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)

Chromosomal proteins from rat liver have been assessed immunologically for changes in specific cytokeratins or primary tumor nonhistone proteins during treatment with an azo dye hepatocarcinogen (3'-methyl-4-dimethylaminoazobenzene), (3'-Me-DAB) or the hepatotoxin alpha-naphthyl-iso-thiocyanate (alpha-NIT). Fisher rats were fed laboratory diets supplemented with either agent and sacrificed sequentially at various intervals. Chromosomal proteins from these livers were electrophoresed in the presence of sodium dodecyl sulfate, transferred to nitrocellulose sheets and reacted with rabbit antisera to Novikoff hepatoma cytokeratin or 3'-Me-DAB induced primary hepatoma dehistonized chromatin. Livers from carcinogen-fed animals exhibited distinct, sequential changes in antigenic nonhistone proteins until the immunological specificity characteristic of the hepatoma was achieved concomitant with the induction of neoplasia. No antigenic changes were observed to occur in hepatotoxin-fed animals. The rat carcinoma-specific cytokeratin antigens p39 and p49 in Novikoff hepatoma were observed to appear as early as three weeks after the start of carcinogen feeding and were present maximally in 23 week livers with in situ carcinoma. These cytokeratins were not detected in alpha-NIT-fed animals. Our results support the concept that the carcinogenic process can be related to temporal changes in the expression of cell-specific cytokeratins in addition to nonhistone chromosomal proteins. Furthermore, these data suggest the expression of these antigenic species to not be the direct result of changes in liver structure and cellular composition associated with carcinogen toxicity; rather, neoplastic transformation is apparently required.
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PMID:Cytokeratin and nonhistone protein antigenic changes in rat liver during azo dye but not hepatotoxin feeding. 619 May 86

Immunization of rats with a purified mouse alpha-fetoprotein (AFP) suspended in Freund's complete adjuvant resulted in the production of antibodies that could precipitate both mouse and rat AFPs. A group of rats was immunized first and then fed a diet containing 0.06% 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) for 10 weeks. In these rats the elevation of serum AFP as well as the development of hepatoma were markedly inhibited. Another group of rats was immunized after feeding the diet containing 3'-Me-DAB for 10 weeks. The development of hepatoma and production of serum AFP were also suppressed. In both groups the life span of the rats was prolonged by the immunization.
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PMID:The effect of active immunization of rats with heterologous alpha-fetoprotein upon hepatocarcinogenesis induced by 3'-methyl-4-dimethylaminoazobenzene. 619 Jun 97

AFP-positive cells during 3'-Me-DAB hepatocarcinogenesis and in hepatomas induced by 3'-Me-DAB were observed by the light microscope immunoperoxidase method, and the location of AFP-immunoreaction products in hepatocytes was determined by the electron microscope immunoperoxidase method. Simultaneously serum concentrations of AFP were measured by radioimmunoassay. Serum concentrations of AFP during hepatocarcinogenesis showed a biphasic pattern, and proliferation of cholangiolar cells in the periportal areas was associated with the first peak of serum AFP in the early stage of hepatocarcinogenesis. AFP-containing cells in the late stage were distributed in clusters in the peripheral areas of hyperplastic nodules. The clusters were composed of two different types of AFP-positive cells, one atypical in shape and structure and the other preserving the structure of hepatic cords. In neoplasms, a heterogeneous AFP immunoreaction was recognized in hepatoma cells. In non-neoplastic nodules, cholangiofibrosis surrounded by AFP-positive cholangiolar cells developed. Ultrastructural immunoperoxidase studies revealed immunoreaction products of AFP on the membrane of r-ER, outer nuclear membrane, s-ER and Golgi complex in hepatocytes of hyperplastic nodules as well as of hepatocellular carcinoma cells. It is suggested that cholangiolar cells detected in hepatocarcinogenesis may form proliferating bile ductules, and the appearance of a cluster in association with AFP in hyperplastic nodules supports the hypothesis that some hyperplastic nodules with clusters of AFP-positive cells are important cell populations which may develop into hepatocellular carcinoma.
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PMID:Immunocytochemical investigation of alpha-fetoprotein-positive cells in hepatocarcinogenesis and hepatomas induced by 3'-ME-DAB. 619 42

Fumaric acid (FA) was examined for its effect on hepatocarcinogenesis in rats fed 3-methyl-4'-(dimethylamino)azobenzene (3-Me-DAB). Male DONRYU rats were given approximately 0.5 g 3-Me-DAB by being fed a diet containing 0.06% 3-Me-DAB for 50 days; they were then given a diet containing 1% FA and drinking water containing 0.025% FA for 51 weeks. The administration of FA effectively suppressed the development of hepatocellular carcinoma, hyperplastic nodules, and hyperplastic areas in the livers of rats fed 3-Me-DAB.
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PMID:Inhibitory effect of fumaric acid on 3-methyl-4'-(dimethylamino)-azobenzene-induced hepatocarcinogenesis in rats. 641 45

