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)

The electron-dense marker which is thought to produce the ruthenium red surface staining is studied. This stain is prepared under conditions which should give its rise in cell surface membrane, and its nature and charge are tested electrophoretically and by measuring the turbidity, respectively. It is a positive colloid resulting from the recharging of colloidal osmium dioxide by RR polycations. Controls on the affinity are carried out by applying positive sol to gelled agarose sections containing hyaluronic acid, polyvinyl sulfate or polylysine. Controls are also carried out on ascites Ehrlich carcinoma and Zajdela ascites hepatoma cells subjected to prior enzymatic and chemical treatments. It is found that the osmium-RR system visualizes all acidic groups in the outer hydrophilic leaflet, that is the greater part of compounds in this external cell layer. A model is presented for the mechanism underlying its rise in cell surface membrane.
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PMID:Ultrahistochemical study on the ruthenium red surface staining. II. Nature and affinity of the electron dense marker. 6 Mar 16

The present study was undertaken to determine the mucopolysaccharide content of cells, AH-100B, and in the ascites, liver, and kidney of a rat bearing this hepatoma. AH-100B is similar to other mixed-type cells in having heparan sulfate as the main component in its mucopolysaccharides but its minor component was different in containing heparin. The main mucopolysaccharide in the ascites of AH-100B bearing rat was hyaluronic acid, which was similar to that of control ascites induced by injection of polypeptone, but minor component contained heparin derived from the cells. The content of hyaluronic acid in the liver of a rat bearing this hepatoma was higher than those of control liver and liver of a rat bearing other tumors. There were no significant differences between control kidney and kidney of a rat bearing this hepatoma.
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PMID:Mucopolysaccharides of rat ascites hepatoma, AH-100B. 17 Nov 92

The glycosaminoglycan composition of AH-130 ascites hepatoma cells and fluid were examined using enzymatic digestion, electrophoresis, and sequential partition fractionation. The cell-associated glycosaminoglycans were found to consist of 93% heparan sulfate, with the remainder consisting primarily of chondroitin sulfate. The glycosaminoglycans isolated from the ascitic fluid were found to consist of 58% heparan sulfate, 26% hyaluronic acid and 16% chondroitin sulfate. Dermatan sulfate was not detected in either cells or fluid. The heparan sulfate isolated from AH-130 cells in low-sulfate and highly heterogeneous with respect to biochemical composition. Fractions isolated by partition fractionation varied from 0.14 mol sulfate/mol uronic acid to 0.6 mol sulfate/mol uronic acid. Of the total sulfate 70--80% is N-sulfate in the former and 50% in the latter. Electrophoresis in 0.1 M HCl showed a highly heterogeneous material with mobility between that of hyaluronic acid and beef lung heparan sulfate. The heparan sulfate isolated from the fluid was similar to that isolated from the cells but was, however, somewhat more homogeneous with respect to charge.
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PMID:Biochemical composition and heterogeneity of heparan sulfates isolated from AH-130 ascites hepatoma cells and fluid. 20 27

The use of a hyaluronic acid-binding proteoglycan (hyaluronectin) as a probe for the detection of hyaluronic acid has facilitated the development of an indirect enzymo-immunological assay for hyaluronidase. Plastic microtest ELISA plates were coated with hyaluronic acid. Incubation with hyaluronidase led to the destruction of insolubilized hyaluronic acid in proportion to the hyaluronidase concentration of samples. Residual hyaluronic acid was assayed by its capacity to bind immune complexes made up of hyaluronectin supplemented with alkaline phosphatase-conjugated anti-hyaluronectin antibodies. The technique was very sensitive and permitted the detection of as little as 10(-10) NFU of bovine testicular hyaluronidase. Hyaluronidase was detected by this technique in human sera, bee venom and culture medium of human hepatoma cell lines.
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PMID:An indirect enzymoimmunological assay for hyaluronidase. 331 96

