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 medical records of 18 dogs that had hepatic disease and received phenobarbital as an anticonvulsant for 5 to 82 months were reviewed. Clinical signs included sedation and ataxia in all dogs, 5 dogs were also anorectic, 2 had coagulopathy, 3 were icteric, and 5 had ascites. Serum biochemical analysis revealed serum albumin concentration less than or equal to 2.2. g/dl in 12 dogs, serum alkaline phosphatase activity greater than or equal to 169 U/L in 18 dogs, serum alanine transaminase activity greater than or equal to 57 U/L in 15 dogs, and total bilirubin concentration greater than or equal to 1 mg/dl (in the absence of lipemia) in 7 dogs. Serum phenobarbital concentration was greater than or equal to 40 micrograms/ml in 12 of 17 dogs. Sulfobromophthalein excretion was prolonged in 8 of 10 dogs. Preprandial serum bile acid concentrations were high in 8 of 10 dogs, and 2-hour postprandial serum bile acid concentrations were high in 9 of 10 dogs. Two of 4 dogs tested had resting plasma ammonia concentrations greater than 200 mg/dl. An ammonia tolerance test was performed on 2 other dogs; both had ammonia concentration greater than or equal to 200 mg/dl in the plasma 30 minutes after receiving 100 mg of ammonium chloride/kg of body weight, PO. Nine dogs died, 1 was euthanatized, and necropsies were performed on these 10 dogs. Biopsies and necropsies of 6 dogs revealed chronic hepatic fibrosis with nodular regeneration (cirrhosis). One dog had hepatocellular carcinoma and mild cirrhosis. In 1 dog, after phenobarbital had been withheld, necropsy revealed complete recovery of the previously observed lesions.
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PMID:Hepatotoxicity of phenobarbital in dogs: 18 cases (1985-1989). 174 13

We evaluated a method for quantifying bone isoenzyme of alkaline phosphatase (ALP) which utilizes wheat-germ lectin to precipitate this fraction. In precision studies, CVs ranged from 3.2 to 11.4% (within-day) and from 3.7 to 11.5% (day-to-day). The assay procedure was linear to 1100 U/L and was easily adapted to automated kinetic measurement. Comparison of the precipitation method with an affinity electrophoretic method, which utilizes cellulose acetate as a support, demonstrated a satisfactory coefficient of correlation (r = 0.886). The reference range was determined in sera from 188 healthy adult subjects. The distribution of bone ALP values was also studied in 73 healthy children and in 30 healthy adolescents. To evaluate the clinical applicability of the method, the bone isoenzyme was determined in samples from several groups of subjects (pregnant women, patients with hepatobiliary diseases, patients with hepatocellular carcinoma without skeletal involvement, and patients with bone, liver or lymph node metastases). We found the method suitable for routine determination of bone alkaline phosphatase and for the screening of bone metastases. Because of its technical simplicity and satisfactory analytical performance, it can be used instead of the heat-inactivation procedure.
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PMID:Precipitation method for separating and quantifying bone and liver alkaline phosphatase isoenzymes. 176 Aug 80

We applied Southwestern and Western blotting and gel retardation techniques to investigate the changes that occur in the cyclic adenosine monophosphate (cAMP)-responsive element (CRE) binding (CREB) proteins in rapidly growing, chemically induced 5123tc and 5123D Morris hepatomas. Using the CRE sequences from the c-fos, E2A, and somatostatin gene promoters, we identified in the nuclear proteins from normal unstimulated or proliferating rat liver cells six different protein factors of Mr 34,000, 36,000, 40,000, 47,000, 56,000, and 72,000 capable of binding to the element. The Mr 47,000 protein had the highest specificity for the core CRE, suggesting its importance in cAMP-mediated gene expression. We could not find the Mr 47,000 CREB protein in the 5123tc and 5123D hepatomas. Our efforts to detect this protein in the tumors by (a) using the CRE sequence from different gene promoters, (b) altering the protocol for extracting nuclear proteins, or (c) attempting to restore its DNA-binding property by phosphorylation [with endogenous protein kinase(s), a catalytic subunit of cAMP-dependent protein kinase, and protein kinase C/dephosphorylation (with alkaline phosphatase)] were unsuccessful. The loss of tje Mr 47,000 CREB protein from solid tumors of the Morris hepatoma is likely to be related to the neoplastic properties of the tumor cell rather than to cell growth because the level of this protein remained unchanged during a 6-day period of liver regeneration. The nuclear extract from the Morris hepatoma that did not have the Mr 47,000 CRE-binding factor contained proteins immunologically related to the CREB, c-Jun, and c-Fos proteins. We conclude that the Mr 47,000 factor represents a distinct member of the CRE-binding protein family and that its absence from the hepatomas may lead to aberrant expression of cAMP-inducible genes.
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PMID:Changes in cyclic adenosine monophosphate-responsive element binding proteins in rat hepatomas. 182 83

