Figure 6.
COX Inhibition Synergizes with Anti-PD-1 Blockade in Immune-Dependent Tumor Growth Control
(A) Left: growth of parental COX-competent tumors following implantation of 105 BrafV600E melanoma cells into C57BL/6 mice. Mice received aspirin in the drinking water and/or 200 μg of anti-PD-1 monoclonal antibody i.p. every 3–4 days from day 3 to day 24. Right: the percentage of mice that fully rejected tumors over time is shown.
(B) Pooled tumor diameters at 19 days post-implantation of BrafV600E melanoma cells into WT or Rag1−/− mice treated as in (A). Each dot represents one independent tumor.
(C) As in (A) but using an inoculum of 106 melanoma cells.
(D) The percentage of tumor-free mice at 6 weeks post-implantation of parental BrafV600E cells into C57BL/6 mice that were untreated (n = 15) (naive) or that previously rejected BrafV600E cells following anti-PD-1 (n = 6) or aspirin + anti-PD-1 treatment (n = 8) (pre-treatment).
(E) As in (A) but C57BL/6 mice received celecoxib i.p. daily from day 0.
(F) As in (A) but Balb/c mice received 105 CT26 colorectal cells. Growth profiles are presented as average tumor diameters ± SEM and are representative of at least two independent experiments with five mice per group.
Samples were compared using two-way ANOVA (A, C, E, and F), one-way ANOVA (B), Fisher’s exact test (D), and log rank test (A and F). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.