Abstract

According to the Centers for Disease Control and Prevention (CDC), breast cancer is currently the 6th leading cause of death of women in the U.S. (CDC, 2007). Currently, estrogen receptor (ER) positive breast cancers are frequently treated with anti‐estrogens such as tamoxifen. Tamoxifen is a selective ER modulator (SERM) that binds to ER and inhibits the expression of genes associated with cell growth. Although tamoxifen therapy has resulted in some success, resistance often develops with prolonged therapy, in which case the patients no longer respond to tamoxifen. How this resistance develops is unclear. To further understand the mechanism of anti‐estrogen resistance, our lab has developed a tamoxifen resistant breast cancer cell line (MCF7‐TamR). Data from our lab suggests that MCF7‐TamR express lower levels of vitamin D receptor (VDR) than parental MCF7 cells. Additionally, resistant cells also display a greater sensitivity to vitamin D inhibition. Whether this increased inhibition by vitamin D is associated with the VDR levels is unclear. The understanding of how vitamin D inhibits resistant and non‐resistant cells may provide further insight into the development of tamoxifen resistant breast cancer and potentially identify new targets for future therapeutics.

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