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)

DNA was isolated from livers of the rats treated with DAB during various steps of hepatoma development. After histological examination the tumor tissue was separated from the normal liver tissue and used as the source of DNA. Chromatographic fractionation on DEAE and Ecteola celluloses shows characteristic patterns for DNA isolated at various steps of hepatoma development. The largest differences in hepatoma DNA as compared to normal liver DNA were demonstrated in the DNA fraction eluated with 2.0 M-NaCl and NH3, gradient 0.1--1.0 M (m. w. 2--9 x 10(6)), and an increase in the first DNA fraction (m. w. less than 1 x 10(6)) was observed. Differences in the chromatographic patterns are discussed in terms of direct DAB action on DNA.
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PMID:Chromatographic pattern of DNA isolated from liver tissue during hepatoma development. 11 86

Samples of sediment and biota were collected from sites in the lower Fox River and southern Green Bay to determine existing or potential impacts of sediment-associated contaminants on different ecosystem components of this Great Lakes area of concern. Evaluation of benthos revealed a relatively depauperate community, particularly at the lower Fox River sites. Sediment pore water and bulk sediments from several lower Fox River sites were toxic to a number of test species including Pimephales promelas, Ceriodaphnia dubia, Hexagenia limbata, Selenastrum capricornutum, and Photobacterium phosphorum. An important component of the observed toxicity appeared to be due to ammonia. Evaluation of three bullhead (Ictalurus) species from the lower Fox River revealed an absence of preneoplastic or neoplastic liver lesions, and the Salmonella typhimurium bioassay indicated relatively little mutagenicity in sediment extracts. Apparent adverse reproductive effects were noted in two species of birds nesting along the lower Fox River and on a confined disposal facility for sediments near the mouth of the river, and there were measurable concentrations of potentially toxic 2,3,7,8-substituted polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), and planar polychlorinated biphenyls (PCBs) both in the birds and in sediments from several of the study sites. Based on toxic equivalency factors and the results of an in vitro bioassay with H4IIE rat hepatoma cells, it appeared that the majority of potential toxicity of the PCB/PCDF/PCDD mixture in biota from the lower Fox River/Green Bay system was due to the planar PCBs. The results of these studies are discussed in terms of an integrated assessment focused on providing data for remedial action planning.
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PMID:Integrated assessment of contaminated sediments in the lower Fox River and Green Bay, Wisconsin. 137 48

A number of plasticizers and lipid-lowering drugs induce peroxisomes and cause hepatocellular carcinoma in rodents by mechanisms which remain unknown. In this study, seven structurally dissimilar peroxisome proliferating agents were shown to uncouple oxidative phosphorylation in isolated rat liver mitochondria. For example, perfluorooctanoate (0.5 mM) increased succinate-induced (state 4) mitochondrial respiration by over 50% while stimulation of state 3 respiration with ADP was minimal (i.e., uncoupling occurred). Interestingly, compounds which are potent carcinogens in vivo (e.g., Wy-14,643 and perfluorooctanoate) were more powerful uncouplers of oxidative phosphorylation in vitro than weak tumor-causing agents (e.g., valproate). Uncoupling also occurred in vivo. Basal rates of oxygen uptake in perfused livers from chronically treated rats were increased from 137 +/- 7 mumol g-1/h in pair-fed controls to 153 +/- 5 mumol g-1/h after 2.5 months of feeding Wy-14,643 (0.1% w/v in diet). Concomitantly, rates of urea synthesis from ammonia, a process highly dependent on ATP supply, were reduced almost completely from 104 +/- 10 mumol g-1/h to 13 +/- 6 mumol g-1/h. Bile flow, another energy-dependent process, was also reduced significantly by treatment with Wy-14,643 in vivo for 24 h. Taken together, these data indicate that energy supply for cellular processes such as urea synthesis and bile flow was disrupted in vivo due to uncoupling of oxidative phosphorylation by Wy-14,643. It is proposed that peroxisomal proliferators accumulate in the liver where they uncouple mitochondrial oxidative phosphorylation and interfere with cellular energetics.
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PMID:Several nongenotoxic carcinogens uncouple mitochondrial oxidative phosphorylation. 139 Aug 25

Inoculation of Buffalo rats with Morris hepatoma produced significant anorexia within four weeks and reduced body weight within two weeks. Blood ammonia concentration was increased by 113% when the rats were euthanized, five days after the development of anorexia. Infusing ammonium salts into normal Buffalo rats also induced anorexia at a blood ammonia concentration comparable to that observed in the tumor-bearing rats. Although ammonia-infused rats exhibited expected increases in brain tyrosine, tryptophan, and metabolites of dopamine and serotonin, these alterations were attenuated in the tumor-bearing rats. These results indicate that hyperammonemia may be a general consequence of experimental cancer and that the increase in ammonia concentration may be of primary importance in the development of experimental cancer-induced anorexia. The rather small alterations in neurotransmitter metabolism in anorectic tumor-bearing rats deemphasize the role aberrations in DA and 5-HT systems in the development of experimental cancer anorexia.
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PMID:Hyperammonemia and anorexia in Morris hepatoma-bearing rats. 168 54

