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Triple-negative breast cancer (*TNBC*) is defined by what it *doesn't* have. Specifically, it lacks three key receptors that are commonly found in other types of breast cancer: estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). These receptors are proteins that can receive signals telling the cancer cells to grow. In other words, TNBC cells don't have these receptors, so treatments that target ER, PR, or HER2 won't work on them. This absence of receptors is determined through a relatively simple test called immunohistochemistry (IHC), which is routinely performed on breast cancer tissue samples. Imagine the receptors as antennas on the surface of the cancer cells; TNBC cells simply don't have those antennas, making them unresponsive to therapies designed to jam those specific signals. Because TNBC lacks these common targets, it can be more challenging to treat. Traditional hormone therapies like tamoxifen, which target ER, and HER2-targeted therapies like trastuzumab (Herceptin) are ineffective against TNBC. Instead, treatment typically relies on chemotherapy, surgery, and radiation. Researchers are actively exploring new targeted therapies and immunotherapies that may be more effective against TNBC, focusing on the unique characteristics of these tumors.
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