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)

A Caucasian male developed florid dermatomyositis documented by serum enzyme elevation, electromyography, and histology of skin and muscle. Serum enzymes, including creatine phosphokinase (CPK), aldolase, glutamic oxaloacetic transaminase (SGOT), and lactic dehydrogenase (LDH), decreased initially during high dose systemic corticosteroid therapy, although profound muscle weakness persisted. Subsequent elevation of serum LDH and SGOT levels during treatment provided a clue to underlying neoplasia. Primary hepatoma with widespread metastases was found at necropsy.
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PMID:Aberrant serum enzyme patterns in dermatomyositis associated with hepatoma. 18 84

Triflavin, an Arg-Gly-Asp (RGD)-containing peptide, purified from snake venom of Trimeresurus flavoviridis, inhibits human platelet aggregation through the blockade of fibrinogen binding to fibrinogen receptors associated with glycoprotein IIb/IIIa complex. In this report, we examined the effect of triflavin on tumor cells (human hepatoma J-5)-induced platelet aggregation (TCIPA) of heparinized platelet-rich plasma (PRP). ADP-scavenger agents, apyrase (10 U/ml) and creatine phosphate (5 mM)/creatine phosphokinase (5 U/ml) did not inhibit TCIPA while hirudin (5 U/ml) completely inhibited it. J-5 cells initially induced platelet aggregation, then blood coagulation occurred. J-5 cells concentration-dependently shortened the recalcification time of normal as well as Factor VIII, IX-deficient human plasmas, while it was inactive at shortening the recalcification time of Factor VII-deficient plasma, suggesting J-5 cells induced platelet aggregation through activation of extrinsic pathway, leading to thrombin formation as evidenced by the amidolytic activity on s-2238 by expressing tissue factor-like activity. Triflavin inhibited TCIPA in a dose-dependent manner (IC50, 0.02 microM). When compared on molar ratio, triflavin was approximately 30,000 times more potent than GRGDS (IC50, 0.58 mM). On the other hand, GRGES showed no significant effect on TCIPA, even its concentration was raised to 4 mM. Additionally, the monoclonal antibodies, raised against glycoprotein IIb/IIIa complex (i.e., 7E3 and 10 E5) inhibited J-5 TCIPA. In conclusion, we suggest the inhibitory effect of triflavin on J-5 TCIPA may be chiefly mediated by the binding of triflavin to the fibrinogen receptor associated with glycoprotein IIb/IIIa complex on platelet surface membrane.
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PMID:Triflavin, an Arg-Gly-Asp containing snake venom peptide, inhibits aggregation of human platelets induced by human hepatoma cell line. 151 27

We studied the creatine kinase (CK) isoenzyme pattern in sera from 332 patients affected by hepatic cirrhosis and several neoplastic diseases (102 cirrhosis, 36 hepatocarcinoma, 16 metastatic liver tumor, 40 breast cancer, 18 other neoplastic diseases and 120 cases of leukemia or lymphoma) to evaluate both its diagnostic utility for cancer diagnosis and its power as a prognostic index. Type-2 macro CK (mitochondrial creatine kinase) was detected, with no statistical difference in cirrhosis (14%), hepatocarcinoma (16%), metastatic liver tumor (31%), breast cancer (5%) and other tumors (6%). It was not detected in any patient with leukemia or lymphoma. The presence of type-2 macro CK was unrelated to the stage of either cirrhosis or hepatocarcinoma, according to Child and Okuda, respectively, nor was it correlated to serum cytolytic enzyme levels or to gamma-globulin levels. In cirrhotics, type-2 macro CK was not linked to serum levels of the following tumor markers: alpha-fetoprotein, pseudouridine and gamma-glutamyltransferase isoenzymes complexed to low-density lipoprotein. In addition, the atypical band persisted in several patients with cirrhosis monitored for six months who did not show any evidence of evolution toward hepatocarcinoma. Thus, type-2 macro CK has poor diagnostic sensitivity for neoplastic diseases, and lacks prognostic value both in cirrhosis and neoplastic diseases.
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PMID:Serum type-2 macro-creatine kinase isoenzyme is not a useful marker of severe liver diseases or neoplasia. 228 11