The serum response element (SRE) is essential for serum and growth factor stimulation of the c-fos gene. We have examined the nuclear proteins, obtained from tissues with elevated expression of the c-fos gene (proliferating rat liver and hepatocarcinoma), that bind to the SRE sequence. A synthetic oligonucleotide containing the SRE sequence from the mouse c-fos gene promoter (-299 to -322) was radioactively labeled, used as a probe for the mobility shift assay and Southwestern (DNA-protein) blotting, and also used for sequence-specific affinity chromatography. We have identified a group of nuclear proteins of molecular sizes 36, 45, 62, 67, 72, and 112 kDa capable of interacting with the SRE sequence. The 36-, 67-, and 112-kDa proteins have DNA-binding properties, but the presence of the others in the SRE-protein complex could be the result of protein-protein interaction. All of these protein factors were present in nuclei obtained from intact and proliferating rat liver as well as from 5123tc Morris hepatoma. The DNA-binding activity (on Southwestern blots) of the 67- and 112-kDa proteins was not affected by alkaline phosphatase treatment, but the ability of the dephosphorylated nuclear proteins to form the complex with the SRE sequence under gel shift assay conditions was severely impaired. The same alkaline phosphatase treatment completely abolished the DNA-binding properties of the c-fos cyclic AMP-responsive element-specific proteins. Therefore, transcriptional activation of the c-fos gene at the SRE must require the presence of a multiprotein complex the formation of which is governed by phosphorylation. The binding of the 67- and 62-kDa proteins to the c-fos SRE has been previously reported; however, the 36-. 45-, 72-, and 112-kDa proteins are novel factors involved in the multifaceted regulation of c-fos gene expression in vivo.
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PMID:Identification of a multiprotein complex interacting with the c-fos serum response element. 190 46

From 1968-1985 a series of thirty-seven patients with primary hepatocellular carcinoma was collected from the tumor registry of the Fairfax County Hospital, in the metropolitan Washington, D.C. area. These patients were found to have a mean age at diagnosis of sixty-two (males) to sixty-six (females). Thirty per cent of patients were previously cirrhotic and nineteen per cent had a history of viral hepatitis. There were no patients with documented birth control pill or steroid use. The most common presenting symptoms were anorexia and right upper quadrant pain. Liver-spleen scan was the most commonly used diagnostic study, but by the 1980's CT scanning was usually diagnostic. Both alkaline phosphatase and serum glutamyloxalotransferase were reliably elevated in twenty-six of twenty-eight and twenty-one of twenty-four patients respectively. Forty-eight per cent of patients with tumor histology reported had multicentric tumors, thirty-eight per cent had nodular tumors, and fourteen per cent had diffuse disease. Survival was as dismal in this as in other studies with a mean of seventy-nine days. No significant difference was noted between cirrhotic and non-cirrhotic patients. Chemotherapy and radiation therapy did not significantly impact upon survival. Finally, a cohort analysis was done and a possibly significant peak in incidence of primary hepatocellular carcinoma was seen in men born from about 1911 through 1920. The authors noted that these males were in the group of draft eligible persons for World War II and questioned a link between veteran status and later development of HCC.
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PMID:Primary hepatocellular carcinoma: hospital based epidemiologic study. 196 92

The hepatoma-specific band of serum gamma-glutamyl transferase II (GGT II) and other three markers were evaluated in 77 patients with primary hepatocellular carcinoma (PHC). The positive rate of GGT II (87%) was much higher than that of the increased alpha-fetoprotein (AFP greater than or equal to 400 ng/ml, 54.5%), the increased alpha-1-antitrypsin (AAT greater than or equal to 400 mg/dl, 64.9%) and alkaline phosphatase isoenzyme I (ALP I, 13.0%). In patients with AFP less than 400 ng/ml, the positive rate of GGT II was 95.2%, higher than that of ALP I (22.8%) and AAT (60.0%). The positive rate of GGT II was positively correlated to the volume of PHC (r = 0.324, P less than 0.05), but even in patients with small PHC (less than or equal to 65 cm3), the positive rate of GGT II (78.6%) was higher than that of AFP (50.0%) and AAT (28.6%). The ALP I positivity was only seen in patients with larger PHC. Follow-up study showed that GGT II, like AFP, might occur before liver tumor could be detected by B-mode ultrasonography and computerized tomography. Therefore, GGT II is a valuable marker of PHC, especially in patients whose AFP was negative or slightly increased; GGT II may be useful for relatively early diagnosis of PHC.
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PMID:Reappraisal of diagnostic significance of a hepatoma-specific band of serum gamma-glutamyl transferase. 197 81

