Figure 3 from Ex Vivo Tumor-Derived Organoid Pharmacotyping Identifies Personalized Therapeutic Options for Patients with Biliary Tract Cancer

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Concordance of ex vivo drug response and genetic biomarkers. A, Heatmap of responses to the FDA-approved FGFR inhibitors futibatinib, infigratinib, and pemigatinib, as well as other FGFR inhibitors derazantinib, AZD4547, dovitinib, lucitanib, and erdafitinib. Dasatinib was included because, as shown here, sensitivity has been detected in several tumors with FGFR alterations that are clinically resistant to FGFR inhibitors. Alterations in FGFR1, FGFR2, and FGFR3 are annotated. B, Heatmap of responses to the HRAS inhibitor tipifarnib; the BRAF inhibitors vemurafenib and dabrafenib; the MEK inhibitors cobimetinib, trametinib, and binimetinib; and the ERK inhibitor ulixertinib. Alterations in KRAS, NRAS, BRAF, and MEK1 are annotated. C, Heatmap of responses to the PI3K inhibitors alpelisib, AZD6482, buparlisib, idelalisib, NVP-BGT226, taselisib, the PI3K/mTOR inhibitor dactolisib, and the mTOR inhibitor everolimus. Alterations in PIK3CA and PIK3CB are annotated. D, Heatmap of responses to the EGFR inhibitors afatinib, dacomitinib, erlotinib, gefitinib, osimertinib, poziotinib, and vandetanib and the ERBB2 inhibitors lapatinib and neratinib. Alterations in EGFR, ERBB2, ERBB3, and ERBB4 are annotated. Asterisks next to a patient number signify that the screen failed a measure of quality control but was still evaluable.

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