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. Author manuscript; available in PMC: 2017 Apr 1.
Published in final edited form as: Cancer Lett. 2015 Dec 3;373(1):88–96. doi: 10.1016/j.canlet.2015.11.029

Fig. 6.

Fig. 6

CPA + CpG treatment delays tumor growth in the non-immunogenic B16F10 melanoma model. (A) Normalized B16F10 tumor volumes, mean ± SE, for: untreated n = 3, CpG-1826, n = 5 until day 6, then n = 4; CPA n = 5, CPA + CpG-1826 n = 5 until day 6 then n = 4. Tumor growth was significantly slowed by CPA (**p < 0.01) and by CPA + CpG-1826 treatment (****p < 0.0001) compared to untreated controls at day 6, as indicated. Tumor volume on days 6, 9 and 12 was significantly lower at p < 0.05 in the CPA + CpG-1826 combination group compared to treatment with CpG alone (dagger symbol) or CPA alone (double-dagger), as indicated. CPA treatment was at 140 mg/kg/injection. (B) qPCR analysis of immune cell marker genes in untreated B16F10 tumors and in treated tumors excised on day 12 (mean ± SE, n = 4–5 mice per group). (C) Basal levels of immune cell marker gene expression in untreated B16F10 tumors compared to untreated GL261 tumors, determined by qPCR, mean ± SE, n = 9–10 mice per group. (D) Comparison of levels of immune cell marker genes induced by CPA + CpG-1826 treatment in B16F10 tumors (day 12, as in panel A), versus GL261 (day 12, as in Fig. 2C), determined by qPCR, mean ± SE, n = 4–5 mice per group.