The Effects of Bisphenol A (BPA) on ErbB2 Positive Breast Cancer
Abstract
This grant investigated whether oral administration of the environmental contaminant Bisphenol A (BPA) could accelerate tumorigenesis in a transgenic mouse model that over-expresses the erbB2 proto-oncogene (erbB2-tg). BPA did not function in a traditional, linear dose responsive manner to induce tumorigenesis. Our data indicate that environmentally-relevant concentrations of BPA (BPA2.5 and BPA25) function in a distinctly different manner than regulatory-based concentrations of BPA (BPA250 and BPA2500). The environmentally-relevant BPA doses significantly accelerated mammary tumorigenesis, decreasing tumor latency and increasing tumor multiplicity, burden, and the rate of metastasis. These effects were absent in the regulatory-based BPA doses. Prior to tumor formation in the mammary gland, all doses of BPA significantly increased the cell proliferation index, but only the regulatory-based doses also increased the apoptosis index. When these two end points were used to estimate a ratio of cell-proliferation-to-apoptosis in the mammary gland, a non-monotonic dose response resulted. This end point provided the best prediction of effects induced by each concentration of BPA on mammary tumor development in erbB2-tg mice.
Document Details
- Document Type
- Technical Report
- Publication Date
- Nov 01, 2010
- Accession Number
- ADA551889
Entities
People
- Coral Lamartiniere
- Sarah A. Jenkins
Organizations
- University of Alabama