772. Inhibition of Ovarian Tumor Growth Following Treatment with an Oncolytic Vaccinia Virus

Background: Recombinant vaccinia virus is currently being explored as a potential replicating oncolytic virus for cancer virotherapy due to its exceptional ability to replicate in tumor cells. Vaccinia tropism is not limited to tumor tissues, but also other tissues including ovarian follicles, possibly due to the presence of angiogenic factors such as vascular endothelial growth factor (VEGF). We therefore investigated the utility of vaccinia virus as an oncolytic therapy in a murine model of ovarian cancer.Methods: A murine ovarian surface epithelial cell (MOSEC) line was employed for this model. Intraperitoneal inoculation of the MOSEC cell line leads to a highly malignant neoplasm containing both carcinomatous and sarcomatous components as well as production of hemorrhagic ascitic fluid. These mice were treated with a thymidine kinase (TK) and vaccinia growth factor (VGF) double-deleted virus with the cytokine deaminase (CD) gene inserted into the TK locus. This recombinant virus (vvddCD) was found to be equivalent to the native WR strain in tumor tropism with minimal systemic growth.Results: Following intraperitoneal (i.p.) inoculation with 7.5x10 6 cells, mice were treated with 109 pfu of the vvddCD strain of vaccinia virus i.p. on the same day (concurrent treatment). In vivo studies appeared to show complete inhibition of tumor growth as compared to the control group (median mouse weight with ascites at 88 days: 40.7+/-1.49 (control [n=10]) vs 27.43+/-1.12 (virus [n=10])) (p