Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We produced monoclonal antibodies (mABs) against human integrins. Competitive enzyme-linked immunosorbent assay (ELISA) revealed that each mAB bound to different antigenic determinants. We then developed sandwich-type enzyme immunoassays (EIAs) to measure the concentration of fibronectin receptor (FNR) and vitronectin receptor (VNR). Serum immunoreactive integrin levels were measured using these EIAs in various liver and malignant diseases. In almost all cases of liver cirrhosis (LC) and hepatocellular carcinoma (HCC), serum integrin levels were significantly elevated, but were in the normal range in gastric, colon, lung cancer, and acute hepatitis (AH). The correlation between serum FNR and VNR levels was statistically significant in all cases of liver disease, and no correlation was observed between these integrin levels and conventional biochemical markers such as AST, ALT, and GGT. The serum integrin levels were demonstrated to be a potential diagnostic marker for hepatic fibrogenesis and carcinogenesis, and these sandwich EIAs could be useful for determination of these integrins in clinical laboratory tests.
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PMID:Sandwich enzyme immunoassay for serum integrins using monoclonal antibodies. 172 78

Two Morris hepatoma-derived cell lines, McA-RH7777 (7777) and McA-RH8994 (8994), exhibit different alterations in morphology upon exposure to glucocorticoid. After treatment with synthetic glucocorticoid dexamethasone (DEX), 7777 cells show increased adhesiveness and more flattened shape, while DEX-treated 8994 cells show decreased adhesiveness to substratum and exhibit a marked increase of round and detached cells. Since fibronectin has been thought to play an important role in cell adhesiveness to substratum in hepatoma cell culture, we have also compared the effects of DEX on the biosynthesis of fibronectin (FN) and the functional level of FN receptor in 7777 and 8994 cells. Northern blot analysis and immunofluorescent studies showed that 7777 cells have a high basal expression level of FN synthesis and that DEX treatment induces FN expression two- to threefold with establishment of an extensive fibrillar FN network around the cells. On the other hand, 8994 cells were shown to express little FN and no apparent FN was localized on nonstimulated 8994 cells. However, DEX-treatment drastically increased FN expression in 8994 cells to the level of more than that of DEX-treated 7777 cells and induced a detectable level of cell-associated FN around DEX-treated 8994 cells, which appears to be contradictory to the decreased adhesiveness to the substratum in DEX-treated 8994 cells. Cell attachment assays using FN-coated plates demonstrated that DEX does not exhibit significant effects on the attachment of either 7777 or 8994 cells to FN-coated dishes. Our results suggest that decrease of adhesiveness to the substratum and increase of round detached cells in DEX-treated 8994 cells are independent of changes in the FN expression and the function of FN receptor.
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PMID:Bidirectional morphological changes induced by dexamethasone in Morris hepatoma cell lines McA-RH7777 and McA-RH8994: independence of fibronectin and its receptor. 182 41

Pooled sera collected from cirrhotic patients was fractionated by affinity chromatography with a fibronectin receptor monoclonal antibody against the beta-subunit of fibronectin receptor. Eluates were assayed using Western immunoblotting. The relative mobility of the protein reactive with fibronectin receptor antibody was nearly identical to that of the beta-subunit of fibronectin receptor, confirming that fibronectin receptor is present in human serum. Serum levels of the beta-subunit of fibronectin receptor were analyzed by sandwich enzyme-linked immunosorbent assay in patients with various liver diseases. The serum level of fibronectin receptor (micrograms/ml) was significantly higher in patients with chronic hepatitis (inactive, 2.59 +/- 0.04; active, 3.45 +/- 0.13), cirrhosis (4.77 +/- 0.30), alcoholic liver disease (2.96 +/- 0.16) and hepatocellular carcinoma (4.71 +/- 0.49) than in normal subjects (2.11 +/- 0.08). Strong positive correlation was observed between serum levels of fibronectin receptor and histological findings, particularly in the degree of hepatic fibrosis. Immunohistochemical studies with fibronectin receptor antibody revealed that the beta-subunit of fibronectin receptor was present on the plasma membrane of hepatocytes and sinusoidal lining cells in the normal liver and was increased in fibrotic areas and on the plasma membrane of hepatocytes and sinusoidal lining cells of fibrotic liver. The serum level of fibronectin receptor in patients with chronic liver diseases may therefore be a useful marker of hepatic fibrosis.
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PMID:Detection of fibronectin receptor in sera: its clinical significance as a parameter of hepatic fibrosis. 183 May 62

