Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serial ascites and plasma volumes were measured during diuresis in nine patients with ascites caused by peritoneal carcinomatosis, four patients with chylous malignant ascites, and three patients with portal hypertension-related ascites caused by massive hepatic metastases. Oral diuretics were given to achieve an adequate natriuresis on a sodium-restricted diet. During the study period (7.8 +/- 3.2 days), patients with peritoneal carcinomatosis and chylous ascites lost 0.49 +/- 0.31 and 0.51 +/- 0.42 kg/day in weight, respectively, with negligible change in ascites volumes (-0.03 +/- 0.11 and 0.02 +/- 0.09 L/day). Patients with ascites caused by massive hepatic metastasis lost 1.06 +/- 0.15 kg/day in weight (P = 0.01 for massive hepatic metastasis vs. peritoneal carcinomatosis) and 0.23 +/- 0.13 L/day of ascites (P less than 0.05 vs. other groups). Plasma volume changes were not significantly different among the three groups. Patients with edema (9/16) had a greater natriuresis and daily weight loss. Three patients with peritoneal carcinomatosis and one with chylous ascites developed renal dysfunction or symptomatic hypotension. No patient with massive hepatic metastasis developed these complications. In patients with ascites caused by peritoneal carcinomatosis or chylous malignant ascites there is no mobilization of ascites, whereas in patients with massive hepatic metastasis, ascites may be mobilized with diuretics.
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PMID:Mobilization of malignant ascites with diuretics is dependent on ascitic fluid characteristics. 139 89

Peritoneal effusion recurrence is one of the most important problem in the palliative management of patients with gastrointestinal malignancies and ovarian cancer. Ten patients with recurrent malignant ascites (three with ovarian cancer, two with pancreas cancer, two with gastric adenocarcinoma and one affected by colon cancer, one patient with peritoneal carcinomatosis, one subject with pleural mesothelioma surgically treated that after three years showed a peritoneal metastases and ascites), were treated with intraperitoneal beta interferon. In all patients a Tenckoff's catheter for peritoneal dialysis was introduced and peritoneal effusion extracted and measured. Three millions of beta interferon in saline solution was infused in peritoneal cavity every three days for nine days. Successively twenty millions every three days for nine days. In the 50% of patients a significant reduction of peritoneal effusion was observed. The locoregional therapy with beta interferon is proposed in palliative management of malignant ascites.
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PMID:[The locoregional treatment of neoplastic ascites with interferon-beta]. 150 25

The aim of the study was to assess the accuracy of fibronectin, a glycoprotein, for the diagnosis of malignant ascites and to compare it with conventional parameters. Ascitic fluid samples from 50 patients, 25 with intra-abdominal malignancy and 25 without it were analysed for total protein concentration, fluid/serum protein ratio, glucose concentration, leucocyte count, pH, fibronectin concentration (by ELISA) and for malignant cell cytology. Twenty-two of the 25 patients with ascites and intra-abdominal malignancy had documented peritoneal metastases in group A. The 25 patients with non-malignant ascites constituted group B. Mean values of ascitic fluid fibronectin, for groups A and B were 538 +/- 46 micrograms/mL and 60 +/- 4.92 micrograms/mL, respectively (P less than 0.001). Within the group with malignant ascites, patients who had positive malignant cytology (n = 12) exhibited a significantly higher ascitic fluid fibronectin concentration than patients with negative cytology (P less than 0.05). While mean ascitic fluid protein concentration showed a significant difference (P less than 0.01) between the two groups, there was no difference in respect to ascitic fluid pH, glucose concentration and leucocyte count. Malignant cell cytology was positive in 54.5% of group A patients with no false positive report in group B. The diagnostic accuracy for differentiating malignant from non-malignant ascites was 100% for a fibronectin value of greater than or equal to 110 micrograms/mL as compared with 78.7% for ascitic fluid protein concentration greater than or equal to 0.5 g/dL, 57.4% for leucocyte count greater than or equal to 1000/mm3, 59.6% for pH less than 7.45 and 78.7% for malignant cell cytology.
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PMID:Evaluation of fibronectin as a marker of malignant ascites. 157 98