The effect of zinc on the growth of a transplantable DAB hepatoma in young male Wistar rats was determined. Both a zinc deficiency (less than 0.5 microgram/g feed) as well as high levels of dietary zinc (500 micrograms/g feed) significantly reduced tumor growth. Both high- and low-zinc diets resulted in reduced activity of the salvage pathway of thymidine synthesis as well as reduced 32PO4 incorporation into DNA and diminished DNA polymerase activity. Blockage of the de novo pathway of DNA synthesis by the folate antagonist methotrexate (MTX) resulted in greatly increased flux through the thymidine salvage pathway and increased DNA polymerase activity but decreased 32PO4 incorporation in the transplantable hepatomas in Wistar rats fed normal zinc diets (50 micrograms/g feed). MTX had the effect of reducing all these activities in the groups fed low- and high-zinc diets. These data suggested a site of action of zinc associated with the salvage pathway of thymidine synthesis.
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PMID:Possible site of zinc control of hepatoma cell division in Wistar rats. 657 40

Expressions of the c-Ha-ras and c-myc genes were studied by Northern blotting of total RNA from primary tumors and non-tumorous parts of the liver of rats given diet containing 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) and from established rat hepatoma cell lines. The expression of the c-Ha-ras gene was found to be high in the primary tumors, non-tumorous parts of 3'-Me-DAB-treated livers and hepatoma cell lines. In contrast, the c-myc gene was expressed at a high level only in primary tumors and hepatoma cell lines. During 3'-Me-DAB treatment, the c-Ha-ras mRNA level in the liver increased by day 5 and then remained high. Increase in expression of the c-Ha-ras gene in regenerating liver was confirmed. These findings suggest that increase in expression of the c-Ha-ras gene is related to proliferation of hepatocytes, whereas expression of the c-myc gene is associated with hepatocarcinogenesis.
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PMID:Expressions of the c-Ha-ras and c-myc genes in rat liver tumors. 671 68

The reaction of indirect inhibition of peritoneal cell adherence to glass was used for a comparative study of the reactivity of lymph node cells of mice injected with the hepatocarcinogen DAB (4-dimethylaminoazobenzene) or with its non-carcinogenic analogue DEAB (4-diethylaminozobenzene, or with hepatoma 22a cells. The ability of regional lymph node cells to sensibilization towards normal cellular antigens decreased following the DAB treatment stronger and for a longer time period than that DEAB treatment. To the contrary, the growth or hepatoma 22a was accompanied by an appreciable sensibilization of cells of the regional lymph nodes. The results obtained are discussed in context of of the problem of immune surveillance of cytodifferentiation.
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PMID:[Effect of carcinogenic exposure and tumor growth on the sensitization of C3HA mouse lymphoid cells to normal cell antigens]. 678 63

Male Sprague-Dawley rats were fed a cube diet containing 2.51 mmol/kg of 3'-methyl-4-(dimethylamino)azobenzene (3'-Me-DAB), 3'-CH2OH-DAB, 3'-CHO-DAB, or 3'-COOH-DAB (at a level equivalent to 0.06% 3'-Me-DAB in the diet) for a period of 1 to 3 months. Almost all the livers of rats given 3'-CH2OH-DAB for a period of 2 to 3 months or 3'-Me-DAB for 3 months showed marked cirrhosis macroscopically. The common histological findings were cholangiofibrosis with or without markedly atypical bile ducts. Moreover, one hepatocellular carcinoma was found in the liver of a rat given 3'-Me-DAB and one in the liver of a rat given 3'-CH2OH-DAB for 3 months. On the other hand, 3'CHO-DAB and 3'-COOH-DAB did not induce these changes (including neoplastic nodules) at all. Consequently, 3'-CH2OH-DAB, like 3'-Me-DAB, was found to be a hepatocarcinogen.
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PMID:Tumorigenicity of 3'-hydroxymethyl, 3'-formyl, and 3'-carboxy derivatives of 4-(dimethylamino)azobenzene in rat liver. 679 85

Inoculation with a crude suspension prepared from autologous liver cell carcinoma inhibited the development of liver tumor in cirrhotic rats exposed to 3'-methyl-4-diethylaminoazobenzene (3'-Me-DAB). The suspension had also an inhibitory effect on the growth of tumor in rats bearing liver cell carcinoma. The results obtained suggest that a close relationship exists between tumor-associated antigens and onco-development.
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PMID:Inhibitory effects of autologous hepatic tumor suspension on the development of liver cell carcinoma in rats. 687 97

DNA-RNA hybridization studies, using nuclear RNA's (nRNA's) labeled in vivo and in vitro with high specific radioactivities, were performed to compare the nRNA populations of normal rat liver, livers treated with 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB), and 3'-Me-DAB-induced hepatomas. The study with normal liver nRNA labeled by i.p. injection of [3H]orotic acid indicated that the nuclei of a 3'-Me-DAB-induced transplanted hepatoma, AH136B, lacked some RNA species present in normal liver nuclei. No qualitative difference in thee RNA populations was seen between normal liver and the livers of rats fed a carcinogenic amount of 3'-Me-DAB, either alone or in combination with 4-nitrostilbene which enhanced the azo dye carcinogenesis. Then, nRNA's of both normal liver and AH136B hepatoma were labeled in vitro by phosphorylation with polynucleotide kinase and adenosine 5'-[gamma-32P]triphosphate. The competitive hybridization with 32P-labeled normal liver nRNA was competed, and the deletion of RNA in the nuclei of AH136B hepatoma or 3'-Me-DAB-induced primary hepatoma was estimated to be 15% or more in the measure of radioactivity of the hybridized normal liver nRNA. 32P-labeled AH136B hepatoma nRNA was completed completely by liver nRNA's, suggesting that no unique RNA species were present in the hepatoma nuclei.
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PMID:Analysis of loss of nuclear RNA in azo dye-induced hepatoma by DNA-RNA competitive hybridization. 705 6


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