Prognostic significance of IL-6 and IL-8 ascites levels in ovarian cancer patients

We measured IL-6 and IL-8 levels in the ascites of 39 patients with newly diagnosed EOC. Commercially available enzyme-linked immunosorbent assay (ELISA) was used to determine IL-6 and IL-8 ascites levels. Ascites cytokine levels were correlated with clinicopathological parameters and progression-free survival.Mean ascites levels for IL-6 and IL-8 were 6419 pg/ml (SEM: 1409 pg/ml) and 1408 pg/ml (SEM: 437 pg/ml) respectively. The levels of IL-6 and IL-8 in ascites were significantly lower in patients that have received prior chemotherapy before the surgery (Mann-Whitney U test, P = 0.037 for IL-6 and P = 0.008 for IL-8). Univariate analysis revealed that high IL-6 ascites levels (P = 0.021), serum CA125 levels (P = 0.04) and stage IV (P = 0.009) were significantly correlated with shorter progression-free survival. Including these variables in a multivariate analysis revealed that elevated IL-6 levels (P = 0.033) was an independent predictor of shorter progression-free survival.Elevated IL-6, but not IL-8, ascites level is an independent predictor of shorter progression-free survival.The incidence of ascites in women presenting with epithelial ovarian cancer (EOC) ranges from 45% to 75% depending on the tumor type but increases in advanced stages [1]. It is a distressing complication carrying substantial morbidity [2]. Unlike most stroma surrounding solid tumors, ascites constitute a unique form of tumor microenvironment. Recent evidences suggest than ascites play an active role in tumor development. EOC ascites may affect cell behaviour such as cell growth, invasion, and de novo drug resistance of EOC cells [3-5]. We recently reported that the acellular fraction of EOC ascites inhibits drugs- and death receptor-induced apoptosis in vitro (de novo resistance) [3,4]. Newly diagnosed women with protective ascites had significantly shorter progression-free survival [6] suggesting that ascites-mediated de novo resistance impacts on EOC progression. Stromal myofibroblasts