We measured the activity of carnosinase, a prominent hepatic peptidase, in sera from 69 patients with liver disorders. Mean values (and SDs) for those with liver cirrhosis (17 cases) and hepatoma (seven cases) were 0.51 (0.28) and 0.68 (0.21) mumol/mL per hour, respectively--clearly less than for normal adults: 4.19 (0.95) mumol/mL per hour. Samples from 17 cases of chronic hepatitis also showed moderately decreased activity, 1.41 (0.97) mumol/mL per hour. In contrast, 14 cases of acute hepatitis generally showed values falling within the normal limits: 3.41 (1.97) mumol/mL per hour. Our results for carnosinase correlated with those for cholinesterase (r = 0.70) and with the concentration of albumin in serum (r = 0.59), but not with the activity of either creatine kinase, aspartate aminotransferase, or alanine aminotransferase in serum. Carnosinase values differed more among groups of disorders than did the values for cholinesterase or albumin. Measurement of serum carnosinase activity may be of clinical value in assessing the severity of chronic liver-cell damage, but not in differentiating liver disease from nutritional, muscle, or endocrine disorders.
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PMID:Decreased activity of carnosinase in serum of patients with chronic liver disorders. 373 53

Guanidinoacetate methyltransferase, the enzyme catalyzing the last step in creatine biosynthesis, has previously been considered to be restricted to a few tissues, but it has been found to occur in the cultured cells H4Az C2 rat hepatoma, N4TG1 mouse neuroblastoma, and IMR-90 human fetal lung fibroblast, as well as in skeletal and cardiac muscle of the rat. Activity was highest in the hepatoma, but tissues and cultured cells of nonhepatic origin had 5-20% of the activity of rat liver. Dialyzed 100,000g supernatants prepared from cultured cells or skeletal muscle tissue yielded values for apparent Km in the range of 1.2-3.4 microM for S-adenosylmethionine and 0.050-0.096 mM for guanidinoacetate. Intact monolayers of the three types of cultured cells converted labeled guanidinoacetate in the culture medium to creatine, which was identified by chromatographic behavior and by reaction with creatine kinase. The amounts of guanidinoacetate converted to creatine by fibroblasts and neuroblastoma cells during an 18-h period of incubation suggested that synthesis was proceeding at rates approaching Vmax, even in medium containing the relatively low physiological concentrations of guanidinoacetate. Fibroblast and neuroblastoma cell monolayers also have the capacity to take up creatine provided in the culture medium. The amounts of creatine taken up by monolayers of those cells were measured under the same conditions that were used for measurement of creatine synthesis. Comparison of the amounts of creatine synthesized with the amounts taken up showed that synthesis can make a significant contribution to intracellular pools of creatine plus phosphocreatine in fibroblasts and neuroblastoma cells.
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PMID:Guanidinoacetate methyltransferase activity in tissues and cultured cells. 397 May 26

A considerable interest has recently been shown for the measurement of isoenzyme BB of creatine kinase as a diagnostic and prognostic indicator of tumor growth. This isoenzyme belongs to the group of oncofetal antigens and in human cancer elevated levels occur frequently in patients with metastatic disease. In this study we have attempted to quantify CK-BB serum levels during the growth of an experimental tumor (Yoshida Hepatoma AH 130) in male albino rats to determine if a significant correlation exists between isoenzyme serum levels and the rate of tumor growth. Creatine kinase-BB was measured spectrophotometrically by immunoinhibition of creatine kinase-M subunits. CK-BB normal values were 4.19 +/- 0.4 U/L and between days 5 and 9, where there is an increase in the rate of proliferation of neoplastic cells, CK-BB serum levels reaches its maximum 69.01 +/- 2.2 U/L. These data are in agreement with the hypothesis that the highest isoenzyme levels are a measure of the aggressiveness of the neoplastic clone. Moreover, this hypothesis is consistent with the proposed mathematical model, and we plan to expand this line of study to evaluate the predictive potential of this tumor marker in man.
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PMID:Evaluation of creatine kinase isoenzyme BB as a marker of neoplastic growth in Yoshida ascites hepatoma of the rat. 406 55

We have developed a new multienzyme control serum, Seraclear-HE, which was designed to function not only as an accuracy and precision control serum but also as an intermethod calibrator for unifying interlaboratory clinical enzyme data in terms of reference method values. Seraclear-HE contains as analytes the following enzymes of human origin only: aspartate aminotransferase (AST, EC 2.6.1.1) and lactate dehydrogenase (LD, EC 1.1.1.27) from erythrocytes; alanine aminotransferase (ALT, EC 2.6.1.2) from a hepatoma cell line; alkaline phosphatase (ALP, EC 3.1.3.1) from an amnion cell line; creatine kinase (CK, EC 2.7.3.2) from an embryo kidney cell line; gamma-glutamyltransferase (GGT, EC 2.3.2.2) from a macrophage cell line; and amylase (AMY, EC 3.2.1.1) from urine and saliva. The seven partly purified enzymes were lyophilized in partially delipidated human serum containing sucrose (50 g/L), pyridoxal 5'-phosphate (30 mmol/L), and other stabilizers. The material is stable for at least 2 years at temperatures < or = 10 degrees C. For two concentrations of this preparation, reference method values (mainly International Federation of Clinical Chemistry and Japan Society of Clinical Chemistry) obtained at both 30 degrees C and 37 degrees C are assigned.
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PMID:Multienzyme control serum (Seraclear-HE) containing human enzymes from established cell lines and other sources. 1: Preparation and properties. 753 43

