Friday, October 28, 2011
Hall 1-2 (San Jose Convention Center)
Though tremendous progress has been made in disease diagnosis and treatment, the breast cancer remains an important cause of female mortality. Breast cancer is the second leading cause for cancer related death in women, and therefore it is a major public health issue. The mechanism of breast cancer development is not well understood. Prolonged exposure to elevated levels of estrogen is a known risk factor for breast cancer. The molecular basis for estrogen-induced breast cancer is not known. Studies suggest that increased cell growth, genetic and epigenetic alterations, and gene expression changes are characteristic features of cancer cells. Therefore, the objective of this study was to determine whether exposure to estrogenic chemicals causes an increase in cell growth and/or changes in gene expression involved in cell growth and epigenetic mechanisms. To achieve this objective, the MCF-7 cells derived from human breast tumors were treated with natural estrogen, 17 beta-estradiol and synthetic estrogen, diethylstilbestrol (DES). DES is a pharmaceutical drug prescribed in the 1940’s to prevent miscarriages. The effect of exposure to these estrogens on the growth of MCF-7 cells was determined by cell count analysis. Our preliminary data suggest that both 17 beta-estradiol and diethylstilbestrol (DES) cause increased growth of MCF-7 breast cancer cells. The result of cell growth analysis will further be verified by MTT assay. The effect of DES on genes expression will also be measured by quantitative real-time PCR. The findings of this study will help to better understand the mechanism of estrogen-dependent breast cancer.