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 urinary level of pseudouridine, primarily a degradation product of transfer ribonucleic acid (tRNA), was determined in 38 patients with primary hepatocellular carcinoma, 18 with liver cirrhosis, 12 with chronic hepatitis, nine with acute hepatitis, and 28 healthy subjects. The mean urinary pseudouridine concentration was significantly higher in the patients with hepatoma [38.2 +/- 12.8 (SD) nmol/mumol creatinine] than in those with liver cirrhosis (20.3 +/- 6.8), chronic hepatitis (24.4 +/- 8.2), and acute hepatitis (21.7 +/- 8.2), and in healthy subjects (23.8 +/- 4.9). Urinary pseudouridine level was elevated above the mean value plus 2 SD for the healthy subjects (33.6 nmol/mumol creatinine) in 71% of our hepatoma cases. Serum alpha-fetoprotein levels correlated poorly with urinary pseudouridine levels, thus, the combination assay for urinary pseudouridine and serum alpha-fetoprotein could detect 79% of the patients with hepatoma. Moreover, urinary pseudouridine level was reduced after effective transcatheter arterial embolization therapy.
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PMID:Urinary pseudouridine as a biochemical marker in the diagnosis and monitoring of primary hepatocellular carcinoma. 245 10

A remarkably high incidence of hepatocellular carcinomas was observed in long-surviving LEC rats with hereditary hepatitis. Among the 60 LEC rats examined between 12 and 28 months of age from F29 and F30, 55 (92%) developed putative preneoplastic and neoplastic lesions such as hyperplastic foci and nodules, and hepatocellular carcinomas. Of these, hepatocellular carcinomas were observed with a high frequency (46/55; 84%). All rats of advanced age that survived more than 18 months developed hepatocellular carcinomas. These results suggest that the development of liver tumors in LEC rats is an age-associated phenomenon with serial hepatic alterations after the subsidence of acute hepatitis. The long-surviving rats had no normal tissue and showed chronic hepatitis in nontumorous tissues of the liver. Cholangiofibrosis was also found in most rats with hepatic lesions. Metastasis of hepatocellular carcinomas was found in four rats. Histologically, the hepatocellular carcinomas were of a well-differentiated type with a typical trabecular structure. Thus, LEC rats seem to be a promising animal model for studying the pathogenesis of hepatitis and hepatocellular carcinoma.
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PMID:High susceptibility to hepatocellular carcinoma development in LEC rats with hereditary hepatitis. 245 92

Serum alpha-L-fucosidase (AFU) was determined in 33 patients with hepatocellular carcinoma (HCC), 4 with secondary metastatic liver cancer, 61 with various liver diseases, 12 with gastrointestinal tumor and 50 healthy controls. The results showed that AFU level was significantly higher in HCC (14.48 +/- 5.77) than that in the controls (3.33 +/- 0.72) and in patient with other diseases (P less than 0.01). Serum AFU level was also increased in fulminant hepatitis (8.96 +/- 3.99), acute hepatitis (8.94 +/- 4.94) and chronic hepatitis (7.27 +/- 2.58), P less than 0.01 or 0.05. There was no significant difference in AFU level between the controls and patients with secondary metastatic liver cancer (6.25 +/- 0.84), cirrhosis (6.30 +/- 3.17), gastrointestinal tumor (4.43 +/- 1.64), liver hemangioma and liver abscess (4.86 +/- 2.22). A level exceeding 10.5u was a useful marker for the diagnosis of HCC with 78.8% sensitivity and 90.0% specificity. The diagnostic positivity was 81.8% in low AFP producing HCC, whereas 93.9% in those with elevated AFP. Our data indicate that serum AFU is a useful tumor marker for HCC, particularly in detection of AFP-low or negative HCC patients.
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PMID:[A preliminary study on serum alpha-L-fucosidase assay in the diagnosis of hepatocellular carcinoma]. 248 Feb 10

We reviewed 40 liver biopsy specimens from 36 patients with non-A, non-B (NANB) hepatitis by light microscopy to characterize the histopathologic features associated with this condition. NANB hepatitis had been acquired from intravenous drug use (6 patients), transfusion (11 patients), sporadic (13 patients), and other routes (6 patients). The major pathologic diagnoses included acute hepatitis, chronic persistent hepatitis, chronic lobular hepatitis, chronic active hepatitis with or without cirrhosis, and hepatocellular carcinoma. Histopathologic changes seen in varied combinations in these specimens included acidophilic degeneration of hepatocytes (100%), fat (85%), formation of portal tract lymphoid aggregates or follicles (52%), bile duct damage (30%), and multinucleate giant hepatocytes (25%). Prominence of sinusoidal cells was variable, but often striking. Hepatocyte atypia (liver cell dysplasia) was noted in 17 specimens. These histologic parameters appear to be diagnostically useful when applied in appropriate clinical settings and will require reevaluation when serologic tests for NANB hepatitis become available.
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PMID:Non-A, non-B hepatitis: characterization of liver biopsy pathology. 250 Apr 77

