Individuals diagnosed with specific diseases may represent subpopulations with heightened sensitivity to environmental compounds. This may be due to their disease-mediated molecular milieu and/or the interference of environmental compounds with
pharmaceutical drug targets.
Prostate cancer represents a significant clinical challenge in the United States. If the disease becomes advanced, standard
therapies are ineffective, leading to high rate of patient morbidity and mortality. Understanding the complex reasons for therapeutic resistance is critical for improving the life expectancy for patients with this
cancer. Recently, it has been identified that common somatically derived genetic mutations that arise following the selective pressure of standard
prostate cancer treatments may facilitate sensitivity to environmental contaminants. These somatic mutations within the
androgen receptor allow the
estrogen mimic,
bisphenol A (BPA), to bind and activate the receptor, resulting in increased proliferation and
tumor growth in the presence of the traditional
therapy regimen for
prostate cancer. In an in vivo xenograft model of
prostate cancer, low level exposure of BPA was sufficient to reduce the efficacy of treatment. Herein, the possible effect of BPA on
prostate cancer treatment and disease management for humans is explored as an example of environmental
endocrine disruptor exposure reducing the efficacy of disease management. These data lend support to the hypothesis that environmental exposure to select compounds may interfere with specific therapeutic regimens.