One of the mechanisms that makes so-called triple-negative breast cancer (TNBC) notoriously aggressive and hard to treat is its ability to disarm proteins that suppress tumors and mutate them into tumor drivers. Seeking to better understand this process, a team from Roswell Park Comprehensive Cancer Center decided to focus not on what these TNBC tumors lack but something they possess: an alternate estrogen receptor, ER-beta. In a new article in JNCI: Journal of the National Cancer Institute, they report that a widely used breast cancer drug, tamoxifen, can turn the ER-beta protein into a double agent capable of disrupting the processes that typically make TNBC tumors so devastating.
