Does exposure of baby boys -- in utero or in infancy -- to bisphenol A, a man-made chemical which mimics natural estrogens, predispose them to prostate cancer later in life?
A five-year, $2.6 million grant to a University of Illinois at Chicago researcher and her colleague aims to answer this question by shedding light on the mechanism by which it may occur.
Gail Prins, professor of urology at the UIC College of Medicine and lead investigator on the grant, and her colleague, Shuk-Mei Ho, professor and chair of environmental health at the University of Cincinnati, established in earlier studies in animals that perinatal exposure to BPA at very low doses results in increased sensitivity to estrogen as the male animal ages and an increased risk of developing prostate cancer.
Demonstrating a similar link in humans in an epidemiological study is difficult because of the small dosages and long lag time between exposure and effect. With the new grant, from the National Institute of Environmental Health Sciences, Prins and Ho will attempt to unravel the genetic mechanism by which the dose-response effect in animals is thought to occur.
Scientists think that sensitization to estrogen due to a much earlier exposure to an estrogen-like compound is an "epigenetic" phenomenon -- a heritable change in gene function that occurs without a change in the DNA sequence, as in mutation.
In this model, the early environment of the fetus causes chemical changes in DNA, called imprinting, which may cause later changes in gene expression. These epigenetic changes, which result in increased or decreased expression of a gene -- or changes in the type of tissues in which the gene is expressed -- can have profound affects on the development of an organism, Prins said. And there is increasing evidence that these changes may be implicated in the origin of a number of adult diseases, like prostate cancer.
"We hypothesize that early 'imprin
|Contact: Jeanne Galatzer-Levy|
University of Illinois at Chicago