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. 2021 Jul 16;13:116. doi: 10.1186/s13073-021-00926-7

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© The Author(s) 2021

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.

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Fig. 9 — In vivo targeted treatment tests. a, b CET-sensitive models with increased baseline GF expression were treated with the indicated mono- or combination therapy aiming at response optimization and delay of SR development. *, each star represents a tumor that was taken out due to weight loss of the mouse. c Individual growth curves for tumors under either CET mono- or CET-trametinib combination therapy from panel a. d–g The indicated CET SR models were treated with the indicated mono- or combination therapy addressing identified SR mechanisms. PD, progressive disease; PR partial response; gray shaded area, stable disease. h Representative immunoblots of total STAT3 protein expression and phosphorylation of STAT3 at Y705 [pSTAT3 (Y705)]. K, untreated BoC32 tumors; 5dC, tumors treated for 5 days with CET; C, tumors which developed SR under chronic CET treatment (left panel) as well SR tumors treated with the indicated mono- or combination therapy (right panel). i Relative quantification of the indicated protein signal intensities to the corresponding intensities of the control tumor normalized with the corresponding beta-actin signal intensities using Image Lab (BioRad). Relative growth curves are derived from mean values ± SEM (error bars); V, Vorinostat; R, Ruxolitinib. j The BoC32 CET SR model with high pSTAT3 was treated with the indicated mono- or combination therapy addressing activated STAT3 signaling