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. 2022 Oct 2;13:5789. doi: 10.1038/s41467-022-33461-z

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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. 5 — a Tumor growth curves of ALMC-1 tumors engrafted in NSG mice, treated with vehicle, venetoclax, or bortezomib. Thicker lines are average tumor size for each treatment (n = 4). b Tumor volume at the indicated number of days post initiation of treatment (n = 4). c Overall survival of mouse cohorts grouped by treatment received. d, e hCD45+ cells from ALMC-1 tumors from vehicle-treated (n = 1), bortezomib-treated (n = 2), and venetoclax-treated (n = 2) mice were BH3 profiled to measure their d overall level of apoptotic priming via sensitivity to the BIM BH3, BID BH3, and PUMA BH3 peptides and their e dependencies on the pro-survival BCL-2 family proteins BCL-2, BCL-X_L, and MCL-1. P-values were calculated using two-way ANOVA with Holm–Sidak’s adjustment for b and Log-rank (Mantel-Cox) test to compare survival curves in c.