Figure 2
Figure 2. PF-04691502 reduces cell viability of CLL cells independently of prognostic markers. (A) CLL samples (n = 25) and normal B (CD19+) and T cells (CD3+) (n = 5) were treated in the presence or absence of PF-04691502 (0.0049-40 μM) for 24 hours. Cell viability was calculated using annexin V/PI assays and measured by flow cytometry. For comparison, a proportion of the same CLL samples were treated with idelalisib (0.0049-40 μM) (n = 12). (B) CLL samples (n = 6, 3 low IC50 and 3 high IC50 at 24 hours) were treated with PF-04691502 (0.0025-2.5 μM) for 24 to 72 hours. Correlation of the response to PF-04691502 with prognostic markers (C) IGHV (n = 21), (D) ZAP-70 (n = 23), and (E) CD38 (n = 23). Error bars represent SEM. M-CLL, mutated IGHV genes; U-CLL, unmutated IGHV genes; +ve, positive; -ve, negative.

PF-04691502 reduces cell viability of CLL cells independently of prognostic markers. (A) CLL samples (n = 25) and normal B (CD19+) and T cells (CD3+) (n = 5) were treated in the presence or absence of PF-04691502 (0.0049-40 μM) for 24 hours. Cell viability was calculated using annexin V/PI assays and measured by flow cytometry. For comparison, a proportion of the same CLL samples were treated with idelalisib (0.0049-40 μM) (n = 12). (B) CLL samples (n = 6, 3 low IC50 and 3 high IC50 at 24 hours) were treated with PF-04691502 (0.0025-2.5 μM) for 24 to 72 hours. Correlation of the response to PF-04691502 with prognostic markers (C) IGHV (n = 21), (D) ZAP-70 (n = 23), and (E) CD38 (n = 23). Error bars represent SEM. M-CLL, mutated IGHV genes; U-CLL, unmutated IGHV genes; +ve, positive; -ve, negative.

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