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One of the themes covered during Thursday's San Antonio Breast Cancer Symposium was hormonal therapies, a very important aspect of breast cancer care.The first study I want to discuss is actually a prevention study looking at aromatase inhibitors. This class of drugs has been around for about two decades, but as a treatment for advanced breast cancer first and early-stage breast cancer a little later. The whole idea began when researchers examined women who were taking aromatase inhibitors (AI) for early-stage breast cancer. They noticed that women on AIs had fewer cancers develop in the opposite breast, which gave them the idea that AIs could be used as a therapy to actually prevent breast cancer.The study presented on Thursday studied women who were at high-risk for breast cancer who were given either anastrozole, which is an AI, or placebo for five years. Researchers discovered that the AI cut the risk of breast cancer by about half.There are side effects with AIs, such as muscle pain, but in the prevention setting, the side effects didn't seem as severe as when women were taking them to treat existing breast cancer.For now, we haven't seen any overall survival benefit, though. It could be that these drugs lower the risk of breast cancer, but whether that actually equates into saving lives is still up in the air. AIs are not currently approved for breast cancer prevention, but other breast cancer therapies--tamoxifen and Evista--are. Another presentation went into the biology of how hormonal therapies work against breast cancer, including drug resistance in advanced disease. Hormonal therapies generally have fewer side effects than traditional chemotherapy. So, if we can delay drug resistance, women can take hormonal therapies for years with few side effects. Once the cancer does begin to spread, that's when we move to chemotherapy. But the longer women can stay on hormone therapies, the better, which is why we're trying to figure out drug resistance.Mutations can make the estrogen receptor stuck in the on position, which can make the cancer unresponsive, or resistant, to certain hormone therapies. These mutations may have been in the original cancer, but once the hormone therapies kill the sensitive cancer cells, it may leave these few resistant cells an opportunity to begin to rapidly grow and spread. This is really the first step in trying to understand how we can counteract these mutation-carrying estrogen receptors.