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 effect of 2-naphthylamine and cyclophosphamide on the urinary bladder and liver of female BALB/c mice was investigated. The bladder mucosa of mice treated with 2-naphthylamine alone for 40 weeks showed diffuse hyperplasia. Oral administration of 2-naphthylamine for 40 weeks plus injections of cyclophosphamide produced bladder carcinomas in 30.8 approximately 35.7% of all animals, associated with downward growth of the bladder epithelium. All the bladder carcinomas were of the transitional cell type and most of them contained pseudoglandular areas. Hepatomas seemed to develop in higher incidence in mice treated with 2-naphthylamine plus cyclophosphamide than in mice treated with 2-naphthylamine alone. Most of the hepatomas were solitary and showed a trabecular pattern. Cyclophosphamide seemed to have a summative or promoting effect on carcinogenesis of the bladder mucosa and liver induced by 2-naphthylamine in female BALB/c mice.
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PMID:Histopathological changes induced in the urinary bladder and liver of female BALB/c mice treated simultaneously with 2-naph-thylamine and cyclophosphamide. 52 Jul 55

Spin-lattice relaxation times (T1) for 31P were determined in normal and malignant tissues by a saturation technique employing a 90 degree -tau-90 degrees pulse sequence. Results for five normal tissues from rat were (in seconds): 2.33 +/- .14 for liver; 2.19 +/- .05 for muscle; 1.13 +/- .05 for brain; 1.43 +/- .15 fro kidney; and 1.97 +/- .12 for intestine. Results for two rat malignancies, Novikoff hepatoma and Walker sarcoma, were 5.98 +/- .57 and 5.38 +/- .68, respectively, and for Crocker sarcoma of mouse, 5.19 +/- 1.42. No individual measurement of malignant tissue overlapped any of the normal measurements; probabilities of insignificance ranged from .029 for Crocker sarcoma to .000184 for Novikoff hepatoma. The data call attention to another nucleus of potential value for NMR detection of internal malignancies in humans. Also suggested, because of the strategic placement of the 31P nucleus in the nucleic acid molecule, is a possible new probe for exploring the mechanism of carcinogenesis.
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PMID:NMR in cancer: VIII. Phosphorus-31 as a nuclear probe for malignant tumors. 61 35

Orthoaminoazotoluol was administered to mice for a period of 9 months. The duration of the G2-and S-periods of the mitotic cycle determined by the autoradiographic method, and mitotic duration--by the stathmokinetics technique with the use of colchicine in the intact liver, the cells of the adenoma nodes, and primary hepatomas. The duration of the S-period of the intact hepatocytes and adenoma nodes proved to be equal (13.8 hours, respectively). As to the primary hepatoma cells--it decreased to 12.8 hours. The duration of the G2-period showed no essential change during the carcinogenesis, and was equal to 2.2--2.7 hours. An average mitotic duration in the course of 24 hours was also constant and was approximately equal to 1 hour. A rise in the number of mitoses and PNA-synthesizing cells in the hepatomas occurred as a result of entering in mitosis and the S-period of a greater number of cells, but not as a result to prolongation of the duration of the S-and M-periods of the mitotic cycle.
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PMID:[Duration of the mitotic cyle of mouse liver cells at different stages of carcinogenesis induced by ortho-aminoazotoluene]. 62 83

Livers of 6- to 7-week-old male C3H/He, CBA, A, and BALB/c mice were examined by electron microscopy for the presence of intracisternal A particles (ICAP) after administration of diethylnitrosamine (DEN) in drinking water. In control mice, ICAP were extremely rare; they were found in the livers of only 2 mice (strains C3H/He and A; none in the other strains). By contrast, the treatment of mice with DEN greatly enhanced the appearance of ICAP in the liver cells of all strains. Within 2 weeks of the treatment, ICAP were found in 8-26% of liver cells examined in all mice and the number of ICAP/cell ranged from 3 to 12. Aside from mild disorganization of the rough endoplasmic reticulum, such as segmentation and vesiculation, liver cells of carcinogen-treated mice showed none of the consistent abnormalities that characterize the appearance of ICAP. The reactivation of ICAP (which are usually suppressed in adult mice) by DEN may become a useful marker for analysis of the sequential alterations of the liver that lead to the development of hepatoma during carcinogenesis.
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PMID:Activation of intracisternal A particles in mouse liver by diethylnitrosamine. 84 86

The composition of total fatty acids in serially transplanted mammary adenocarcinomas of C3H mice which were fed a fat free diet or a stock diet containing 4% fat for 8 weeks were significantly different, although fatty acid amounts were similar. The difference in composition was manifested in the triglyceride, phosphatidyl choline, and phosphatidyl enthanolamine fractions. Tumors of mice fed fat free diet has appreciable amounts of eicosatrienoic acid, whereas neoplasms of stock diet fed animals had none. In addition, higher levels of oleic acid and lower contents of linoleic acid were found in tumors from mice fed fat free diet than in those from mice fed the stock diet. Thus, mechanisms which maintained the triglyceride fatty acid composition in some tumors, such as 7288CTC hepatoma, were not observed in mouse mammary adenocarcinomas, and, therefore, were not a general phenomena associated with carcinogenesis.
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PMID:Dietary alteration of fatty acid composition of lipid classes in mouse mammary adenocarcinoma. 118 51