To evaluate the level of serum thyroxine-binding globulin (TBG) in various liver diseases, TBG and T4, T3, FT4 were measured by radioimmunoassay in 29 HBsAg carriers (C), 27 patients with acute hepatitis (AH), 18 patients with inactive chronic hepatitis, 70 patients with chronic active hepatitis (CAH), 31 patients with active cirrhosis (AC), 20 patients with inactive cirrhosis (IC), 38 patients with hepatocellular carcinoma (HCC), 12 patients with metastatic Ca to the liver (Met.) and in 81 normal controls. All the patients were clinically euthyroid. The TBG as well as T4 in patients with AH, CAH, AC HCC and, Met. were significantly higher than those in controls. The T3 level was significantly elevated in CAH and AC patients. The TBG level did not correlate with serum albumin or bilirubin levels, but did correlate significantly with alanine transaminase (ALT) (r = 0.54, p less than 0.01). However, the correlation was positive in chronic active hepatitis (r = 0.40, p less than 0.01) but negative in hepatocellular carcinoma (r = -0.32, p less than 0.05). The data suggested: (1) Significant TBG and T4 elevation was found in all active liver diseases and HCC. (2) In the presence of high T4 in patients with liver disease, normal FT4 excluded the diagnosis of hyperthyroidism. (3) The elevation of TBG levels in chronic hepatitis appeared to parallel the severity of hepatocytolysis, and therefore might be the result of hepatocytolysis; while the elevation of TBG in HCC might be due to increased synthesis by the malignant cells.
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PMID:[Changes in thyroid hormone concentration in liver disease]. 250 36

Patients with liver disease frequently have multiple hemostatic abnormalities. Coagulation and fibrinolytic factors and inhibitors may decrease as the result of impaired synthesis and/or enhanced catabolism. In order to assess the actual degree of activation of coagulation and fibrinolytic systems in liver disease, plasma levels of thrombin-antithrombin III complex (TAT) and plasmin-alpha 2-antiplasmin complex (PAP) were measured together with cross-linked fibrin derivatives (XDP), tissue-type plasminogen activator (t-PA), and plasminogen activator inhibitor (PAI-1) in 31 patients with liver disease (five patients with acute hepatitis, seven with chronic hepatitis, nine with liver cirrhosis, and ten with hepatocellular carcinoma). Mean plasma levels of TAT (mean 4.2 +/- SD 4.0 micrograms/L), PAP (0.7 +/- 0.7 mg/L), and XDP (374 +/- 518 micrograms/L) were significantly elevated in patients with liver disease as compared with normal subjects (TAT of 1.7 +/- 0.3 micrograms/L, PAP of 0.2 +/- 0.1 mg/L, and XDP of 30 +/- 14 micrograms/L; P less than 0.005). Plasma concentrations of t-PA and PAI-1 antigens were also elevated. When plotted by the disease categories, the magnitude of elevations of these parameters was variable among subgroups. Patients with acute hepatitis had considerably higher TAT levels. The mean PAP values were relatively high in chronic hepatitis and hepatocellular carcinoma, in which an elevation of the t-PA/PAI-1 ratio was observed. Although clearance of TAT and PAP should be evaluated in the future, these findings suggest that excessive amounts of thrombin and plasmin are actually generated in patients with liver disease.
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PMID:Thrombin and plasmin generation in patients with liver disease. 252 2

Interaction between woodchuck hepatitis virus surface antigen and proteins of hepatocyte plasma membranes were examined in the course of woodchuck hepatitis virus infection. Membranes purified from animals with histologically confirmed acute hepatitis, active or persistent chronic hepatitis and the virus-related hepatocellular carcinoma were evaluated for the virus surface antigen contents, treated with agents eluting plasma membrane-bound antigen to test the extent of the antigen-membrane associations and incubated with purified, particulate woodchuck hepatitis virus surface antigen to determine membrane potential for the antigen adsorption. Hepatocyte plasma membranes originating from woodchucks chronically infected with the virus showed the highest quantities of the incorporated virus surface antigen among membranes studied, the behavior of bound antigen as an integral and a peripheral membrane protein and the resistance to bind an exogenous antigen. Similar properties were expressed by plasma membranes prepared from hepatocytes of nontumor parenchyma displaying chronic active hepatitis of a woodchuck hepatitis virus carrier with hepatoma. Furthermore, plasma membranes originating from animals with active or persistent chronic hepatitis demonstrated identical properties, implicating that histologic activity of the chronic liver inflammatory process is not dependent on the quantity of the virus surface antigen insertion into the membrane. In contrast, hepatocyte plasma membranes from animals with acute hepatitis showed significantly lower antigen quantities, presence of the antigen specificity exclusively behaving as an integral membrane protein and noticeable ability to bind an exogenous surface antigen of the virus. Comparable, but not identical, features were observed for hepatocyte membranes purified from nodules of hepatocellular carcinoma, suggesting that neoplastic transformation of infected hepatocytes is associated with loss of the membrane-bound antigen and with simultaneous, partial recovery of the membrane potential for the antigen binding. Comparative analysis of the properties on the woodchuck hepatitis virus surface antigen incorporation into hepatocyte plasma membranes in studied cases indicated that sustained infection with woodchuck hepatitis virus leads to an increase in the quantity of the membrane-incorporated antigen and to the appearance of the virus surface antigen specificity behaving as a peripheral membrane protein. In conclusion, this study demonstrated that the extent and the character of the antigen interaction with hepatocyte plasma membranes undergoes significant variations in the natural course of hepadna viral infect
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PMID:Characterization of the incorporation of woodchuck hepatitis virus surface antigen into hepatocyte plasma membrane in woodchuck hepatitis and in the virus-induced hepatocellular carcinoma. 253 20