Hepatoma is a rare disease in Natal Indians. It occurs in male patients in the fifth decade. They have no history of alcohol intake. The main presenting feature is abdominal pain, weight loss and hepatomegaly. Blood tests reveal a raised alkaline phosphatase, hypoalbuminaemia, hypergammaglobulinaemia and markedly raised gamma glutamyl transferase. The tumour is a single large expanding mass in the right lobe. The patient usually presents in a late stage of the illness and shows a progressive downhill course. Hepatitis B virus infection is emerging as the likeliest carcinogen.
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PMID:Hepatocellular carcinoma in South African Indians resident in Natal. 198

We have detected the in situ activities of DNA glycosylase, endonuclease, exonuclease, DNA polymerase, and DNA ligase using a novel polyacrylamide activity gel electrophoresis procedure. DNA metabolizing enzymes were resolved through either native or SDS-polyacrylamide gels containing defined 32P-labeled oligonucleotides annealed to M13 DNA. After electrophoresis, these enzymes catalyzed in situ reactions and their [32P]DNA products were resolved from the gel by a second dimension of electrophoresis through a denaturing DNA sequencing gel. Detection of modified (degraded or elongated) oligonucleotide chains was used to locate various enzyme activities. The catalytic and physical properties of Novikoff hepatoma DNA polymerase beta were found to be similar under both in vitro and in situ conditions. With 3'-terminally matched and mismatched [32P]DNA substrates in the same activity gel, DNA polymerase and/or 3' to 5' exonuclease activities of Escherichia coli DNA polymerase I (large fragment), DNA polymerase III (holoenzyme), and exonuclease III were detected and characterized. In addition, use of matched and mismatched DNA primers permitted the uncoupling of mismatch excision and chain extension steps. Activities first detected in nondenaturing activity gels as either multifunctional or multimeric enzymes were also identified in denaturing activity gels, and assignment of activities to specific polypeptides suggested subunit composition. Furthermore, DNA substrates cast within polyacrylamide gels were successfully modified by the exogenous enzymes polynucleotide kinase and alkaline phosphatase before and after in situ detection of E. coli DNA ligase activity, respectively. Several restriction endonucleases and the tripeptide (Lys-Trp-Lys), which acts as an apurinic/apyrimidinic endonuclease, were able to diffuse into gels and modify DNA. This ability to create intermediate substrates within activity gels could prove extremely useful in delineating the steps of DNA replication and repair pathways.
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PMID:Characterization of DNA metabolizing enzymes in situ following polyacrylamide gel electrophoresis. 200 53

In conclusion, we report the cases of two patients with large hemangiomas of the liver, abdominal pain, increased ESR and fibrinogen, increased serum alkaline phosphatase and gamma-glutamyltransferase activity, and normal white blood cell counts. Clinical and biochemical abnormalities disappeared after surgical resection. Increased ESR and fibrinogen are probably related to thrombosis within the tumor. This mode of presentation may suggest a diagnosis of hepatocellular carcinoma.
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PMID:Giant hemangioma of the liver with pain, fever, and abnormal liver tests. Report of two cases. 200 71

A perspective on serum alkaline phosphatase isoenzymes in liver disease is provided with a brief discussion of the location of the enzyme in liver and its presumed function. Mechanisms of entry of alkaline phosphatase into serum in liver disease are discussed. Characterization of high molecular weight alkaline phosphatase in obstructive jaundice is reviewed. The relationship between blood group O and the appearance of the intestinal enzyme in sera of such subjects with cirrhosis of liver is discussed. Properties of hepatoma alkaline phosphatase and the genesis of liver alkaline phosphatase in diseases not related to the liver are explored. Methods for detection of serum alkaline phosphatase isoenzymes in liver disease are discussed from the standpoint of the limitations of electrophoretic procedures, and the promise of procedures such as isoelectric focusing and high performance liquid chromatography that are currently non-routine.
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PMID:Serum alkaline phosphatase isoenzymes as markers of liver disease. 201 75


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