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Your doctor may also to withdraw ascites fluid from your belly. The fluid is tested to look for the cause of ascites.|

A peritoneal fluid alpha-fetoprotein (AFP) concentration >6.0 ng/mL is suspicious but not diagnostic of ascites related to hepatocellular carcinoma (HCC). This clinical decision limit cutoff yielded a sensitivity of 58%, specificity of 96% in a study of 137 patients presenting with ascites. AFP concentrations were significantly higher in ascites caused by HCC. Ascites caused by malignancies other than HCC routinely had AFP concentrations <6.0 ng/mL. Therefore, negative results should be interpreted with caution.|

Runyon BA. Ascites and spontaneous bacterial peritonitis. In: Feldman M, Friedman LS, Brandt LJ, eds. 9th ed. Philadelphia, Pa: Saunders Elsevier; 2010:chap 91.|

As discussed above, ascites is a source of tumor material from which valuable information can be extracted not only to understand the pathophysiology of ovarian cancer progression but also for the development of markers which will predict prognosis and monitor the progression of the disease. The frequent presence of ascites at first presentation, and subsequent relapses, provides an accessible pool of tumor material that can be studied to determine the molecular characteristics of cells as the disease progresses. With the establishment of methods which can separate the different soluble and cellular components of the ascites (), it may now be possible to identify and differentiate the true molecular perturbations that exist between the chemonaive, chemoresistant, and recurrent status of the disease. Isolated cellular components of the ascites can be preserved as paraffin embedded blocks for immunohistochemical analysis (, ), or can be frozen for molecular analysis at the RNA and protein levels (, ). Moreover, ascites provides a substantial amount of biological material which can be obtained to design studies which require relatively larger amounts of tumor material, which previously were only limited to genome-based studies due to the scarce availability of primary and metastatic tumors leftover after pathological diagnosis. These studies include methods to elucidate the protein profile of ascites-derived tumor and associated cells by proteomic methods such as matrix-assisted laser desorption and ionization (MALDI), surface enhanced laser desorption and ionization (SELDI), and liquid chromatography followed by mass spectroscopy (MS) (, ), all of which require larger amounts of samples than that used by genomic methods. In addition, high-throughput automated array-based proteomics techniques such as reverse phase protein arrays (RPAs) can be used to understand the differential expression of proteins in the isolated ascites cellular components from chemonaive and chemoresistant patients. A recent study which used the RPA analysis on ascites samples and pleural effusions obtained from ovarian cancer patients showed significantly higher expression of AKT, cAMP-responsive element binding protein (CREB), and Jun-N-terminal kinase (JNK) in malignant ascites compared to benign effusions (). Given that deregulation of PI3 kinase and the downstream AKT pathway has been demonstrated in ovarian cancer (, ), and high levels of p38 and an increase in the ratio of phosphorylated EGFR and phosphorylated JNK were associated with bad prognosis in ovarian cancer patients (), it seems that the proteomic profile of the ascites environment may imitate the protein expression profile of the original tumors (). These observations suggest the enormous potential of using ascites samples for diagnostic, prognostic, and therapeutic endpoints.|

It is important to stress that a requirement to use alternatives to ascites has no more to do with experimental design, than does a requirement to use a particular anesthetic or veterinary procedure.|

Your health care provider may diagnose ascites by doing a physical exam and asking about your symptoms. He or she may also order tests to confirm ascites, such as:|

Accessibility to ascites also provides a means of comparing the secretory components of the chemonaive and chemoresistant patients. A recent study has determined the cytokine expression profile of the ascites of ovarian cancer patients. Out of 120 cytokines analyzed OPG, IL-10, and leptin was found to be associated with worst prognosis in ovarian cancer patients (). The concept that the damage of tumor cells in response to chemotherapy treatment can activate autocrine and paracrine secretory responses of residual tumor cells (, , ), suggest that the soluble component of the ascites microenvironment of chemonaive and chemoresistant patients may be significantly different. In addition, the tumor growth promoting effect of exosomes released by ovarian tumors has been reported (). Malignant ascites-derived exosomes of ovarian carcinoma patients have been shown to contain CD24 and EpCAM (). The exosome-associated proteolytic activity in the tumor vicinity has been suggested to augment tumor invasion into the stroma (). Exosomes released by ovarian cancer cells have been shown to induce apoptosis of mature dendritic cells and peripheral blood nuclear cells suggesting they have a negative effect on host immunity (). In addition, ascites have been shown to contain pro-survival factors which compromised the therapeutic effects of TRAIL and were shown to be associated with shorter disease-free intervals in ovarian cancer patients (). These data suggest that the signals derived from the soluble ascites microenvironment plays a crucial role in regulating ovarian tumor cells and targeting the survival promoting activity of the soluble component of ascites may be mandatory for the development of efficient therapies for ovarian cancer patients.|

