## 1 Introduction  
About 35% of patients with advanced ovarian cancer have astic fluid present at initial diagnosis and during the course of treatment [1]. Ascites is positively correlated with a poor prognosis, chemoresistant tumour features and deterioration in the patient's quality of life [2; 3]. Ascitic fluid contains biological components including cytokines, chemokines, growth factors, small molecules, white blood cells, mesenchymal cells and ovarian cancer cells [4; 5; 6]. Therefore, this unique microenvironmental milieu within the peritoneal cavity may promote tumour cell growth and modulate tumour cells responding to chemotherapy.  
The dissemination of ovarian cancer cells occurs at an early stage of the disease. Tumour cells detach from the primary tumour; many form small clusters and move around in the peritoneal cavity with the movement of the peritoneal fluid [7; 8]. In addition, increasing numbers of these cell clusters are found in the ascitic fluid of the advanced disease [9; 10]. Genotypic and phenotypic signatures of these floating cancer cells are poorly understood. However, it is widely recognised that these cancer cells are the major source of secondary metastasis growth [11]. Therefore, acknowledging the unique phenotypic features, associated with certain oncogenic proteins of the floating cancer cells, is necessary to understand the biology of metastasising ovarian cancer. The identification of specific proteins that may have oncogenic potential and that can be inhibited with existent clinical drugs may offer clinical benefits to a subset of ovarian cancer patients.  
It is widely recognised that tumour cells manifest rapid growth and sustained survival processes, which are facilitated by oncogenic protein-specific pathways. Elevated levels of the protein family of epidermal growth factor receptors, including EGFR and HER-2 in tumour tissue, have been linked with the poor prognosis of women with advanced ovarian cancer [12; 13; 14]. The activation of EGFR and HER-2 has been well documented in several solid tumours, in which the receptors were crucial to sustain growth and survival during the course of chemotherapy treatment [15; 16; 17]. Many in vitro studies and preclinical models have also demonstrated the effectiveness of EGFR and HER-2 inhibitors in delaying growth, reducing cancer cell survival and the metastatic potential of ovarian cancer [18; 19; 20]. Furthermore, the combination of these targeted inhibitors with standard cytotoxic agents have demonstrated enhanced anti-tumour activities compared with mono treatments [21].  
Even though the expression of these receptors in ovarian tumour tissues has been well described, the role they play in metastasis and chemoresistance is still poorly understood. Investigating the receptors' status in cells derived from ascites from ovarian cancer patients will somewhat delineate this role. In addition, the efficacy of EGFR and HER-2 inhibitors has not yet been studied in these types of cells. In this study, we hypothesised that cells isolated from ascitic fluid will have detectable expression levels of EGFR and HER-2, and in turn the efficacy of the inhibitor will be notable in these EGFR and HER-2 positive cells.