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. 2020 Feb 22;13:13. doi: 10.1186/s13045-020-0846-y

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© The Author(s). 2020

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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Fig. 4 — In vivo response to targeted therapies and chemotherapy in metaplastic PDXs. a, b Relative tumor growth (RTV) in HBCx-60 and HBCx-165 PDX models treated with BYL-719 (PI3KCa inhibitor) monotherapy, selumetinib (MEK inhibitor) monotherapy, chemotherapy with adriamycin and cyclophosphamide (AC), a combination of BYL-719 + selumetinib, BYL-719 + AC, and selumetinib + AC. Mean ± SD, N = 10 xenografts/group. c Relative tumor growth in the HBCx-178 PDX treated with BYL-719 (PI3KCa inhibitor) monotherapy, selumetinib (MEK inhibitor) monotherapy, chemotherapy with AC, or the combination of BYL-719 + selumetinib. d Western blot analysis of AKT, p-AKT (ser 473), S6, p-S6 (Ser235/236), ERK, p-ERK (Thr202/Tyr204), MEK, p-MEK (Ser217/221), and GAPDH in treated tumors of HBCx-60, HBCx-165, and HBCx-178. N = 3 − 4