Anti-VEGF Antibody Suppresses Tumor Growth And Metastasis Of Wilms' Tumor

Background and objectives: Angiogenesis is indispensable to both tumor growth and metastasis of tumor on physiology and pathology. So antiangiogeneic therapy is paid more and more attention to as a new method of dealing with cancer, previously findings showed the start of tumor angiogenesis stemmed from the vascular endothelial growth factor which initiates endothelial cells proliferation and transferation. VEGF plays a crucial role . Because VEGF actives karyokinesis and build up blood vessel networks. Interdiction of angiogenesis can hold back the development of tumors, with people mastering VEGF and VEGF receptor, a new therapy methd is provided. VEGF is a perfect target on tumor. In this study, Serum VEGF was measured with immuneohistochemical (ELISA) method in 35 children of nephroblastoma at preoperation. lw. 2w after surgery respectively. Wilms' tumor cells were implanted in nude mice right kidneys to set up experimental models. The mice were randomly divided into the control group and the anti-VEGF treatment group. To study VEGF' s function ofpredicting metastasis in nephroblastoma and whether the treatment with anti-VEGF antibodies would suppress both tumor growth and metastasis of Wilms' tumor in mice models.Subjects and methods: (1) Serum VEGF was measured with immuneohistochemical (ELISA) method in 35 children of nephroblastoma at preoperation. lw. 2w after surgery respectively. Simple visiting happened after surgery 4w. 8w. 16w. 32w. The countrol group was 35 healthy children. (2)Wilms' tumor cells were implanted in nude mice right kidneys to set up experimental models. The mice were randomly divided into the control group and the anti-VEGF treatment group. Anti-VEGF and phosphate-buffered saline (PBS) were begun with injection intraperitoneally in the anti-VEGF treatment group and the control group respectively. Mice were killed and tumor weights and the incidence of lung metastases were evaluated after 6w. The anti-VEGF treatment group had not received treatment any longer, and all animals were killed after 9w.Results: (1) Before surgery, the median VEGF in the children was 89. 47?2. 45 ng/ml and was 0. 75?. 12ng/ml in the countrol group . This difference is statistically highly significant (PO. 01). After surgery lw. 2w , levels in the children fell significantly to 2. 75?. 31ng/ml, 1. 52 0. 18ng/ml. There is a significant difference compared withpreoperation (P<0.01). Nine children had metastasis in lungs through simple visiting after surgery 4w. 8w. 16w. 32w. Five children died among them. Serum VEGF was measured from the deteriorate children and un-deteriorate children: 1. 25?. 1 Trig/ml, 144. 7642. 62ng/ml (KO. 01) (2)Anti-VEGF treatment resulted in a great reduction in tumor weight compared with the control group (P < 0.0001). Anti-VEGF treatment also abolished the establishment of lung metastases (50% in control animals, P<0. 05). Cessation of treatment resulted in rebound tumor growth in 3 weeks (P < 0.0001).Conclusion: (1) Serum VEGF expression indicate a rapid reduction following surgery, but the level rapidly increase during the metastasis. The findings revealed nephroblastoma' s occurring, developing, and metastasis signif icently correlated with production of VEGF. VEGF can be used as a clinical marker to predict the adverse prognosis of nephroblastoma. (2) Anti-VEGF therapy can suppress both tumor growth and metastases of Wilms' tumor in mice models. The findings supports the antiangiogenic therapy for Wilms' tumor and might become an important way of adjuvant therapy for Wilms' tumor.