Vascular endothelial growth factor (VEGF) is a strong endothelial cell mitogen and vascular growth factor [1]. The unbalanced pathological state of cell proliferation and apoptosis is closely related to tumorigenesis and development. In this study, we examined the expression of VEGF in ovarian cancer tissues and its relationship with apoptosis in ovarian cancer cells, and conducted a preliminary investigation of its significance. 1. Materials and methods 1. 1 Clinical data 45 ovarian cancer specimens were obtained from archived wax blocks after surgical resection in our hospital from 1994 to 2001, including 27 cases of plasmacytic cystic adenocarcinoma, 3 cases of mucinous cystic adenocarcinoma and 15 cases of endometrioid adenocarcinoma. The age ranged from 35 to 70 years, with a median age of 51 years. According to the 1986 FIGO staging, 14 cases were in stage I-II and 31 cases were in stage III-IV. Eleven cases of normal ovarian tissues removed for uterine fibroids during the same period were selected as controls, aged 46 ~ 51 years, with a median age of 50 years, and the two groups were comparable. 1,2 Methods. The expression of VEGF was detected by immunohistochemistry SP method. polyclonal antibody for VEGF was purchased from Beijing Zhongshan Biotechnology Co. Apoptosis was detected by terminaldeoxynudeotide transferase mediated nick end labeling (TUNEL), and the reagents were purchased from Beijing Zhongshan Biotechnology Co. Paraffin block specimens were serially sectioned at a thickness of 4 μm, and tumor tissue sections were subjected to microwave antigen repair. PBS was used as a negative control instead of primary antibody. 1, 3 Determination of results 1, 3, 1SP method VEGF staining was localized in the cytoplasm of tumor cells and/or the cell membrane was stained brownish yellow (see Figure 1). Referring to the method reported by Liu Wei et al [2], five high magnification fields (× 400) were randomly selected to count the total number of tumor cells and the number of positive cells, and the percentages of positive cells were derived and classified according to the positive rate as: clear background without staining as -, positive cells <10% as +, positive cells 10%-70% as +++, and positive cells >70% as ++++. In this study -, is negative; +, is weakly positive; ++ and ++++ are strongly positive. 1,3,2TUNEL:Apoptotic cells had lavender nuclei with fragmented, irregular and variable size, while normal non-apoptotic cells and negative controls had blue nuclei re-stained by hematoxylin, relatively large nuclei and more uniform morphological size. Five high magnification fields (× 400) were randomly selected to count the number of apoptotic tumor cells ≥ 5% as positive and < 5% as negative [3]. 1, 4 Statistical methods. One-way ANOVA was performed using SPSS10.0 statistical package. 2, Results 2, 1 Expression of VEGF in ovarian cancer tissues 86.7% (39/45) of ovarian cancer cells expressed VEGF, of which, 12.8% (5/39) expressed weakly positive (+) and 87.2% (34/39) were strongly positive (++~+++); weakly positive expression was seen in normal ovarian tissues. The rate of strong positive VEGF expression in stage I-II ovarian cancer tissues was 35.7%, while that in stage III-IV was 93.5%, with significant differences between the two (P=0.001). 2, 2 Apoptosis in ovarian cancer tissues. 60% (27/45) of the 45 ovarian cancer cases were apoptosis positive and 40% (18/45) were apoptosis negative. The rate of strong positive expression of VEGF in the apoptosis negative group was 88.9% (16/18), and the rate of strong positive expression of VEGF in the apoptosis positive group was 40.7% (11/27), and the difference between them was significant (P=0.039). 3, Discussion 3, 1 Tumor growth and metastasis is a complex multi-step process, which is influenced by many factors. Among them, tumor angiogenesis plays an important role. VEGF is one of the important angiogenic factors, which plays an important role in tumor angiogenesis. The results of this study showed that 39 (86.7%) of 45 ovarian cancer specimens had different degrees of VEGF protein expression, among which 34 cases had strong positive expression, mainly in stage III-IV ovarian cancer, while only 5 cases had weak positive expression, mainly in stage I-II ovarian cancer, while no strong positive expression of VEGF was seen in normal ovarian cortex, and the tumor-free survival time and overall survival time were shortened with increased VEGF levels. survival time was shortened with elevated VEGF levels, which is consistent with the literature [4, 5]. It indicates that VEGF not only correlates with the malignant phenotype of tumor but also plays a key role in ovarian cancer progression, and its expression is closely related to prognosis, which can be used as an indirect indicator to predict the prognosis of ovarian cancer. 3, 2 VEGF expression and apoptosis in ovarian cancer Most scholars believe that the occurrence and development of tumor is not only the result of uncontrolled cell proliferation, but also may be due to blocked apoptosis, that is, the imbalance between cell proliferation and apoptosis determines the growth rate of tumor. Whether cells proliferate or apoptosis is influenced by many factors and is a two-way regulatory process. The experimental application of TUNEL method revealed that ovarian cancer tissues were accompanied by apoptosis, with a positive rate of 60%, suggesting a relationship between apoptosis and ovarian cancer. It was confirmed that neovascularization occurs early in tumorigenesis and development, and the spontaneous apoptosis of tumor cells is significantly influenced by the degree of neovascularization in tumor tissues. It has been reported [6] that vascular growth factor promotes tumor cell growth and inhibits tumor cell apoptosis by mediating angiogenesis. In the present study, the positive rate of VEGF expression in the ovarian cancer apoptosis-negative group was significantly higher than that in the ovarian cancer apoptosis-positive group, thus we have reason to infer that blocking the angiogenic effect of VEGF may achieve inhibition of tumor growth by promoting tumor cell apoptosis.