Fig. 4.

V-aCD3^Mu promotes tumor regression and prevents growth of non-established tumors. A 4T1 tumors were peritumorally treated on day 1, 3, 6, and 8 after cancer cell inoculation (indicated by red arrows),before the tumors were established. The mice were treated with either PBS (number of mice (n) = 5), rVAR2 (n = 5), aCD3^Mu (n = 5), CpG (n = 3), V-aCD3^Mu (n = 5), or V-aCD3^Mu + CpG (n = 3). CpG was only administered on day 5 (indicated by a blue arrow).Numbers in parentheses indicate the number of tumor-free animals out of all animals in the group. B Quantification of bioluminescence in vivo imaging of C57BL/6 mice following orthotopic implantation of 5 × 10⁴ Luciferase⁺ primary pancreatic cancer cells (CHX2000) derived from KPC mice (LSL-Kras^G12D/+; p53^f/f; Pdx1-Cre). The mice received intratumoral injections of V-aCD3^Mu (n = 5) or PBS (n = 5) on day 8, 11, 14, 32, 35, and 38. Tumor volumes of treatment versus control group were compared using the Mann–Whitney test. (Left) Tumor growth in individual mice. Baseline luminescence levels of non-tumor-bearing mice are indicated. (Right) Quantification on day 22 and day 43 displays responders and non-responders. On day 22 all mice in the treatment group are responders