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. Author manuscript; available in PMC: 2022 Jan 6.
Published in final edited form as: Cancer Discov. 2021 Jun 14;11(10):2544–2563. doi: 10.1158/2159-8290.CD-20-0872

Figure 4: Inhibiting Bcl-xL sensitizes FLC but not PHH (next page).

Figure 4:

(A) Normalized percent survival of FLC1-6 and PHH with anti apoptotic inhibitors navitoclax (Bcl2/Bcl-xL), obatoclax (Bcl2/Bcl-xL) and venetoclax (Bcl2). (B) Differential expression analysis of Bcl-xL in non-tumor liver (N), tumors (T) and PDX (P), from RNA-Seq (left). Differential expression of Bcl-xL in non-tumor liver, sensitive (FLC1 and 4) versus resistant (FLC 2,3 and 5) tumors and derived PDX (right). (C) Differential expression analysis of additional antiapoptotic (Bcl2, Mcl1) and proapoptotic (BIM, BID, NOXA, PUMA) genes in non-tumor liver, tumors and PDX, from RNA-Seq. (D) The ZIP synergy score of combination therapy with panobinostat and A1331852 (Bcl-xL inhibitor), AZD5991 (Mcl1 inhibitor) and Venetoclax (Bcl2) for FLC1,3,5 and PHH. (E) Dose response curves of panobinostat in the absence (full circles) and presence (empty cicles, dotted lines) of A1331852, showing the normalized percent survival for FLC1,3,5 (blue, green and orange, respectively) and PHH (black). (F) Synergy scores (ZIP, Bliss and HSA) for A1331852, Navitoclax and Venetoclax anchor screens.