This study was performed in 65 patients with cytologically proved malignant ascites to describe and classify direct and indirect sonographic signs of peritoneal carcinomatosis. Abdominal sonography revealed tumour-associated abnormalities which account for malignant ascites in 60 cases (92%). This includes visualisation of peritoneal metastases (n = 16, 25%); matting together of bowel loops (17, 26%); distribution of fluid (19, 29%); echoes within the fluid space (3, 5%); omental matting (8, 12%); associated masses (21, 32%); lymphoadenopathy (31, 48%); and hepatic metastases (26, 40%). Sonography enables the physician to demonstrate direct and indirect signs of peritoneal carcinomatosis in almost all tumour patients with ascites and is therefore useful in determining whether the cause of ascites is malignant or benign disease.
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PMID:Malignant ascites: sonographic signs of peritoneal carcinomatosis. 182 11

Several lysosomal proteinases including the cysteine proteinase cathepsin B have been implicated in malignant progression of tumors. Many investigators have demonstrated correlations between increased activity of cathepsin B and increased metastatic capability of animal tumors or malignancy of human tumors. Such increases in cathepsin B activity in malignant tumors may reflect alterations in synthesis, in activation and processing, and/or in intracellular trafficking and delivery as well as in the endogenous inhibitors of cathepsin B. Increases in mRNA transcripts for cathepsin B have been observed in both murine and human tumors and multiple transcripts for cathepsin B have been identified, but an association of multiple transcripts with malignancy has not been confirmed. Cathepsin B precursors found in human malignant ascites fluid do not possess mannose-rich carbohydrates suggesting that a defect in the post translational processing of carbohydrate moieties on tumor cathepsin B may be responsible for the release of cathepsin B observed in many tumor systems. However, the intracellular trafficking of cathepsin B responsible for its association with plasma membrane/endosomal systems and for its release will require further study as both latent, precursor forms of cathepsin B and native forms of cathepsin B are involved. We speculate that malignant tumor cells adherent to basement membrane are capable of forming a digestive microenvironment in which lysosomal proteinases such as cathepsin B function optimally, a microenvironment similar to that formed between adherent osteoclasts and bone. One of the endogenous cysteine proteinase inhibitors, stefin A, also is affected by malignancy. Reduced expression (mRNA and protein) of stefin A is found as well as a reduction in its inhibitory capacity against cysteine proteinases. The data to date at both the molecular and protein levels supporting a functional role(s) for cathepsin B and its endogenous inhibitors in cancer progression are only correlative. Experimental approaches utilizing well-defined model systems in conjunction with genetic manipulation of cathepsin B and its endogenous inhibitors are needed to provide convincing evidence that cathepsin B has an important role in cancer.
Cancer Metastasis Rev 1990 Dec
PMID:Cathepsin B and its endogenous inhibitors: the role in tumor malignancy. 209 84

A prospective study of 14 malignant ascites examined with high frequency ultrasonic probes enabled he authors to achieve a diagnosis of peritoneal metastases in 78% of cases. Peritoneal metastases appear as areas of peritoneal thickening or scalloping, as nodules, with sometimes a strong bulging, and as intestinal masses. Soft part ultrasound should be employed systematically in the diagnosis and follow up of malignant ascites.
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PMID:[Echographic diagnosis of peritoneal metastases in patients with ascites]. 221

A variant of CEA which is less readily endocytosed by macrophages has been isolated from malignant ascites. In vivo, CEA is cleared more slowly by the liver (t1/2 = 15.1 minutes) than CEAs isolated from hepatic metastases (t1/2 = 3.1 minutes). In vitro, rat and human Kupffer cells and rat alveolar macrophages endocytose this CEA less effectively. This slow clearing form of CEA is associated with a smaller (45kD) acidic glycoprotein (CORA) with which it forms a stable complex. CORA can be visualized on reducing gels but not on non reducing gels or by HPLC run under non reducing conditions. This suggests a non-covalent complex between the two glycoproteins. Analysis of protein conformation by circular dichroism revealed changes in the ascites CEA consistent with binding of CORA to the molecule. Western blot showed that CORA crossreacts with antisera to alpha 1-acid glycoprotein and double immunodiffusion demonstrated cross-reactivity but not identify. Sequencing of CNBr peptides showed sequence homology with alpha 1-acid glycoprotein but areas of unique sequence were also found. It is suggested that binding of CORA to CEA blocks the macrophage receptor binding of CEA.
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PMID:A carcinoembryonic antigen (CEA) binding protein from ascites influences CEA uptake by macrophages. 240 53

