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 gamma-glutamyltransferase (EC 2.3.2.2) (=gamma-glutamyltranspeptidase, gamma-GTP) activity in hepatoma induced by 3'-methyl-4-(dimethylamino)azobenzene (3'-Me-DAB) was 120-fold higher than that of normal liver and high activity was also found in bovine hepatocellular carcinoma. gamma-GTPs from these malignant tissues responded more and showed broader specificity to gamma-glutamyl group acceptors than those from normal tissue such as bovine, rat, and mouse liver and bovine kidney. Three species of gamma-GTP were isolated from bovine kidney by DEAE-cellulose chromatography, whereas only two species were isolated from bovine hepatocellular carcinoma. The carcinoma lacked the least acidic enzyme species. Appropriate gamma-glutamyl group acceptors stimulated more-acidic enzyme species more than less-acidic species in both tissues. The fractions separated from the hepatoma were stimulated more than those of kidney by gamma-glutamyl group acceptor. The enzymes from normal tissues responded similarly to a gamma-glutamyl group acceptor irrespective of the difference in their activity. Thus, gamma-GTPs of malignant tissues appear to be more versatile for amino acid transport, both qualitatively and quantitatively. In these properties the enzyme of mouse fetal liver which showed the highest activity in the last period of pregnancy resembled the enzymes of malignant rather than normal tissues. The activity of hepatic gamma-GTP is not parallel with the rate of cell proliferation during normal development.
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PMID:Higher transpeptidation activity and broad acceptor specificity of gamma-glutamyltransferases of tumors. 0 27

In the hepatoma cells, AFP synthesis was found to occur through ribosomes of the rough endoplasmic reticulum, since AFP was demonstrated around ribosomes of the rough endoplasmic reticulum by the peroxidase antibody technique. The secretory process was suggested to be as follows: smooth endoplasmic reticulum takes a part and the Golgi apparatus does not. Concerning the early transitory appearance of AFP in the course of hepatocarcinogenesis by 3'Me-DAB, AFP might be produced by proliferated ampulla cells, which exist between the cholangioles and liver cell cords.
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PMID:Immunoelectronmicroscopic study of alpha-fetoprotein synthesis in hepatoma cells. 5 22

Localization of alpha-fetoprotein (alpha-FP) has been followed in hepatal tissue and tumors during induction of primary hepatomas with the aid of 0.12% 3'-Me-DAB (3'-methyl-4-dimethylammoazobenzene) in Wistar rats. The indirect immunofluorescence method was used for the localization of alpha-FP positive cells. During the course of carcinogenesis, alpha-FP in serum was detected by means of the crossing over immunoelectrophoresis. This study has yielded the following results: Alpha FP positive cells resembling small hepatocytes occurred dispersed and in groups beginning with the 5th week of a carcinogenic diet until the appearance of tumors. No alpha-FP positive oval cells have been found. Alpha-FP positive cells were always found in rats with alpha-FP positive serum, but they were rarely present in rats with alpha-FP negative serum. From the 10th week, tumors of the cholangiohepatoma type began to be formed in which variously scattered alpha-FP positive cells of the type of small hepatocytes were present, with the serum being negative. Between week 14 and 21 hepatoma nodules began to be formed. At week 21 frequent alpha-FP positive cells close to normal hepatocytes were observed both singly and in groups. These are considered to be the sites of developing tumor nodules. In all the hepatoma nodules, the number of positive tumorous cells and the intensity of fluorescence proved to be directly proportional to alpha-FP concentration in serum.
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PMID:Localization of alpha-fetoprotein by immunofluorescent method during induction of rat liver tumors by 3'-methyl-4-dimethylaminoazobenzene. 7 94

Hepatomas were induced by feeding rats laboratory chow containing 0,6375 g of 3'-methyl-4-dimethylaminoazobenzene per kg for 3 to 5 months. DAB-1 was a hepatoma induced in randomly bred Wistar rats and was transplanted for 3 years after which it failed to grow in vivo but not in vitro. DAB-2 and DAB-3 are new transplantable hepatoma lines established in highly inbred DBIX rats. DAB-3 has a metaplastic morphology showing, inter alia, goblet cells, cartilagenous areas, duct-like structures and glandular follicles. This is unlike DAB-1 and DAB-2 which showed poorly differentiated trabecular or anaplastic carcinomatous patterns.
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PMID:The induction and transplantation of hepatomas in Wistar and BD IX rats. 10 17

NADPH- and ascorbic acid-induced microsomal lipid peroxidation was almost absent in subcutaneously implanted DAB-induced hepatomas D23, D30 and D192A, and present at greatly reduced levels in DAB-induced primary hepatomas when compared with normal liver controls. Fatty acid analysis of the microsomal lipid from passaged tumours demonstrated adequate levels of substrate in the phospholipid fractions to support lipid peroxidation. Lipid extracted from hepatoma microsomal fractions was shown to undergo ascorbic acid-induced lipid peroxidation, but to a lesser extent that the corresponding liver extract. This may be partially explained by a decrease in the phospholipid content of hepatoma microsomal membranes. However, phospholipid extracted from microsomal fractions of hepatoma and liver supported lipid peroxidation to a similar extent. The possible role of the non-lipid component of the membrane in the process of lipid peroxidation is discussed.
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PMID:Lipid peroxidation of the microsomal fraction and extracted microsomal lipids from DAB-induced hepatomas. 10 13

