for a subset of prostate cancers.

According to a study published in the January 1 issue of Cancer Research, such prostate cancer cells proved to be vulnerable to exposure to the chemical BPA (bisophenol A), an industrial chemical and nonsteroidal environmental estrogen used in the manufacture of food cans, milk container linings, food storage containers and water supply pipes. About 2.5 billion pounds of the chemical are produced each year.

In particular, the study showed that the affected class of prostate cancer cell, 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 Karen Knudsen, Ph.D., an assistant professor in the University of Cincinnati’s Department of Cell Biology and Center for Environmental Genetics. Scientists estimate that anywhere from eight to 25 percent of all prostate cancer patients may fall into this category.

In the United States 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, said Dr. Knudsen, the study’s senior author. 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,” said Dr. Knudsen. The effect of the environmental non-steroidal BPA on human prostate cancer tumor implants in laboratory animal models will shed additional light on whether the synthetic pseudo-estrogen encourages tumor growth in whole animal systems. “We’ll know more about the ’hormone sensitizing’ ability of BPA in prostate cancer cells from studies on animals. It is also important to note that our study demonstrates that the actual dose of BPA exposure may change the biological response,” Dr. Knudsen said.

The safety of BPA has been under intense debate for several years, with some arguing that exposure to the chemical among humans is safe, with others contending 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, Ph.D., Nicola Fisher, B.S., and Ann Staubach, B.S., all with the University of Cincinnati; Mark Danielsen, Ph.D., Georgetown University, Washington, D.C.; and Ralph De Vere White, M.D., the University of California, Davis.