| Background:The growth and metastasis of solid tumors requires the formation of microvessel.Vascular endothelial growth factor (VEGF) is found to be the most important inducer of angiogenesis and cound improve vascular permeability.VEGF is often secreted by tumor cells and acts on its receptors 桲DR/Flk-1 and Flt-1 in vascular endothelial cells. It has been proved that VEGF is associated with micro vessel density (MVD) and progression in many kinds of carcinomas . nm23-H, is a metastasis suppressor gene and plays an important role in suppressing the metastasis phenotype. Hepatocellular carcinoma (HCC) is a well-known hypervascular tumor ,and easy to produce invasion and metastasis. However, the combined examination of VEGF, Flk-1, Flt-1 and nm23-H, in HCC and the relationship with MVD, growth and metastasis has not been reported up to now. Objective: To analyse the role of VEGF, Flk-1, Flt-1, nm23-H, and MVD expression in patients with hepatocellular carcinoma. Methods: A total of 76 HCC samples were examined for VEGF, Flk-1, Flt-1, nm23-H, and MVD expression by immunohistochemical staining. Results: The positive expression rate of VEGF is 84.2% (64/76) ,and nm23-H,is 52.6% (40/76) ;VEGF, MVD expressed higher (P<0.05 ft]P<0.05) and nm23-H, expressed lower (P<0.05) in non-encapsulated and matastatic HCC samples than those in the other samples. The expression of VEGF was related with the angiogenesis ,growth and metastasis of HCC, but there was an inverserelationship between nm23-H, expression and metastasis of HCC. Flk-1, Flt-1 were expressed in vascular endothelial cells and a part of the HCC cells. Conclutions: The expression of VEGF, Flk-1, Fit-land nm23-H, in HCC is associated with tumor angiogenesis ,growth and metastasis, VEGF is an inducer and nm23-H, is a suppressor, so there is a relationship between them and the progression of HCC. So, combined examination of VEGF, Flk-1, Flt-1, nm23-H, and MVD in HCC is very significant.
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