The metabolism of acid mucopolysaccharides in Novikoff hepatoma and in hepatoma BW7756 was studied using the precursors -35S-sulfate, -H-glucosamine and -14C-galactosamine. There is an active formation of sulfated mucopolysaccharides at the mitochondria and cell membrane level. Hepatoma cells synthesize heparin to a lower rate than liver cells. In ascitic as well as in solid tumors there is a considerable accumulation of hyaluronic acid which does not seem to be elicited by the tumor cells but by the surrounding tissues. The possible implication of the low heparin production in the cell membrane characteristics is discussed.
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PMID:Metabolism of acid mucopolysaccharides in hepatoma and in normal liver. 437 92

Polyamine-responsive protein kinase, a cyclic nucleotide-independent protein kinase from the cytosol of Morris hepatoma 3924A, was stimulated 8-9 fold by several different polymers of polylysine, polyornithine and random copolymers of lysine-alanine; spermidine, spermine, and mixtures of spermine and spermidine stimulated 2, 3, and 5 fold, respectively. The protein kinase was not stimulated by poly-carboxybenzyl-lysine, random copolymer of lysine-tyrosine, polyhistidine, polymethionine, polyglutamic acid, polyaspartic acid, dipeptide (Lys-Lys), lysine, ornithine, and putresine. The polyamine stimulation of the protein kinase was prevented by certain specific charged carbohydrates: heparin, chondroitin sulfates A, B, and C, dextran sulfate and hyaluronic acid. It was not prevented by noncharged carbohydrates: dextran, glycogen, starch, sucrose, etc; or by sulfate salts: ammonium sulfate, potassium sulfate, sodium thiosulfate, etc. The inhibition was reversed by increased polylysine. Heparin was non-competitive inhibitor of Mg2+-ATP. It would appear that this enzyme is regulated by certain highly specific molecules with certain sizes and charges; plus charge is stimulatory, negative charge prevents the stimulation.
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PMID:Regulation of polyamine-responsive protein kinase by certain highly specific polyamines and charged carbohydrates. 682 33

The basis of the differential effect of anionic polysaccharides on replicative DNA synthesis in liver and hepatoma cell nuclei was investigated. The differential effect of heparin was lost when more than 40% of its sulfate was removed. DNA synthesis in liver nuclei was optimally stimulated by heparin of molecular weight 22600 and sulfate to hexosamine ratio 2.42, but inhibited by heparin of molecular weight 4300 and sulfate to hexosamine ratio 2.35. A heparin fragment (molecular weight 2800 and sulfate to hexosamine ratio 1.81), prepared by partial nitrous acid treatment was a potent inhibitor of DNA synthesis in hepatoma nuclei. There was no significant difference in the rate of entry of heparin or its subfractions into either liver or hepatoma nuclei. In both cases less than 15% of added polysaccharide entered the nuclei and only about 4.5% was found associated with the chromatin. The influence of the anionic polysaccharides on DNA synthesis was correlated with their ability to complex with histones as determined by relative light scattering in a laser nephelometer. The relative light scattered on mixing with histones (H1, H2A + H3, H4) was high for DNA synthesis stimulators (heparin, dextran sulfate); medium for DNA synthesis inhibitors (chondroitin 4- and 6-sulfates, heparan sulfate) and low for non-effectors (keratan sulfate, hyaluronic acid). Heparin and chondroitin sulfate H, which at low concentrations stimulate DNA synthesis in liver nuclei, inhibited DNA synthesis by calf thymus DNA polymerase alpha at all concentrations. This inhibition was not simply due to electrostatic interactions.
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PMID:Influences of anionic polysaccharides on DNA synthesis in isolated nuclei and by DNA polymerase alpha: correlation of observed effects with properties of the polysaccharides. 688 67

Serum levels of circulating intercellular adhesion molecule-1 (cICAM-1) were measured in 23 patients with chronic hepatitis (CH), 22 with liver cirrhosis (LC) and 45 with hepatocellular carcinoma (HCC) using an ELISA. Serum samples from all patients showed significantly higher cICAM-1 levels than serum from 50 normal controls. The cICAM-1 level was significantly increased in LC or HCC when compared with CH, but no differences were noted between LC and HCC. Levels of cICAM-1 correlated well with serum bilirubin, retention rate of indocyanine green, hyaluronic acid, type IV collagen 7-S and type III procollagen peptide levels but not with tumor size or circulating tumor markers (alpha-fetoprotein and des-gamma-carboxyprothrombin). Our findings indicate that the measurement of cICAM-1 is useful for the determination of the severity of liver disease and hepatic fibrosis. HCC tissues obtained from 10 patients were immunohistochemically stained for ICAM-1. Enhanced ICAM-1 expression was found on the tumor cell membranes. Sequential measurements of cICAM-1 levels showed that they changed in a similar manner to those of alpha-fetoprotein during the course of treatment of HCC in a patient with very high pretreatment levels of both markers. These results suggest that HCC cells shed ICAM-1 into the circulation. We conclude that cICAM-1 is not a diagnostic marker for HCC, but may be useful for monitoring the response to treatment.
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PMID:Detection of circulating intercellular adhesion molecule-1 in hepatocellular carcinoma. 750 59