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

A factor has been purified from rabbit liver which decreases the incorporation of 3H-thymidine in DNA of regenerating rat liver slices. This effect is due mostly to an inhibition of DNA synthesis from the deoxynucleoside triphosphates. The purified rabbit liver factor thus interferes with the liver cell division cycle. This inhibitor of DNA synthesis is specific for liver cells; it is not toxic for cultured hepatocytes and its action on DNA synthesis is reversible: at low dose, the inhibition of DNA synthesis in regenerating liver slices is transitory. The purified rabbit liver inhibitor is thus a chalone. The purified rabbit liver chalone ultrafiltrates through 1.2 nm pores, is destroyed by trypsine and pronase, carries a negative charge at pH 8.8 and a positive charge at pH 4.6; it is thermostable and likely a small peptide. It also inhibits RNA and protein synthesis in regenerating liver slices. The inhibition of protein synthesis is immediately maximal then decreases with time, while the maximum inhibition of DNA and RNA synthesis appears after a delay. When a low dose of chalone is used (0.2 unit per 5 ml), the inhibition of DNA and RNA synthesis disappears after some time: this is not due to a destruction of the chalone, but to a loss of sensitivity of the slices incubated in Hanks solution. The inhibitor content of liver cells, normal or malignant, seems inversely correlated with their state of growth. It is much lower in the liver of a young animal or in regenerating liver than in adult liver. Hepatomas produced by feeding DAB contain three times less inhibitor than the normal liver. The purified liver chalone is 5-10 times less active on the incorporation of 3H-thymidine in DNA of DAB hepatoma slices than in DNA of regenerating liver slices. It has no apparent action on adult liver slices; this might be due to the fact that 3H-thymidine incorporation into DNA of the adult organ depends, for the greater part, on other processes than DNA replication in hepatocytes.
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PMID:The hepatic chalone. II. Chemical and biological properties of the rabbit liver chalone. 16 23

The location of binding sites for 3'-methyl-p-dimethylaminoazobenzene (3'-Me-DAB) or metabolites on components of rat liver cells and hepatoma cells in tumors induced by this carcinogen was determined at 2 stages during the induction of tumors in rats: (a) in normal liver immediately following the application of a massive dose of the azocarcinogen by intragastric feeding, and (b) in liver and tumor after hepatomas had developed following repeated exposures to the carcinogen by s.c. injections. Bound 3'-Me-DAB or metabolites were detected by the use of rabbit antisera directed against either p-azoazobenzene or p'-azo-p-dimethylaminoazobenzene in an indirect fluorescent antibody technique. Soon after massive intragastric doses of 3'-Me-DAB, the staining observed when the anti-p-azoazobenzene antiserum was used was principally on cytoplasmic components of liver cells with some staining of the intranuclear components. When the second antiserum, anti-p'-azo-p-dimethylaminoazobenzene antiserum, was used, the most intense fluorescent staining was on the nuclear membranes, although there was some cytoplasmic and intranuclear staining as well.
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PMID:Binding of the azocarcinogen 3'-methyl-p-dimethylaminoazobenzene to cellular components of normal rat liver and azocarcinogen-induced hepatomas. 17 35

Aldolase (ALD) consists of three different types of isozyme, i.e. muscle or A type, liver or B type and brain or C type, their relative proportions being fixed for each tissue. In this study, isozyme profiles in the serum and DAB induced hepatoma as it grows were examined in comparison with those in the fetal liver, in the hope to obtain information for early detection of the malady. In the very early phase of hepatoma growth with no elevated enzyme activity, ALD-A fraction after electrophoresis was found to increase. In the course of hepatoma growth, ALD-B decreased while ALD-A increased with appearance of hybrid of ALD-A and ALD-C. In the normal adult liver, no hybrid of ALD-A and ALD-C was encountered. Serum profile of the rat with DAB induced hepatoma was similar to that of the cancer tissue. On the other hand, the fetal liver shows a profile with high ALD-A fraction and even with hybrid of ALD-A and -C. These features disappeared gradually as maturation proceeded and became close to the adult pattern. Thus it is clear that DAB induced hepatoma exhibits retrogressive change in hepatic differentiation in its isozyme profile. The results also indicate usefulness of isozyme profile for early detection of the hepatoma.
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PMID:[Experimental study on aldolase isozyme during the development of hepatoma in the rat (author's transl)]. 17 23

The effects of dietary polychlorinated biphenyls (PCBs) on hepatocarcinogenesis in female rats of Donryu strain receiving 3'-methyl-4-dimethylaminoazobenzene (3'-Me-DAB) were investigated. Oral administration of PCBs after administration of 3'-Me-DAB resulted in a high incidence (64%) of hepatocarcinoma. In contrast, administration of a similar amount of PCBs before, or together with 3'-Me-DAB did not induce hepatic tumors. Administration of a slightly larger amount of PCBs alone did not induce liver tumors, while administration of a slightly larger amount of 3'-Me-DAB alone caused only a low incidence (13%) of hepatocarcinoma. These results strongly suggest that PCBs exert a potent promoting action in experimental azo dye hepatocarcinogenesis.
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PMID:Polychlorinated biphenyl(s) as a promotor in experimental hepatocarcinogenesis in rats. 18 20


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