Hif-1 Alpha, P53, Expression Of VEGF In Endometrial Carcinoma And Its Relationship With Tumor Angiogenesis

【Objective】To detect the expression of hypoxia-inducible factor 1α(HIF-1α) and VEGF, P53and MVD in endometrial carcinoma ,and to investigate their association with angiogenesis of endometrial carcinoma under hypoxia.【Methods】Immunohistochemical staining(s-p method)was used to detect HIF-1αand VEGF, P53and MVD expression in 46 cases of endometrial adenocarcinoma,16 cases of endometrial complex hyperplasia with atypical hyperplasia and 12 cases of endometrial simple hyperplasia.Spearman coeffcient of correlation was used to test correlation between HIF-1αand VEGF, P53, MVD.【Results】1,The positive rates of HIF-1 alpha,VEGF and P53 in endometrial Carcinoma were both significantly higher than those in endometrial complex hyperplasia with atypical hyperplasia and endometrial simple hyperplasia.2,The expression of HIF-1 alpha,VEGFand P53 in endometrial Carcinoma had no Relationship with surgical stages and muscular invasion. There were significant correlations between the expression of HIF-1 alpha,VEGFand P53inendometrial carcinoma and histological grading.Close positive relation was observed between microvessel density (MVD)level and surgical clinical stage ,histological grading,muscular invasion of endometrial carcinoma.3,HIF-1 alpha expression was found significant association with VEGF,P53and MVD expression .Patients with expression of HIF-1 alpha had a higher VEGF,P53and MVD expression compared with those with no expression.【Conclusion】1,There are overexpression of HIF-1α,P53 and VEGF in endometrial carcinoma, There were significant correlations between the expression of HIF-1 alpha,VEGFand P53 in endometrial carcinoma and progression of endometrial carcinoma .2,HIF-1 play a very important role in angiogenesis of endometrial carcinoma through regulating the expression of VEGF.3,HIF-1 cooperates with P53deletion or mutation taking part in the regulation of endometrial carcinomatumor cells under hypoxia probably.