Lipiodolization--selective regional cancer chemotherapy using Lipiodol plus an anticancer drug (LPD)--can prolong survival time of patients with an unresectable hepatocellular carcinoma (HCC). To enhance understanding of LPD's influence on the cirrhotic liver, we carried out related studies. Forty-three cirrhotic patients with HCC were treated with LPD (epirubicin in a dose of 15-40 mg/m2 and Lipiodol of 0.02-0.25 ml/kg). Seven cirrhotic patients with HCC were subjected to hepatic angiography alone, and these subjects selected randomly served as controls. Among the 43 treated with LPD, 23 belonged to Child's class A, 15 to class B, and 5 to class C. Blood samples were taken before angiography (pre) and at 24 hours after angiography (post) from each patient. Post/pre ratio of the following parameters were compared between patients of the two groups: sGOT, sGPT, and LDH as a marker for hepatocyte injury; t. bilirubin and hepaplastin test (HPT) as hepatocyte function; alkaline phosphatase and gamma-GTP to examine bile duct injury; and serum hyaluronic acid level to determine an endothelial cell functions. Post/pre ratio of serum GOT, GPT, LDH levels, and HPT in patients treated with vs. without LPD were 1.32 +/- 0.59 vs. 0.92 +/- 0.09 (P < 0.001), 1.18 +/- 0.43 vs. 0.88 +/- 0.09 (P < 0.001), 1.11 +/- 0.20 vs. 1.00 +/- 0.07 (P < 0.05), and 0.95 +/- 0.10 vs. 1.09 +/- 0.12 (P < 0.01), respectively. There were no significant differences in post/pre LPD ratio of other parameters, rates of complications, and hospital stay after LPD for patients with Child's class A, B, and C. Hepatocytes are apparently the primary site of injury in cases of LPD. LPDs, using epirubicin in a dose of 15-40 mg/m2 and Lipiodol in a dose of 0.02-0.25 ml/kg, proved to be safe for cirrhotic patients with HCC.
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PMID:Influence of lipiodolization on a cirrhotic liver. 772 71

The collagen-binding activity of plasma vitronectin was measured in 15 control subjects and 64 subjects with chronic liver disease. The assay of collagen-binding vitronectin was performed by an enzyme immunoassay using a monoclonal antibody to human vitronectin and type I collagen from human placenta. The plasma collagen-binding vitronectin concentration (mean +/- S.D.) was 5.6 +/- 1.9 micrograms/ml in the controls, 8.3 +/- 1.1 micrograms/ml in chronic persistent hepatitis, 8.3 +/- 2.9 micrograms/ml in chronic active hepatitis, 7.8 +/- 2.9 micrograms/ml in liver cirrhosis and 8.2 +/- 2.1 micrograms/ml in hepatocellular carcinoma with cirrhosis. The percent collagen-binding vitronectin to total plasma vitronectin was 2.2 +/- 0.8% in the controls, 3.9 +/- 2.2% in chronic persistent hepatitis, 3.9 +/- 1.2% in chronic active hepatitis, 5.8 +/- 3.3% in liver cirrhosis and 4.1 +/- 1.2% in hepatocellular carcinoma with cirrhosis. The plasma collagen-binding vitronectin also correlated with the serum levels of 7S collagen and hyaluronic acid. These findings suggest that vitronectin may play an important role in the progression of liver disease and/or in hepatic fibrosis through its collagen-binding domain.
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PMID:Collagen-binding activity of plasma vitronectin in chronic liver disease. 881 65


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