Figure 1.

The addition of IDO1 inhibitor does not further improve the antitumor activity achieved by the combination of radiation and anti-PD-1 antibody therapies. (A, B) IHC staining of PD-L1 expression in PDACs from patients (n=20) treated without (A) and with (B) neoadjuvant treatment. (C) The treatment scheme. Mice underwent orthotopic implantation procedure receiving 2–3 mm KPC cancer tissues, followed by the combinational treatments with hypofractionated radiation treatment (3 fractions of 8 Gy during days 6–8), a small-molecule inhibitor of IDO1 (60 mg/kg, oral gavage during day 6–26) and/or anti PD-1 antibody (10 mg/kg, intraperitoneal injection for every 4 days, six times). (D, E) Growth curves of tumors evaluated by ultrasound imaging. (D) Growth curves of all treatment groups until day 26 following tumor implantation. (E) Growth curves of selected treatment groups during the entire course of the experiment (till day 56). Shown are the αPD-1 alone, RT/αPD-1, RT/IDO1i, and RT/αPD-1/IDO1i groups. The remaining groups are not shown because mice in these groups started to reach the survival endpoint on day 26. (F) Kaplan-Meier survival curves of mouse pancreatic cancer implantation model treated with combinations of radiation, anti-PD-1 antibody and IDO1 inhibitor. No mice were excluded for survival analysis. Data represent results obtained from experiments with five mice per group that was repeated at least twice. The error bars represent mean with SD. *P<0.05, **P<0.01; NS, not significant, by unpaired t-test or log-rank test. IDO1i, indoleamine 2,3-dioxygenase 1 inhibitor; IHC, immunohistochemistry; PDACs, pancreatic ductal adenocarcinomas; RT, radiation therapy.