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. Author manuscript; available in PMC: 2019 May 15.
Published in final edited form as: Cancer Res. 2018 Feb 22;78(10):2732–2746. doi: 10.1158/0008-5472.CAN-17-1990

Figure 5. A WHIM12-derived cell line is sensitive to regimens that combine PI3K inhibition with agents that target PI3K downstream signaling components or the MEK/ERK pathway.

Figure 5

A, a schematic network indicates targets for in vitro validation. B, buparlisib in combination with the MEK inhibitor trametinib shows synergistic decrease of cell viability of the WHIM12 cell line. C and D, cells were treated with buparlisib alone or in combination with a PI3K or mTOR inhibitor, respectively, showing synergistic effects on the WHIM12-derived cell line. E, a combination of PI3K and/or mTOR inhibition leads to synergistic decrease of cell viability. F, the dual PI3K and mTOR inhibitor omipalisib shows a marked decrease in cell viability on its own. B-F, mean and error bars (standard deviations) of cell viability treated with indicated drug(s) relative to control from three independent experiments are shown; * ≤ 0.05 and ** ≤ 0.01 as significance.