Abstract
The current view is that breast cancer is a stem cell disease characterized by the existence of cancer cells with stem-like features and tumor-initiating potential. These cells are made responsible for tumor dissemination and metastasis. Common therapies by chemotherapeutic drugs fail to eradicate these cells and rather increase the pool of cancer stem cells in tumors, an effect that may increase the likelyhood of recurrence. Fifteen years after the first evidence for a small stem-like subpopulation playing a major role in breast cancer initiation has been published a large body of knowledge has been accumulated regarding the signaling cascades and proteins involved in maintaining stemness in breast cancer. Differences in the stem cell pool size and in mechanisms regulating stemness in the different breast cancer subtypes have emerged. Overall, this knowledge offers new approaches to intervene with breast cancer stem cell activity. New options are particularly needed for the treatment of triple-negative breast cancer subtype, which is particularly rich in cancer stem cells and is also the subtype for which specific therapies are still not available.
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