Fig. 6.

Increased CD8⁺ T cell infiltration and impaired tumor growth in FGFR1 KO tumors. (A) Expression of FGFR1, in mouse PDAC FGFR1 WT and KO cells, was measured by immunoblotting. (B) In vitro comparison of PD-L1 cell surface expression in mouse PDAC cells and their FGFR1-KO cells, quantified by FACS analysis. (C) C57BL/6 mice were inoculated with syngeneic pancreatic cancer cells (FGFR1 WT or KO; n=7) expressing K-ras^G12D (2 × 10⁶ cells per injection). Tumor size data (means ± SD) were log-transformed before statistical analyses using generalized linear model. (D) BALB/c nude mice were inoculated with syngeneic pancreatic cancer cells (FGFR1 WT or KO; n=7) expressing K-ras^G12D (1 × 10⁶ cells per injection). Tumor size data (means ± SD) were log-transformed before statistical analyses using generalized linear model. (E) C57BL/6 mice were inoculated with syngeneic pancreatic cancer cells as described in (C). The mice were sacrificed at day 21 after tumor inoculation. PD-L1 protein expression was evaluated by IHC and scored as described in methods. (F) Tumor tissues were processed for immunostaining of CD8⁺ T cells (same tumor samples than E). The number of CD8⁺ lymphocytes was quantified in each group. (G-I) Quantitative RT-PCR analysis of IFNγ (IFNG), Granzyme B (GZMB) and Perforin (PRF1B) mRNA expression in tumor tissues from mice (same tumor samples than E). Statistical analysis: Data are mean ± SEM of three independent experiments (B) or three biological replicates (E–I); One-way ANOVA followed by Tukey post hoc test for B, E-I. *, P < 0.05; **, P < 0.01; ***, P < 0.001.