**P < 0.01. In vitro experiment LY2090314 manufacturer demonstrating the effect of bevacizumab on VM SKOV3 cells were cultured in 3D culture, which formed VM channels. Then, we compared the cell viability and the ability to form VM in 3D culture after treatment with bevacizumab (0, 1, 10, 100 and 1000 μg/ml)for up to 48 h. Cell viability was examined by a CCK8 assay. Bevacizumab treatment did not affect SKOV3 cell viability and the number of tubules (Figures 4 and 5). Figure 4 Bevacizumab treatment did not affect SKOV3 cell viability. Bevacizumab treatment (0, 1, 10, 100 and 1000 μg/ml) does not affect SKOV3 cell viability in 3D culture. There were no statistically significant

difference (P > 0.05). Figure 5 Bevacizumab treatment did not affect the number of tubules. The effect of bevacizumab (0, 10 and 1000 μg/ml) on the formation of VM channels (× 100). (A) Bevacizumab

at 0/(B) 10/(C) 1000 μg/ml. (D) Bevacizumab treatment did not affect the number of tubules (P > 0.05). Discussion Antiangiogenic therapy is one of the most significant advances in cancer treatment. Its clinical value has been investigated, but is still too limited. A number of recent clinical and preclinical observations have been reported. In a neoadjuvant phase II trial of advanced epithelial ovarian cancer patients find more treated with the combinational therapy of carboplatin/paclitaxel with the angiogenesis inhibitor sorafenib, Pölcher M et al. reported that progressive disease was Tubastatin A diagnosed in two patients out of four, and surgical exploration showed an increased number of peritoneal tumor implants [11]. Furthermore, after short-term treatment, varous forms of antiangiogenic therapy can lead to increased metastasis in mouse

models of multiple tumor types [12, 13]. Thus, there is a strong need to improve Orotidine 5′-phosphate decarboxylase treatment strategies and to better understand the mechanisms of failure that hinder targeted antiangiogenic therapies. Here, we address the effect of short-term bevacizumab treatment using ovarian cancer xenografts. The data show that short-term bevacizumab treatment induces a reduction in tumor growth and an increase in distant tumor metastasis as measured by bioluminescence. Importantly, similar results were obtained when nu/nu mice were treated with bevacizumab + cisplatin and cisplatin alone. It should be noted that in mouse models of ovarian cancer, antiangiogenic therapy can elicit an adaptive response involving increased dissemination and the emergence of distant metastasis. To investigate this metastatic “”conditioning”" effect, a better understanding of the biological effects of anti-VEGF treatment is required. Antiangiogenic therapy inhibits the development of new blood vessels, i.e.