| Esophageal carcinoma is one of the most common cancer and rate ranks the forth among all cancers in China. It is important to invetigate the mechanism of carcinogenesis and the new strategy of prevention and therapy. The carcinogenesis and development of esophageal carcinoma is multistage and associated with lesions of esophagus . Long-term lesions of esophageal mucosa result in dysplasia and carcinogenesis. Prostaglandin E2(PGE2) increases during the repairing of these lesions and plays an important role in protection , repairing and cell renewing, however, it also contributes to carcinogenesis by affecting mitosis, suppressing apoptosis, degrading immunity and so on. Cyclooxygenase(COX) is the rate-limiting enzyme in the conversion of arachidonic acid to PGE2. Two isoforms of COX have been identified: constitutive COX-1 and inducible COX-2. COX-2 is induced by inflammatory substance, growth factors and carcinogen.lt cntributes to the pathologic process of inflammation, cancer and others. COX-2 may exert benefical effects hi tumor growth and invasion by suppressing cell apoptosis, facilitating cell proliferation, promoting angiogenesis in tumor, degrading extracellular matrix(ECM). COX-2 makes the new vessel growing mainly through up-regulation of vascular endothelial growth factor(VEGF). VEGF is the main factor in regulating angiogenesis and penetrating vessels , it can degrade basement membrane(BM), stimulate angiogenesis and benefit tumor growth and invasion. Microvessel density(MVD) is the basic way of counting new microvessels in tumor . MVD is helpful to evaluatingthe angiogenesis and development of tumor . Up to now, the study of COX-2 and VEGF expression in esophageal squamous cell carcinoma and the MVD in it has not been much reported.ObjectivestTo evaluate the role of COX-2 and VEGF in carcinogenesis, development, metastasis of esophageal carcinoma as well as the relationship to angiogenesis and the clinicopathology of tumor, and to provide theoretical foundation for esophageal carcinoma prevention and new clinical theropy using selective COX-2 inhibitor acting as a chemopreventive strategy and anti-angiogesis in tomour.Materials and methods: 41 cases of surgically resected esophageal squamous cell carcinoma samples, 20 cases of normal mucosa and 12 cases of dysplasia biopsy specimens were collected. Expressions of COX-2 and VEGF were observed by immunohistochemical staining(SABC) method, MVD was examined using antibodies against CD34 (endothelial cell specific) by immunohistochemical staining (SP) method .Satistical analysis: The SPSS 10.0 statistical package program was used for all analysis. x2-test , Fisher, s exact probability test , Student,s t test and analysis of variance were used to analyze the data. P<0.05.were deemed significant.Results: The positive staining of COX-2 is mainly located in cytoplasm , minority located nucleus membrane. COX-2 protein was undetectable in normal esophageal mucosa. in low and middle-grade dysplasia, high-grade dysplasia ,and esophageal squamous cell carcinoma, the positive rates of COX-2 were 16.7%(1/6), 50.0%(3/6), 53.7%(22/41) respectively, There were significant differences(P<0.05) when esophageal carcinoma group and high-grade dysplasia group compared with normal group. There were no significant differences(P>0.05) when the other groups compared with each other.In the well-differentiated group, moderately-differentiated group and poor-differentiated group, the positive rates of COX-2 were 70.6%(12/17), 42.9%(6/14), 40.0%(4/10) respecttively,There were no significant differences(P>0.05) when the expression of COX-2 of these three groups were compared with each other. Of 41 cases esophageal carcinoma, in the group with tunica adventitia invasion and the group without tunica adventitia invasion, thepositive rates of COX-2 were 60.0%(12/20) and 47.6%(10/21), There were no significant differences(P>0.05). In the group with lymph node metastasis and the group without lymph node metastasis, the positive rates of COX-2 were 73.7%(14/19) a... |
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