To investigate the clinical significance of ascitic fluid in patients with a malignancy, an abdominal paracentesis to evaluate the ascitic fluid was performed in 10 patients with a hepatocellular carcinoma (HCC) and in 7 patients with liver cirrhosis (LC). The AFP levels in the ascitic fluid and in the serum of the HCC patients was found be significantly higher than that of the LC patients. In addition, the ratio of albumin/total protein in ascitic fluid was also higher in the HCC patients. However, no significant findings were uncovered with regard to the concentration of lipid in ascitic fluid, in either type of patient although 2 HCC patients were found to have a very high concentration of total cholesterol. The cytological findings provided no reliable marker because of significant number of false negatives in the HCC patients. Also, there was no significant difference between the fibronectin levels in the ascitic fluid of either type of patients. This finding differs from previous studies, and suggests that the fibronectin levels in the ascitic fluid may not be a useful marker in determining a malignancy.
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PMID:[Clinical analysis of ascitic fluid in patients with liver cirrhosis and hepatocellular carcinoma]. 197 86

Chemical analysis of ascitic fluid may be helpful in determining the underlying disease. We discuss the diagnostic accuracy of the common and newer chemical parameters (protein, LDH, lactate, glucose, cholesterol, triglycerides, phospholipids, fibronectin, albumin gradient [value of serum minus value of ascites], ferritin, tumor markers, immunomodulators, leukocytes, bacterial and cytologic examinations). We also review the pathogenesis and clinical findings of the most frequent ascites forms (benign hepatic, infective, malignant ascites, ascites associated with liver metastases or hepatocellular carcinoma, cardiac and pancreatic ascites) and the most important diagnosis criteria. In the malignant ascites a high cholesterol, a narrow albumin gradient or a high ferritin value have high diagnostic accuracy, but diagnosis is by the finding of malignant cells. For the diagnosis of infective ascites, bacteriology is mandatory even though the results are negative in most cases, particularly in spontaneous bacterial peritonitis where diagnosis has to be established clinically, by a low pH or by a high leukocyte count. Benign hepatic ascites is diagnosed by demonstrating an underlying chronic liver disease and laboratory examinations of the peritoneal fluid to exclude other causes. The laboratory tests in ascites associated with liver metastases or with hepatocellular carcinoma were similar to those in benign hepatic ascites and the two ascites forms must be separated by other clinical and technical findings. Pancreatic ascites can easily be distinguished from the other forms by the high amylase and lipase content.
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PMID:[Laboratory chemical analysis in ascites]. 203 10

An Image Analysis program was used for the quantitative evaluation and comparison of the fibronectin (FN) mRNA detected by dot-blot and in situ hybridization in different cell lines. These techniques were applied for the evaluation of FN mRNA synthesized by human normal fibroblasts (Flow 7000) and by four tumour-derived cell lines (HeLa, epithelioid carcinoma; 8387, fibrosarcoma; RD, rhabdomyosarcoma; SK Hep-1, hepatocarcinoma). Dot-blot analysis showed that the cell types analysed synthesize different levels of FN mRNA. Flow 7000 are the highest producers while HeLa the lowest. In situ hybridization confirmed these results and furthermore showed that while Flow 7000, 8387 and HeLa cells synthesized homogeneous levels of FN mRNA, RD and SK Hep-1 could be subdivided into two populations expressing high or low levels of FN mRNA. The combined analysis of dot-blot, in situ hybridization and Image Analysis allowed the quantitation of the number of FN mRNA molecules expressed by single cells. This approach is therefore an invaluable tool when evaluating mRNA expression in heterogeneous cell populations like tumour-derived cell lines, during cell cycle or in histological tissue sections.
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PMID:Study of fibronectin expression in tumour cells by dot-blot and in situ hybridization: quantitative evaluation by image analysis. 222 84

High molecular weight hepatoma-associated nonhistone chromosomal proteins (NHPs) in transplantable rat hepatoma cells were reported previously from this laboratory. A cDNA library prepared from Morris hepatoma 7777 cells was screened with the polyclonal antibodies against hepatoma NHPs and a positive cDNA clone (lambda P2A1) was isolated. DNA sequence analysis revealed that the cDNA clone was identical to that of rat fibronectin (FN). The polyclonal antibodies against hepatoma NHPs were shown to bind specifically to both rat plasma FN and the fusion proteins encoded by lambda P2A1. A monoclonal antibody specific to rat plasma FN also recognized high molecular weight antigens of hepatoma NHPs in a pattern similar to that demonstrated with the polyclonal antibodies. These results suggest the existence of FN or FN-like antigens in the chromatin preparations from rat hepatoma cells. The antigenic proteins are localized in the nuclei of neoplastic foci of liver undergoing hepatocarcinogenesis.
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PMID:Association of fibronectin-like antigens in chromatin preparations from rat hepatoma cells. 227 52

