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. Author manuscript; available in PMC: 2017 Aug 15.
Published in final edited form as: Leukemia. 2017 Jan 23;31(10):2075–2084. doi: 10.1038/leu.2017.32

Figure 1. Ex vivo BTK inhibition increases CLL cell BCL-2 dependence as shown by dynamic BH3 profiling.

Figure 1

Primary CLL cells were co-cultured with the NKTert stromal cell line, and subjected to single drug or combination treatment with ibrutinib alone (panel A), venetoclax alone (panel B), or the ibrutinib + venetoclax combination (panel C). Analogous experiments were performed with acalabrutinib alone (panel D), venetoclax alone (panel E), or the acalabrutinib + venetoclax combination (panel F). Ibrutinib and acalabrutinib were both used at 1 uM for 72 hours, while venetoclax at 1.5 nM was added only for the last 20 hours. Cells were then harvested for BH3 profiling. Delta priming is the difference in mitochondrial response to a BH3 peptide between DMSO- and drug treated samples (Y-axis). The response from BAD peptide, a specific indicator for BCL2 dependence, is shown side-by-side with BIM peptide response. Means are depicted as horizontal bars +/− SD error bars. p values were calculated using a one sample t test to validate if delta priming is different from 0. Ib, ibrutinib; ACP, acalabrutinib. * and ** indicate statistical significance.