The January 21, 2013 issue of The Journal of Cell Biology published a report by Susana Gonzalo at Saint Louis University and her associates that indicates a possible benefit for vitamin D in triple-negative breast cancer, one of the more treatment resistant forms of the disease. Triple-negative breast cancer tumors do not express receptors for estrogen, progesterone or HER2, and are therefore unresponsive to hormone-targeted therapies.
Dr Gonzalo's research discovered a molecular pathway in women with triple negative breast cancer and mutations in a tumor suppressor gene known as BRCA1. Loss of BRCA1 function impairs the cells' ability to repair DNA double-strand breaks and halt the proliferation of damaged cells.
It was recently discovered that the loss of another DNA repair factor known as 53BP1 enables the proliferation of BRCA1-deficient cells. Dr Gonzalo's team discovered that the protease cathepsin L degrades 53BP1, and that vitamin D restores it. "It's a new pathway that explains how breast cancer cells lose 53BP1," stated Dr Gonzalo, who is an assistant professor of biochemistry and molecular biology at Saint Louis University. She added, however, that the mechanism behind the increase in cancer cells' nuclear cathepsin L has not been defined.
In further research utilizing tissue samples from breast cancer patients with BRCA1 mutations or triple-negative breast cancer, the team found high levels of nuclear cathepsin L and decreased levels of 53BP1 and vitamin D receptor. These markers identify which populations might best benefit from cathepsin inhibitors or vitamin D therapy.
The Science of Skin Care
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