Flow cytometry was used to detect fibrinogen (platelet associated fibrinogen: PAFbg) and fibronectin (PAFn) on the surface membrane of platelets in leukemia (9 cases), lung cancer (15 cases) and hepatoma (8 cases) patients (by one color analysis method), and simultaneously to investigate the binding of monoclonal anti-glycoprotein (GP) IIb/IIIa and anti-GP Ib antibodies (by two color analysis). All patient groups showed higher Fbg values than the normal control group, but no differences were found between patient groups. The values of Fbg and Fn showed a correlation, but the pattern of binding did not show a regular tendency in any patient group. There also was no significant correlation between Fbg values and the positive percentage of monoclonal anti-GPIIb/IIIa and anti-GPIb antibodies, and the binding of Fbg did not inhibit that of monoclonal antibody. The results suggest the following. 1. There are no differences in platelet activation in leukemia, lung cancer and hepatoma patients, and the degree of platelet activation is decided by the degree and the kind of stimulation. 2. The increase of both PAFbg and PAFn prove to the existence of activated platelet.
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PMID:[Analysis of adhesive proteins on the surface membrane of platelet in malignant neoplasm]. 232 78

Ascitic fluid concentrations of fibronectin, cholesterol and protein were determined in 95 patients: 38 with cirrhosis of the liver, 10 with miscellaneous nonmalignant diseases, 43 with peritoneal carcinomatosis and 4 with liver metastases or hepatocellular carcinoma. Fibronectin, cholesterol and protein at discrimination values of 7.5 mg/100 ml, 45 mg/100 ml and 3.0 g/100 ml, respectively, separated patients with peritoneal carcinomatosis from patients with cirrhosis with an efficiency of 94%, 90% and 85%, respectively. Thus, ascitic fluid determinations of fibronectin and cholesterol offer good discrimination of cirrhotic ascites from ascites related to peritoneal carcinomatosis, superior to the conventional protein determination. However, the failure of all parameters to distinguish ascites caused by miscellaneous nonmalignant diseases from malignancy-related ascites underscores the importance of highly specific methods to confirm a suspected diagnosis of malignancy-related ascites.
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PMID:Ascitic fluid concentrations of fibronectin and cholesterol: comparison of differential diagnostic value with the conventional protein determination. 238 56

Hepatocytes adhere well on plastic in the presence of serum or fibronectin and subsequent spreading is not prevented when protein synthesis was blocked by cycloheximide. Protein synthesis-independent spreading was also observed in cultures containing serum depleted of fibronectin by affinity chromatography. This indicates that serum-mediated adhesion is independent of fibronectin and suggests the existence of an adhesion factor other than fibronectin in serum. The involvement of different membrane components for fibronectin- and serum-mediated adhesion was demonstrated by experiments where the different adhesion-inhibiting activities of antisera raised against plasma membranes of rat liver and Morris hepatoma 7777 (Neumeier et al., FEBS lett 168 (1984) 241-244) were used. Whereas anti-liver antibodies inhibited both types of adhesion, anti-hepatoma antibodies were only able to prevent fibronectin-mediated adhesion. This indicates again that two different mechanisms are responsible for fibronectin- and serum-mediated adhesion. Fractionation of fetal calf serum (FCS) by size exclusion HPLC revealed that proteins of molecular weights of 60-80 kD promoted attachment and spreading of hepatocytes. Spreading was not perturbated by anti-hepatoma antibodies, indicating that an adhesion factor of 60-80 kD is responsible for serum-mediated adhesion. 'Serum-spreading factor', also called vitronectin, from human plasma has been described as having a similar molecular weight. The purified factor was found to mediate hepatocyte adhesion which was not inhibited by anti-hepatoma antibodies. This suggests that serum-mediated adhesion depends on an adhesion factor present in FCS, which is similar to or identical with vitronectin.
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PMID:Hepatocyte adhesion on plastic. Different mechanisms for serum- and fibronectin-mediated adhesion. 241 65


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