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. 2020 Oct 30;40(2):322–333. doi: 10.1038/s41388-020-01530-6

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© The Author(s) 2020, corrected publication 2023

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. 7 — Transformation and breast cancer progression are driven by ErbB signaling through EGFR and HER2. These signaling pathways can be effectively blocked through the use of several small molecules that directly act on these RTKs, collectively referred to here as ErbB inhibition (ErbBi). Induction of epithelial–mesenchymal transition (EMT) is a shared mechanism of acquired resistance to ErbBi. Through this process tumor cells originally driven by ErbB signaling upregulate FGFR1 and NRP1. FGFR1 can be directly targeted through the use of small molecule kinase inhibitors (FGFRi). In addition to FGFR1, NRP1 can also enhance signaling from other RTKs that are present such as PDGFR and the MET receptor. Twist-mediated expression of NRP1 during EMT requires BRD4 binding to acetylated H3K27. Therefore, the use of BET inhibitors such as JQ1 in conjunction with targeted inhibition of FGFR may present an effective means to block ErbBi bypass signaling.