| Background:China is a country where the esophageal carcinoma is in higher morbidity, accounting for 60% of all across the world, and the 5-year survival rate of postoperative cases is less than 20%, life is threatened deadly. In China, 95% cases are squamous cell carcinoma, drawing more attention. It is well known that angiogenesis is the prerequisite to the tumor progression. Studies show that the inflammatory cells and cytokins in tumor stroma are the important resources of pro-angiogenesis factors. Macrophage is the main inflammatory cell characterized by infiltration, therefore, defined as tumor associated macrophage(TAM). Some data argue that high TAM count leads to the adverse prognosis in many kinds of malignancy, but some protest yet, controversy lies here. Cyclooxygenase-2 is not only one of cytokins secreted by macrophage but also an important rate-limiting enzyme involved in the inflammation, and over-express in multiple digestive system cancer. Recent studies tell us the expression of COX-2 contributes to the angiogenesis of tumor. However, the reports regarding the relationship between TAM count and COX-2 in esophageal carcinoma are unsufficient , nether TAM to the prognosis.Objectives:To detect the significant infiltration of TAM and expression of COX-2 and their correlations with angiogenesis and clinicopathologic features in esophageal squamous cell carcinoma, as well, to determine the relationship of TAM count with prognosis.Methods:1. Collecting the specimen of postoperative esophageal carcinoma. 2. By means of immunohistochemistry, the expression of TAM marked by CD68 and COX-2 and microvessel density were determined, meanwhile, the relationship of the expression of TAM and COX-2 with angiogenesis, invasion depth, lymph nodes metastasis, as well as 3-year survival rate were also observed.3. Statistical analysis: The data were analyzed by SPSS 10.0. Student's t-test, Chi-square test, Fisher's exact test of probabilities, Spearman rank-correlation test and Cox's proportional hazard regression model were used to analyze the date, P<0.05 were deemed significant. The survival curve was obtained with Kaplan-meier test.Results:1. The count of TAM in esophageal squamous cell carcinoma and normal mucosa were 47.60±13.68, 70.33±9.66 respectively, showing significant difference(P<0.05). In cases with regional lymph nodes involved, TAM count was obviously higher than those in cases of non-metastasis of regional lymph nodes, 77.01±2.98 and 39.11±6.42. TAM count of cases with serous membrane involved and no-invasion to serous membrane were 76.36±3.63, 46.78±6.47, respectively. TAM count and gender were independent from differentiation.2. The expression rate of COX-2 in esophageal squamous cell carcinoma was 65.9%, however, 10% in normal mucosa, showing the significant difference; in lymph node positive and negative were 19/21, 10/23; serous membrane positive and negative were 22/29, 7/15(P< 0.05).3. MVD in normal esophageal and carcinoma were 37.32±2.12 and 50.18±5.34, respectively(P<0.05). Both TAM and MVD, COX-2 and MVD were correlated, correlation coefficient(r) were 0.933 and 0.849, (P<0.01). The expression of TAM count and COX-2 were correlated, r=0.934, (P<0.01). In addition, the sites of their expression were similar.4. Three-years survival rate was lower in the higher TAM count cases.Conclusion:Macrophage infiltrated count, MVD and the expression of COX-2 in ESCC are obviously higher than those in normal esophageal mucosa, associated with lymph node metastasis, the depth of tumor invasion, and angiogenesis, however, no relationship with the differentiation and gender. The increase of TAM count and over-expression of COX-2 are correlated with the invasive features of ESCC. It is uncertain that whether the high TAM count is one independent adverse prognosis factor of ESCC or not. It will be improved for the survival of esophageal carcinoma if the expression of COX-2 can tend to be inhibited by selective COX-2 inhibitor accompany with the routine therapy. And it is constructive for the prognosis of esophageal carcinoma to inhibiting the inflammation angiogenaesis.
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