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. 2022 Aug 5;13(8):678. doi: 10.1038/s41419-022-05133-9

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© The Author(s) 2022

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

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Fig. 2 — A Tumor sections from four PDX models (ACCx9, ACCx11, ACCx5M1, and ACC6) collected at baseline (before implantation) were stained for NICD1, MYC, and Ki67 using an IHC. Representative images are shown. B Transactivation activity of wild-type full-length NOTCH1 (FL-NOTCH1), constitutively active γ-secretase dependent form of the NOTCH1 receptor (ΔECD-NOTCH1), and alleles containing mutations carried by ACCx9 and ACCx11 PDX tumors (ACC9-I1680N and ACC11-S1723ins28, respectively) was assessed using a dual-luciferase reporter assay. Bars represent the average of five independent experiments performed in triplicates and indicate fold-change relative to FL-NOTCH1 (red line). Percent inhibition induced by AL101 (gray bars) relative to DMSO (white bars) is indicated in blue. ***p < 0.001.