In heparinized human platelet-rich plasma (PRP), J-7 human hepatoma cells initially induced platelet aggregation; then a clot formed. ADP-scavenger systems, apyrase and creatine phosphate/creatine phosphokinase did not inhibit this tumor-cell-induced platelet aggregation (TCIPA), whereas hirudin and concanavalin A completely blocked it. J-7 cells also shortened the recalcification time of normal and of Factor-VIII- and IX-deficient human plasma, although it was inactive in shortening the recalcification time of Factor-VII-deficient plasma. After treatment with phorbol 12,13-dibutyrate (PDBu) for 5 to 90 min, the aggregation and coagulation abilities of J-7 cells were unaffected. Prolonged treatment of J-7 cells with PDBu but not with alpha-PDBu for 24 and 72 hr resulted in gradual loss of aggregation and coagulation. Staurosporine antagonized the effect of PDBu and restored aggregation and coagulation in J-7 cells. Protracted treatment with PDBu (24 or 72 hr) did not affect adherence of J-7 cells to the extracellular-matrix proteins (i.e., fibrinogen, fibronectin, laminin, vitronectin and collagen types I and IV) or to the surface of plastic culture dishes. The treatment also did not affect J-7 cell detachment from plastic culture dishes. These in vitro results demonstrate that protracted phorbol ester treatment diminishes TCIPA and blood coagulation of tumor cells.
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PMID:Protracted treatment with phorbol ester modulates J-7 human hepatoma-cell-induced aggregation and coagulation of human platelet-rich plasma. 796 Feb 44

We have compared the levels of creatine kinase (CK) activity and the distribution of CK isoenzymes determined by agarose gel electrophoresis in normal colon, liver and lung tissues, and in colon, liver and lung adenocarcinomas, lung squamous cell carcinomas and lung carcinoids. Colon and lung adenocarcinomas, and squamous cell carcinomas presented lower CK activity than the normal tissues and no differences were found between hepatocarcinoma and normal liver tissue. In contrast, lung carcinoids had higher CK activity than normal lung tissue. Type BB-CK was the predominant isoenzyme in normal lung, colon and liver tissues. Type MM isoenzyme was detected in normal lung and type MB-CK was found in normal colon. In most lung tumours the CK isoenzyme electrophoretic pattern did not change. However, no type BB-CK was detected in some hepatocarcinomas, type MM-CK decreased in lung carcinoids and type MB isoenzyme was not observed in colon adenocarcinomas. It is concluded that in most tumours there is a decrease in the expression of type B- and type M-CK subunits, whereas in lung carcinoid the expression of type B-CK activity increases. Thus, the increase in type BB-CK observed in the serum of patients with lung and colon adenocarcinomas is probably due mainly to enhanced enzyme release as a result of tumour cell necrosis.
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PMID:Creatine kinase activity and isoenzymes in lung, colon and liver carcinomas. 930 58

A case of hepatocellular carcinoma associated with polymyositis is reported. A 70-year-old man noticed muscular weakness mainly in the proximal limb muscles. The clinical course, a raised level of serum creatine kinase and electromyographic findings suggested polymyositis, and the pathological findings on muscle biopsy were compatible with this diagnosis. Computed tomography of the upper abdomen revealed a mass lesion in segment VII and VIII of the liver, which was diagnosed pathologically as hepatocellular carcinoma. The patient underwent systematic resection of segment VII and the dorsal part of segment VIII of the liver. After surgery, the weakness improved and the serum creatine kinase level normalized without medical treatment for the polymyositis. The relief of neurological symptoms and signs after complete resection of the tumor strongly suggests paraneoplastic polymyositis, which has been described only rarely in association with hepatocellular carcinoma.
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PMID:Polymyositis as a paraneoplastic manifestation of hepatocellular carcinoma. 1110 Mar 67


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