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. 2018 Sep 24;9(10):976. doi: 10.1038/s41419-018-1034-7

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — (Left side) In primary breast cancer, EGFR signaling is dominated by pro-growth and pro-survival signaling pathways such as Erk1/2, driving several oncogenic processes. In contrast, in metastatic breast cancer (MBC), STAT1 signaling is enhanced, supporting EGF-induced apoptosis. (Right side) EGFR signaling can be biased toward STAT1-mediated apoptosis through pharmacologic inhibition of MEK/Erk signaling using the allosteric inhibitor Trametinib