Hepatocellular carcinoma cells obtained from ascitic fluid after diethylnitrosamine treatment of Sewall Wright strain-2 guinea pigs produce solid (primary) tumors, lymph-node metastases and malignant ascites when reinjected into animals of the same strain. When brought into culture the cells settle, form multilayer cultures and can be maintained in passage. In addition to epithelium-specific cytokeratin intermediate filaments (IF), these latter cells, like most cultured cells, also contain vimentin. Hepatocellular carcinoma cells in solid tumors and in metastatic tumors retain their original keratin IF and in general do not have an additional vimentin-IF system. When the tumor cells are present in ascites they develop vimentin-IF in addition to cytokeratin filaments. Vimentin is gradually lost when these cells sediment onto the peritoneal surface and proliferate continuously to form papillary projections, or when they are detected as circumscribed metastases. It seems likely, therefore, that in this system the synthesis of an additional vimentin cytoskeleton is related to reduced cell-to-cell contact and to the ability of the cells to survive individually or as cell clusters in body fluids, without being part of a cohesive tissue.
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PMID:Changing intermediate-sized filament patterns in metastatic hepatocellular carcinoma cells of the guinea pig. 242 67

A Sewall Wright strain-2 guinea pig model producing malignant ascites after injection of a diethylnitrosamine-induced hepatocellular carcinoma cell suspension (Line-10) was used to demonstrate the multilayered settling of tumor cells on the peritoneal surface, frequently followed by the formation of papillary projections and the early invasion in a proliferating submesothelial tissue. At the border of tumor cells and the desmoplastic tissue the malignant cells changed their shape and generally two categories were recognized. Often multilayering, atypical flat cells covered the stromal tissue, while mostly rounded ones invaded using their branched penetration processes, being devoid of cationized ferritin, which was only present on the luminal sides of all cellular elements. Flattened malignant cells, penetrating processes and invading cells lost their microvillous surface pattern. The infiltrating cells were often only detectable with the monoclonal antibody 10 TL 40 and the anti-cytokeratin OV TL 12-5, demonstrating the need for immunohistochemistry in diagnosing solitary invading malignant cells in light microscopy. It appeared that still numerous mesothelial cells were found scattered deeply within the desmoplastic tissue. These former lining cells were identified by their junctions and the presence of remnants of basal lamina as well as by their microvillous 5'-nucleotidase activity.
Clin Exp Metastasis
PMID:Tumor cell settling and early invasion of the peritoneum. 246 62

Hepatocellular carcinoma cells (Line-10), obtained from ascitic fluid after diethylnitrosamine treatment of Sewall Wright strain-2 guinea pigs, produce solid (primary) tumours, lymph-node and lung metastases and malignant ascites when reinjected into animals of the same strain. Monoclonal antibodies were raised against the tumour cells by immunizing BALB/c mice with viable ascitic hepatocellular Line-10 tumour cells. Three hybridomas producing anti-Line-10 monoclonal antibodies were selected for further studies (10TL1, 10TL40 and 10TL43) and compared with monoclonal antibodies against intermediate filament keratins. The anti-Line-10 monoclonal antibodies did not cross react with Line-1 hepatocellular carcinoma cells, nor with normal guinea pig hepatocytes. When ascitic Line-10 cells form high papillary projections on the peritoneal surface, they significantly reduced their antigen expression of 10TL40 and of 10TL43 defined antigens, while the expression of 10TL1 defined antigens remained unaltered. Invading Line-10 cells in the deep submesothelial stromal tissue, however, lost reactivity with MoAb 10TL43 but not with the MoAb's 10TL40 and 10TL1. The antigens on lung- and lymphnode metastases remained largely unaffected. The reactivity with MoAb's 10TL40 and with 10TL43 was also lost upon prolonged culturing of Line-10 cells. The reactivity of Line-10 and Line-1 cells with all monoclonal antibodies against keratin filaments remained unaltered. Line-1 cells could be distinguished from Line-10 cells by the absence of any reactivity with the MoAb's 10TL1, -40, -43, but also by the fact that 100% of the Line-1 cells were positive with antibodies against keratins 5/8, 18, and 7.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changing tumour antigen expression in metastatic hepatocellular carcinoma cells of the guinea pig. 246 49


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