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

A 40-yr-old man presented with encephalopathy and was found to have hepatocellular carcinoma without cirrhosis. A large vascular hepatic mass was defined by CT scan and angiography; laparoscopy with biopsy confirmed the absence of chronic liver disease. A definitive tissue diagnosis of hepatocellular carcinoma was made at laparotomy; the tumor was unresectable. Peripheral arterial and selective portal and hepatic venous ammonia levels were high, and this finding suggested that the encephalopathy was nitrogenous and hepatic in origin. The proposed mechanisms of the encephalopathy are generation of ammonia from tumor breakdown and portosystemic shunting, a result of partial tumor occlusion of the hepatic veins. An unusually high urinary excretion of orotic acid was found similar to that seen in hereditary orotic aciduria.
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PMID:Hepatic encephalopathy and orotic aciduria associated with hepatocellular carcinoma in a noncirrhotic liver. 282 14

Dynamic positron emission tomography (PET) of the liver tumor was performed with a whole body multi slice PET device and 13N-ammonia. Sixteen patients with hepatocellular carcinoma (HCC) and seven patients with metastatic liver tumor were studied. In 12 of 16 patients with HCC, in which cases rich tumor vessels and dense tumor stain were proven by hepatic angiography, the tumors showed remarkable uptake of 13N-ammonia from the first scan, whereas the radionuclide accumulation was more gradual in the other part of the liver, and high tumor to liver ratio (T/L ratio) (2.62 +/- 1.09) was observed in the 1st scan, so that the tumor was clearly visualized by high contrast. However, HCC with poor blood supply from the hepatic artery or central necrosis of the tumor were demonstrated as low T/L ratio. In seven cases with metastatic liver tumor, the accumulation of 13N-ammonia was also lower than the normal liver throughout the scan. The results suggested that hepatic arterial blood flow of the liver tumors can be assessed with dynamic PET, which may provide valuable information for the characterization of tumors as well as for the evaluation of the treatment.
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PMID:Dynamic positron emission tomography with 13N-ammonia in liver tumors. 285 65

Yoshida AH-130 ascites hepatoma cells were grown in rats and were examined by quantitative electron microscopy 4 days (exponential growth phase) and 10 days (stationary phase) after intraperitoneal inoculation. No significant differences between growing and growth-inhibited tumors were found in the composition of the cytoplasm, except for a slight increase in the cytoplasm, except for a slight increase in the volume fraction of mitochondria (from 9.6 to 12.1%) and, in particular, a prominent (4.2-fold) increase in the volume fraction of early stage of autophagic vacuoles (from 0.31 x 10(-4) at day 4 to 1.37 x 10(-4) at day 10; P less than 0.001). At the same time, the rate of cell protein degradation was increased twofold, namely from 0.67%/h at day 4 to 1.37%/h at day 10, as measured in vitro after labeling cells with 3H-leucine in vivo. Such elevated proteolytic activity was entirely suppressed by ammonia, which inhibits the lysosomal pathway for protein degradation. The data show that: (i) the regulation of autophagic degradation of cytoplasmic constituents depending on the growth state was maintained in these tumor cells, and (ii) the increase in autophagy measured by morphometric analysis contributed to, yet did not quantitatively explain, the acceleration of protein degradation characterizing the transition from the logarithmic growth phase to the growth-inhibited state.
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PMID:Regulation of protein turnover versus growth state. III. Growth cessation is associated with activation of autophagy in Yoshida ascites hepatoma AH-340. 290 92

Dynamic PET using [13N]ammonia was performed in patients with primary hepatocellular carcinoma (hepatoma). All the tumors started to show remarkable accumulation of radioactivity from a very early period (within 150 sec after the radionuclide injection), whereas the radionuclide was more gradually accumulated in the liver. Central necroses of the tumors were visualized as low radioactivity areas. Daughter nodules of less than 2 cm were also visualized. This dynamic PET study is a valuable technique for the detection of the hepatoma.
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PMID:Imaging of the hepatocellular carcinoma using dynamic positron emission tomography with nitrogen-13 ammonia. 298 53

Cell protein turnover states as related to growth phase have been analyzed in a rat ascites hepatoma (Yoshida AH-130), which after transplantation entered a period of exponential growth, followed by a quasi-stationary state. Evaluation of AH-130 cell protein turnover in the animal (slow-turnover protein pool) was combined with rapid assays of proteolytic rates of cells transferred in vitro. Protein accumulation in the exponential phase reflected the balance between sustained synthetic rates and relatively low degradative rates. Cessation of growth resulted from convergent reduction of synthesis (from 3.10 to 1.49%/h) and enhancement of protein breakdown (from 0.61 to 1.43%/h). Endogenous proteolytic rates in vitro were very close to the above degradation rates. As shown by incubation with ammonia or other lysosomal inhibitors, the acidic vacuolar pathway for protein degradation, while totally suppressed in exponential tumor cells, was activated in cells from stationary tumors to such an extent that it fully accounted for the enhanced proteolysis. In contrast, energy metabolism inhibitors were effective on cells in either growth state, the residual ongoing proteolysis being similar in both cells. The possible contribution of cell death to activation of the acidic vacuolar proteolysis in stationary tumors is discussed.
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PMID:Regulation of protein turnover versus growth state: ascites hepatoma as a model for studies both in the animal and in vitro. 359 79


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