
Early in tumorigenesis, the previously highly maintained balance of pro-angiogenic and anti-angiogenic factors that regulate normal ovarian function is tipped, with the downregulation of anti-angiogenic signaling and the upregulation of pro-angiogenic growth factors.5 Although VEGF is expressed in healthy ovaries, it is overexpressed in ovarian cancer.2,6,8 VEGF expression is hypothesized to mediate multiple functional and structural characteristics of the disease.1
In one preclinical model, tumor xenographs overexpressing VEGF-A formed larger cysts lined with tumor cells relative to xenographs that weakly expressed VEGF-A.6 In another study that examined gonadotropin levels, elevated levels of luteinizing hormone and follicle-stimulating hormone increased VEGF expression and significantly contributed to the angiogenic potential of ovarian carcinomas.9
The growth of ovarian tumor cells is supplied by ascites, and ascites accumulation is associated with progression.4,10 Experimental models have demonstrated a positive correlation between ascites volume and VEGF expression.10
