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The Korean Journal of Pathology 2001;35(5): 401-407.
Microvessel Density and Expressions of bcl-2, p53, and Vascular Endothelial Growth Factor in Endometrial Carcinoma.
Soon Young Kim, Hae Jin Jeong, Myeng Sun Park, Bang Hur
Department of Pathology, Kosin University Medical Center and Eonyang Boram Hospital, Busan 602-702, Korea. hurbang@ns.kosinmed.or.kr
ABSTRACT
BACKGROUND: Recent studies have shown that oncogenes and tumor suppressor genes are involved in tumorigenesis and tumor progression. The inverse role of bcl-2 and p53 in endometrial carcinomas has been debated. Moreover, their roles in angiogenesis as well as the interrelationship between prognostic clinico-pathological factors and angiogenesis have not been elucidated in endometrial carcinomas. METHODS: The expression rates of bcl-2, p53 and vascular endothelial growth factor (VEGF) in thirty-eight cases of surgically removed endometrial carcinomas were investigated using an avidin-biotin complex method of immunohistochemistry. CD34 immunostain for microvessel density (MVD) was also performed. RESULTS: The expression rate of bcl-2 was higher in the endometrioid type carcinoma (43.8%) than in the non-endometriod type carcinoma (16.7%). There was a significantly increased bcl-2 expression in grade I compared to grades II and III (P<0.05). The p53 expression rate was significantly higher in the non-endometriod type carcinoma than in the endometrioid type carcinoma (P<0.05).The VEGF expression rate was higher in the non-endometriod type carcinoma (83.3%) than in the endometrioid carcinoma (28.1%). Differences of MVD according to stages, histological types, grades and bcl-2, p53 and VEGF expressions were not noted. CONCLUSIONS: The expression rate of bcl-2 increases in the low grade endometrial carcinoma more than in the high grade one, so it may be suggested that bcl-2 expression could be used for an ancillary prognosticator. However, p53 and VEGF expressions and microvessel density may not have any prognostic value.
Key Words: Carcinoma; Endometrium; Genes; bcl-2; p53