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. 2023 Jan 9;21:9. doi: 10.1186/s12967-022-03848-z

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© The Author(s) 2023

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. 6 — Sensitivity of PTC-derived organoid lines for BRAF and MEK inhibitors. a Dose–response curves after 5 days of treatment with BRAF and MEK inhibitors. Each data point represents mean ± SEM of 3 independent biological replicates. IC₅₀ values are calculated and indicated beside the curve graphs. b Scatterplots of the correlation of 1-AUC values for targeted agents and chemotherapeutic drugs screened by two biological replicates (different passages of PTC organoids). Each data point represents 1-AUC for a PTC organoid line treated by the indicated drug. c Drugs with a common target have similar activity profiles across the PTC organoid lines. 1-AUC values are plotted for the inhibitors of BRAF^V600E (vemurafenib and dabrafenib) and MEK (selumetinib and trametinib)