Figure 1
Figure 1. Small-molecule XIAP antagonist induces apoptosis of DLBCL patient cells. (A) Dose-response curves for each DLBCL sample after 4 hours of treatment with the XIAP antagonist (●) 1396-12 (left) or the inactive control (○) 1396-28 (right). (B) Detection of the percentage of cell death after 4 hours of treatment with 25 μM XIAP antagonist in DLBCL samples, tonsil GC B cells, and PBMC B cells. The observed percentage of XIAP antagonist-induced cell death was defined as the percentage of cell death induced by XIAP antagonist 1396-12 minus the percentage of cell death induced by the inactive compound 1396-28. When the percentage cell death greater than 2 times the standard deviation of the mean value of the nonneoplastic cells (GC B cells and PBMC B cells) was taken as the cut-off value (indicated by ¦), we found that 16 of 20 tested samples were sensitive to the XIAP antagonist.

Small-molecule XIAP antagonist induces apoptosis of DLBCL patient cells. (A) Dose-response curves for each DLBCL sample after 4 hours of treatment with the XIAP antagonist (●) 1396-12 (left) or the inactive control (○) 1396-28 (right). (B) Detection of the percentage of cell death after 4 hours of treatment with 25 μM XIAP antagonist in DLBCL samples, tonsil GC B cells, and PBMC B cells. The observed percentage of XIAP antagonist-induced cell death was defined as the percentage of cell death induced by XIAP antagonist 1396-12 minus the percentage of cell death induced by the inactive compound 1396-28. When the percentage cell death greater than 2 times the standard deviation of the mean value of the nonneoplastic cells (GC B cells and PBMC B cells) was taken as the cut-off value (indicated by ¦), we found that 16 of 20 tested samples were sensitive to the XIAP antagonist.

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