Trichloroethylene (TCE), a structural analog of vinyl chloride, is known to induce hepatocellular carcinoma and other tumors in C57BL/6 X C3H/He F1 (hereafter known as B6C3F1) hybrid mice. TCE epoxide, a possible metabolite, is expected to be highly reactive toward cellular nucleophiles, e.g., proteins and nucleic acids. Hence, the microsomal metabolism of TCE and its covalent binding to microsomal protein were examined. Rat liver microsomes were incubated in vitro with [14C]TCE. The results showed that TCE binds covalently to microsomal protein since extensive organic extractions and Pronase digestion do not dissociate the TCE-protein complex. The binding was decreased by 7,8-benzoflavone, blocked by SKF-525A, and enhanced by i.p. administration of phenobarbital. The possibility that TCE epoxide, once formed, could be converted to water-soluble products through enzymatic hydrolysis by epoxide hydrase was also investigated. Addition of 3,3,3-trichloropropene oxide, a potent inhibitor of epoxide hydrase, to the incubation system markedly enhanced the binding of TCE. These observations support the view that, in order to bind to protein, it is necessary for TCE to be metabolized to its epoxide, a reactive intermediate that is most likely involved in TCE carcinogenesis and toxicity.
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PMID:Covalent interaction of metabolites of the carcinogen trichloroethylene in rat hepatic microsomes. 127 48

We have demonstrated that rat liver contains at least four types of sialidase differing in subcellular location, in catalytic property and immunologically. They are intralysosomal, cytosolic and membrane-associated sialidases I and II. Membrane sialidase I locates mainly in plasma membrane and sialidase II in lysosomal membrane. Immunological study reveals that the same types of sialidase exist in various tissues of rat and of other mammalian species. Based on these results, we examined the sialidases in rat hepatomas and in transformed cells of JB6 mouse epidermal cell. Hepatomas were found to possess four types of sialidase and the three of them altered quantitatively. Intralysosomal sialidase activity was higher but cytosolic and lysosomal membrane sialidase activities were lower in hepatomas than in control liver. When the sialidases of transformants of JB6 cells were compared with those of control cells, the activities of two lysosomal sialidases were decreased and contrarily plasma membrane sialidase was increased. We discussed a possible significance of the sialidase alterations in carcinogenesis.
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PMID:Multiple forms of mammalian sialidase: altered expression in carcinogenesis. 130 7

Short-term cultures of three primary hepatocellular carcinomas were cytogenetically analyzed. Case 1 displayed a normal karyotype. Case 2 had, in addition to cells with a normal male chromosome complement, a clone with -Y. In case 3, two abnormal clones were found, one with -Y and one with a highly aberrant karyotype: [formula: see text] Our results, collated with the findings in one previously published primary hepatocellular carcinoma and in three cell lines, suggest that structural changes of chromosomes 1 and 6, leading to loss of 1p and 6q material, and loss of chromosome 16 are frequent events in hepatocellular carcinogenesis.
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PMID:Cytogenetic findings in three primary hepatocellular carcinomas. 131 94

Liver-cell dysplasia is a well known histological entity with preneoplastic significance in experimental hepatic carcinogenesis. However, while the association of liver-cell dysplasia with hepatitis B virus can be considered as established, it is still controversial whether this lesion represents a premalignant condition in cirrhotic patients. Efforts have been made to render its morphological assessment more reliable, but no firm conclusions can be drawn from the available clinical studies, which are mainly retrospective or based on autopsy series. Preliminary results from a prospective study argue that liver-cell dysplasia is associated with an increased risk to hepatocellular carcinoma. The emergence of liver-cell dysplasia as a preneoplastic lesion in cirrhotic patients will have some impact in the future on their management, including selection for closer monitoring in early detection of hepatocellular carcinoma and for liver transplantation.
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PMID:Liver-cell dysplasia and hepatocellular carcinoma. 131 75

This study was undertaken to investigate the relationship between morphometrical characteristics of noncancerous liver tissues and clinicopathological features of hepatocellular carcinoma (HCC) in 89 cases which underwent either hepatectomy (n = 56) or autopsy (n = 33). Using Automatic Image Analyzer (IBAS-2), we determined interstitial ratio (IR) of the non-cancerous liver tissues as a morphological parameter in all cases. In addition, mean values of area (MA), maximal diameter, and shape factor of pseudolobules were determined in the cirrhotic patients. IR in cases with main tumors smaller than 3 cm was higher than that in cases with tumors larger than 3 cm (23.5 +/- 6.7% vs 18.5 +/- 8.9% mean +/- SD: p less than 0.01), and IR in cases with histologically proven intrahepatic metastases (im positive) was also higher as compared to im negative cases (17.5 +/- 9.0% vs 21.3 +/- 8.0%; p less than 0.05). Among the other parameters determined in the cirrhotics, MA was higher in cases with tumors larger than 3 cm than in cases with smaller tumors (2.54 +/- 1.87 mm2 vs 1.78 +/- 1.01 mm2; p less than 0.05), and MA was higher in im positive cases as compared to im negatives (2.67 +/- 1.91 mm2 vs 1.67 +/- 0.96 mm2; p less than 0.01). These data indicated that non-cancerous liver tissue has a close relation not only to the carcinogenesis but to subsequent tumor growth and progression of HCC.
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PMID:[Morphometrical analysis of non-cancerous liver tissue with special reference to clinicopathological features of hepatocellular carcinoma]. 131 43


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