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. Author manuscript; available in PMC: 2015 Dec 15.
Published in final edited form as: Cancer Res. 2014 Oct 13;74(24):7191–7197. doi: 10.1158/0008-5472.CAN-14-1379

Figure 3.

Figure 3

Dusp1 deficiency enhances tumor-associated inflammation and disease progression. A, Tumor inflammation scores and expression of pan-leukocyte marker Ptprc by qPCR. n= 12–13 (vehicle), 31 per group (4NQO), p <0.001 (inflammation), n = 7 per group, p = 0.0175, Mann-Whitney (Ptprc). B, Nanostring analysis of chemokine, cytokine, and receptor gene expression. n = 6 per group, p < 0.05. C, FACS analysis of myeloid-lineage cells in spleen and cervical lymph nodes from tumor-bearing mice, using markers CD11b, Ly6C, Ly6G, and F4/80. n = 6 per group. p< 0.05. Immunohistochemistry of F4/80, CD11b, and Ly6G-positive cells quantified in a 10X field of view of oral tumor sections. n = 17–18 (F4/80), 8 (CD11b), 8–9 (Ly6G). p = 0.0176 (Ly6G). D, Volumes of subcutaneous EO771 tumors with daily intraperitoneal injections of SB203580 (5mg/kg) or vehicle control, starting on day 7. Rate of tumor growth is increased in Dusp1-deficient vehicle-treated animals (p < 0.0001) and Dusp1-deficient SB203580-treated animals (p = 0.0098). Dusp1-deficient animals had decreased survival compared to wild-type animals (p = 0.0123). Survival was enhanced in Dusp1-deficient animals treated with SB203580 compared to vehicle treatment group (p = 0.0086). n = 6–8.