NK activity in acute viral hepatitis, chronic hepatitis, liver cirrhosis (LC), metastatic liver cancer and hepatocellular carcinoma (HCC) was preserved and had no significant change compared with the normal control in each disease. In acute hepatitis, NK activity was higher in convalescent phase than in acute phase. Although in LC and HCC, some liver functions such as total bilirubin, the rate of ICG 15' excretion, AFP and IAP did not have significant correlation with NK activity, advanced cases according to Child's classification and E factor which was anatomical extent of HCC in liver showed significantly low NK activity. The low NK activity group advanced much more in Child's classification, performance status, stage and E factor of HCC than high NK activity group significantly. According to those facts, LC or HCC is not a single entity of disease in view point of NK activity. NK activity may change in accordance with the advancement of hepatic disease and reserve function of the liver in LC and HCC.
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PMID:[NK activity in various liver diseases--especially the relation between NK activity and reserve function of the liver in liver cirrhosis and hepatocellular carcinoma]. 255 27

In the present study, we have measured the serum concentration of PIIIP in patients with various liver diseases, and studied serial changes in serum PIIIP after TAE and its gel filtration pattern in 10 cases of hepatocellular carcinoma undergone TAE. The following results were obtained. 1) Serum concentration of PIIIP was 12.3 +/- 6.1 ng/ml in normal controls and elevated significantly in liver cirrhosis, liver cirrhosis with hepatocellular carcinoma, chronic active hepatitis, and acute hepatitis. 2) There was no significant difference in the serum concentrations of PIIIP between liver cirrhosis and liver cirrhosis with hepatocellular carcinoma. The result suggested that serum PIIIP cannot be a specific marker of hepatocellular carcinoma. However, the serum PIIIP concentration was decreased 2 or 4 weeks after TAE in effective cases, whereas increased in ineffective cases. Thus, the measurement of serial change in the serum PIIIP after TAE was considered to be useful for evaluating the effectiveness of TAE. 3) In analysing the elution patterns of serum PIIIP by gel chromatography, the peak of 125I-PIIIP antigen decreased 4 weeks after TAE in effective cases, whereas, no change was observed in the elution profile by gel chromatography 4 weeks after TAE in ineffective cases. These results seem to be caused by necrosis of hepatocellular carcinoma by TAE, and suggest the possibility that PIIIP is produced in hepatocellular carcinoma tissue.
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PMID:[Serial change in serum concentration of type III procollagen N-terminal peptide after TAE in hepatocellular carcinoma, and analysis of gel filtration pattern of the peptide]. 256 Apr 88

A high risk group of hepatocellular carcinoma (HCC) was statistically established using multiple regression analysis of 331 cases with liver cirrhosis (LC), in which 78 cases later developed HCC. Highly contributing factors to hepatocarcinogenesis were found to be positive HBsAg, age, drinking history, sex (male), history of blood transfusion, history of acute hepatitis (or jaundice) and elevated plasma levels of alpha-fetoprotein. A prospective study was initiated in April, 1985 employing another 122 LC patients to clinically evaluate the significance of the high risk group of HCC. 28 cases with small HCC (less than 3 cm in diameter) were newly found: 4 with chronic hepatitis and 24 with LC, among whom 22 developed from the high risk group (sensitivity 92%, specificity 44%). Three year survival rate of 28 cases thus found was 56%, and causes of death of 9 fatal patients were 4 cancer death, 4 hepatic failure and 1 gastrointestinal bleeding. In conclusion, the high risk group is valuable for the screening of early liver cancers, and treatments of hepatic failure as well as of HCC itself are important to improve the prognosis of HCC patients thus diagnosed.
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PMID:[A high risk group of hepatocellular carcinoma in man, with special reference to its clinical significance for the screening of early liver cancer. Gifu Study Group for Early Liver Cancer]. 256 Apr 92


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