Malignancy accounts for approximately 7% of cases of ascites formation. Malignant disease can cause ascites by various mechanisms including: peritoneal carcinomatosis (53%), massive liver metastasis causing portal hypertension (13%), peritoneal carcinomatosis plus massive liver metastasis (13%), hepatocellular carcinoma plus cirrhosis (7%), and chylous ascites due to lymphoma (7%). The evaluation and diagnosis of malignancy-related ascites is based on the patient clinical history, ascites fluid analysis, and imaging tests.|

Ascites is a condition in which fluid collects in spaces within your abdomen. Although the most common cause of ascites is cirrhosis of the liver, for about 10 percent of people with ascites, the cause is cancer.|

The prevention of ascites largely involves preventing the risk factors of the underlying conditions leading to ascites.|

In a minority of patients with advanced cirrhosis that have recurrent ascites, shunts may be used. Typical shunts used are , , and the (TIPS). However, none of these shunts has been shown to extend life expectancy, and are considered to be bridges to . A of by the international concluded that "TIPS was more effective at removing ascites as compared with paracentesis...however, TIPS patients develop hepatic encephalopathy significantly more often"|

Ascites is an indicator of poor prognosis in ovarian cancer patients, with the tumor cells within the ascites postulated to play dominant roles in metastatic spread, chemoresistance, and ultimately, the recurrence of the cancer (, ). Hence, a thorough understanding of the biology of the ascites microenvironment is essential for developing effective therapeutic intervention for metastatic ovarian cancer. Established ovarian cancer cell lines, often originally isolated from ascites, are readily available, immortalized, and low-cost options to assess tumor cell behavior. However, the distinct disadvantage of cell lines is their accumulation of numerous genetic and phenotypic abnormalities over years of culture which no longer accurately reflect the clinical disease (). Ascites isolated from ovarian cancer patients represents a readily accessible source of primary cancer cells and cancer-associated cells with the potential to provide direct insights into the molecular and cellular pathophysiology of ovarian cancers as they metastasize within the peritoneal cavity. Reviewed below are some of the clinically relevant model systems which have provided novel insights into the contribution of ascites-derived cells and the ascites microenvironment to ovarian cancer tumorigenicity and the metastatic progression of the disease.|

Pancreatic ascites can be seen in people with chronic (long standing) or inflammation of the pancreas. The most common cause of chronic pancreatitis is prolonged alcohol abuse. Pancreatic ascites can also be caused by acute pancreatitis as well as trauma to the pancreas.|

Cancers which spread through the blood and lymphatic vasculature undergo repeated intravasation and extravasation through vessel walls. In contrast, during ovarian cancer metastasis, cancer cells are shed from the primary tumor into the peritoneal cavity and must survive suspended within the ascites (, ). To model this stage of ovarian cancer metastasis, ovarian cancer cell lines or primary ascites-derived cells are maintained under non-adherent conditions, such as in hanging-drops, in a liquid overlay, or in low-attachment culture dishes (, ). Under non-adherent conditions, cancer cells inherently aggregate together to form multicellular spheroids, which exhibit enhanced abilities to avoid anoikis (). The main advantage that spheroid cultures have over monolayer cultures is that spheroid cultures more accurately model the complex three-dimensional structures assumed by ovarian cancers metastasizing within the peritoneum and recapitulate the molecular (e.g., oxygen, nutrient, metabolite) gradients found . Thus, multicellular spheroids cultured under non-adherent conditions which mimic the ascites more accurately predict behaviors and responses to therapies. For example, cancer cells grown as spheroids can be up to 100 times less sensitive to chemotherapies than the same cells cultured as monolayers, reflecting the inherent chemoresistance exhibited by metastasizing ovarian cancer spheroids in a clinical setting (). The enhanced survival capabilities of spheroids were recently demonstrated using primary ascites-derived epithelial ovarian cancer cells (). In this study, when grown as spheroids in non-adherent culture, ascites-derived tumor cells exhibited resistance to Myxoma-virus-mediated death despite the virus entering and replicating within the spheroids. In contrast, if the tumor cells were grown as monolayers in adherent culture or if spheroids were replated onto adherent surfaces, they exhibited sensitivity to Myxoma-virus-mediated death (). This study has important implications for the development of treatments for advanced, metastatic ovarian cancers, underscoring the need to study the non-adherent spheroid stage of ovarian cancer metastasis in the development of new therapeutic regimens in order to ensure that new treatment options are effective against tumor spheroids floating within the ascites.|