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. 2016 Jan 8;5(5):e1122860. doi: 10.1080/2162402X.2015.1122860

Figure 6.

Figure 6.

Exogenous HMGB1 promotes leukocyte recruitment into the peritoneal fluid and supports tumor growth. (A) Schematic representation of mice treatment with HMGB1. Treatment (1 µg/mouse) started 2 d after MC-38 carcinoma cell injection. Mice were treated every other day until animal sacrifice (day 15). (B) Tumor growth was monitored by [18F]FDG scans of HMGB1- or PBS-treated mice. Coronal (a) and transaxial (b) view of reconstructed images at the level of tumor location (dashed white line) are reported. Sites of [18F]FDG accumulation are indicated with arrows. Images were presented with the same scale and corrected for injected dose and animal weight. (C) Representative pictures of abdomens of HMGB1- or PBS-treated mice. Arrows indicate neoplastic lesions. (D) Volume of neoplastic lesions of HMGB1- or PBS-treated mice measured at PET (cm3, y-axis). Results are expressed as mean ± SEM. n = 5 per PBS- and n = 4 per HMGB1-treated groups, two independent experiments. (E) Weight of neoplastic lesions of HMGB1- or PBS-treated mice retrieved at sacrifice. Results are expressed as mean ± SEM of four independent experiments, n = 20. (F) CD68+ macrophages per Field of Vision (FOV) were identified by immunohistochemistry (y-axis) in peritoneal lesions of HMGB1- or PBS- treated mice retrieved at sacrifice (x-axis). Results are expressed as mean ± SEM of CD68+ cells/FOV. n = 10 animals per group, two independent experiments. (F) The mean vascular area (y-axis) was calculated in peritoneal lesions of HMGB1- or PBS-treated mice retrieved at sacrifice (x-axis) by digital image analysis. Data are expressed as mean ± SEM of results obtained. n = 10 animals per group, two independent experiments. *p < 0.05, **p < 0.005, ***p < 0.001, significantly different from control (Unpaired T test).