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Introduction: Surgical trauma-related increased rates of metastasis formation and tumor growth have been noted in murine models. In humans, major abdominal surgery has been associated with persistent proangiogenic plasma protein changes and postoperative plasma been shown to promote Endothelial cell (EC) proliferation, migration, and invasion. The current murine study was done to determine: 1) if tumor angiogenesis and growth was increased after sham laparotomy (SL) vs. anesthesia alone (control, AC) and 2) to assess postoperative (postop) serum levels of four proangiogenic proteins.
Methods: Fifty BALB/cJ mice were subcutaneously inoculated with syngeneic CT26 colon adenocarcinoma cells on Day 1. On Day-15 the mice were randomized into 2 groups (n=25/group), one underwent SL and the other anesthesia alone (AC). Tumor Study: On Day-29 the mice were sacrificed and the tumors excised, measured, and weighed. The tumor microvessel density was determined via IHC CD34 staining. Serum Study: Blood samples were taken and serum harvested from a second group of mice that underwent SL or anesthesia alone (total n=84). The sampling points were: preoperative (Preop), POD1, 3, 5, 7, 10, and 14. Serum levels of FGF, VEGF, sVCAM and PDGF-BB were determined via ELISA. Results: The median tumor volume of the SL group (625.9 mm3) was significantly larger than the AC group result (510.2 mm3, p=0.01). Also, the SL group’s median tumor mass (0.55g) was greater than that of the AC group (0.35g, p=0.04). Lastly, a higher microvessel density was found in the SL group tumors (8.5/field) than in the AC group (6.7/field, p=0.001). Elevated serum PDGF-BB levels were observed in the SL group on POD5 (SL, median level 15.40 ng/ml, vs AC, 8.90 ng/ml, p=0.002) and POD7 (SL, median 10.85 ng/ml, vs AC, 7.59 ng/ml, p=0.02). Conclusion: Tumor growth was increased after SL as was tumor angiogenesis and serum PDGF-BB levels. These results support the hypothesis that increased tumor growth after SL may, at least in part, be due to proangiogenic plasma protein alterations that promote tumor angiogenesis.