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. 2023 Dec 18;20(1):28–55. doi: 10.1038/s44320-023-00004-7

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© The Author(s) 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 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/. Creative Commons Public Domain Dedication waiver http://creativecommons.org/publicdomain/zero/1.0/ applies to the data associated with this article, unless otherwise stated in a credit line to the data, but does not extend to the graphical or creative elements of illustrations, charts, or figures. This waiver removes legal barriers to the re-use and mining of research data. According to standard scholarly practice, it is recommended to provide appropriate citation and attribution whenever technically possible.

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Figure EV3 — (A) Phenotypic drug response of two sarcoma lines towards 11 PDGFRB inhibitors. (B) Distribution of activity scores of proteins in RD-ES (top panel) and RD cells (bottom panel) showing that MAP2K1 and its downstream substrates MAPK1 and MAPK3 have different activities in the two cell lines. This translates into differences in phenotypic response of the two cell lines to MAP2K inhibitors (right panel). (C) Ranked list of kinases either considering kinase abundance, substrate phosphorylation abundance or computed activity in SK-ES-1 cells (left panel) showing that AURKA phosphorylation and activity is substantially higher than protein abundance. This translates into a strong response of the cell lines to AURKA inhibitors (right panel). (D) Same as panel (C) but for DDR2 in A204 cells. (E) Left panel: list of kinases ranked by activity score in SW684 cells. The asterisk denotes a kinase that is a target of the kinase inhibitor. Middle panel: relative sensitivity of SW684 cells to all drugs in the screen. Right 2 panels: CDK1 activity score and drug responses toward Dinaciclib among 17 sarcoma lines. (F) The heatmap summarises the Pearson correlations of proportions of cell cycle clusters (from Kelly et al) and drug responses from 87 drugs (AUC <0.8).