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Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aflatoxin B1 content of liver tissue was measured in patients who died from chronic liver disease [hepatocellular carcinoma (HCG) (5), schistosomal liver fibrosis (1), chronic aggressive hepatitis (1)] and compared with fifteen controls who died of motor traffic accidents (10), drowning (1), malnutrition (1), idiopathic cardiomegaly (1) and lung infection (2). Significant levels of aflatoxin B1 were found in hepatocellular carcinoma patients who were also hepatitis B surface antigen (HBsAg) negative. Histology showed HCC arising in macronodular cirrhosis.
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PMID:Aflatoxin B1 in hepatocellular carcinoma. 625 85

Aflatoxin B1, B2, G1, G2 levels were determined in sera of 20 patients with primary liver cell carcinoma (CC). Values of B1 above 0.15 microgram/ml were obtained in sera of three patients. Hepatitis B surface antigen (HBsAg) was detected in only 35% of patients. 50-90% of serum levels were cleared in 24 h in three patients studied. Although it is inconclusive as to the carcinogenic potential of aflatoxins in adult man, foodstuffs should be protected from excessive aflatoxin contamination.
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PMID:Aflatoxins, B1, B2, G1, G2 in primary liver cell carcinoma. 628 48

The metabolism of chemical carcinogens by a human hepatoma cell line, huH-1, was studied. The huH-1 line has been derived from a hepatoma of a 57-year-old HBs-antigen carrier and cultivated for several years. The hepatoma cells metabolized about 90% of 5 microM benzo[a]pyrene into water-soluble products within 24 h. Aryl hydrocarbon hydroxylase activity in huH-1 cells was induced to 24 times higher than the basal level by treatment with 13 microM benz[a]anthracene for 24 h. Metabolic activation of benzo[a]pyrene, dimethylnitrosamine and aflatoxin B1 by huH-1 cells was observed by cell-mediated sister-chromatid exchange assay. Sister-chromatid exchanges in human diploid fibroblasts were observed in the cultures mixed with or without huH-1 cells. All 3 chemicals induced sister-chromatid exchanges in human fibroblasts far more efficiently in the cultures mixed with huH-1 cells than in those without huH-1 cells. Some characteristics of huH-1 cells as a human cell-mediated metabolic activation system for carcinogens are discussed.
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PMID:Metabolic activation of benzo[a]pyrene, aflatoxin B1, and dimethylnitrosamine by a human hepatoma cell line. 628 53

Two closely related hepatoma cell lines were examined for their response to carcinogens requiring metabolic activation: H5, a dedifferentiated line expressing cytochrome P-448-dependent monooxygenase(s); and HF1-4, a differentiated line which also expresses cytochrome P-450-dependent monooxygenase(s). The hepatocarcinogens dimethyl- and diethylnitrosamine and aflatoxin B1, preferred substrates for cytochrome P-450-dependent monooxygenase(s), and the non-hepatocarcinogen benzo[a]pyrene, which is preferentially metabolized by cytochrome P-448-dependent monooxygenase forms, were used as test agents. Their effects were compared to those of the directly alkylating agents N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and N-ethyl-N-nitrosourea (ENU). The cytotoxicity was evaluated by plating efficiency, the genotoxicity by the appearance of alkaline labile DNA sites. The nitrosamines had a cytotoxic and genotoxic effect on the differentiated HF1-4 cells, but had no effect on H5 cells. Aflatoxin B1 affected both cell lines, but was approximately 10-times more potent in the HF1-4 than in the H5 cells. In contrast to the nitrosamines and the mycotoxin, benzo[a]-pyrene exerted a stronger effect on the dedifferentiated cell line. Pretreatment of cultures with dexamethasone increased both the cytotoxicity and genotoxicity of the hepatotoxic agents. MNNG and ENU induced a similar degree of DNA-damage after short-term (2 h) exposure in the two cell lines. When cells were allowed to recover for 16 h HF1-4 cells, but not H5 cells, regained their full growth potential suggesting a marked capacity for the repair of MNNG- and ENU-induced lesions in the HF1-4 cells. The results indicate that continuous lines of mammalian cells may retain a considerable degree of organ-specific response to chemical carcinogens. Hepatoma cells of the type described above may be useful for screening the wide spectrum of chemicals which are potentially genotoxic in liver and in extrahepatic tissues and for analyzing their metabolic activation and mechanism of action.
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PMID:Geno- and cytotoxicity of nitrosamines, aflatoxin B1, and benzo[a]-pyrene in continuous cultures of rat hepatoma cells. 629 36

2 human hepatoma cell lines (C-HC-4 and C-HC-20), in which aryl hydrocarbon hydroxylase activity was induced with benz[alpha]anthracene in vitro to about 140- and 64-fold of the respective basal levels, yielded an increased frequency of sister-chromatid exchanges (SCEs) when exposed to benzo[alpha]pyrene (BP), 7,12-dimethylbenz[alpha]anthracene and 3-methylcholanthrene in vitro. Analysis of the metabolism of BP by these cells by high-pressure liquid chromatography revealed that both cell lines produced various BP metabolites including the proximate form BP-7,8-dihydrodiol which has been reported to be the most potent inducer of SCEs among the metabolites of BP. In addition, aflatoxin B1 and cyclophosphamide also induced SCEs in these cell lines. The above findings suggest that these cells may be capable of metabolizing a range of indirect mutagens/carcinogens into DNA-active forms. These cells may therefore serve as a useful test system in vitro for the detection of genotoxic agents, without the use of an exogenous activating system.
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PMID:Sister-chromatid exchange induction by indirect mutagens/carcinogens, aryl hydrocarbon hydroxylase activity and benzo[alpha]pyrene metabolism in cultured human hepatoma cells. 630 Jun 68

Hepatomas were induced in rats with aflatoxin B1, and nephroblastomas with dimethylnitrosamine. Microscopic examination of livers of aflatoxin-treated rats revealed multinodular hepatocyte hyperplasia at 8 months, and by 13 months all rats had hepatomas. Nephroblastomas were observed by 4 months and by 8 months all rats had developed them. The urinary excretion of several modified nucleosides and bases by normal rats is dependent on body weight and reflects, to a certain extent, their concentrations in tissue tRNA. Increased levels of several modified nucleosides and bases were found in all rats that had cancer. Rats with hepatomas excreted essentially the same modified nucleosides and bases as did those with nephroblastomas; the quantitative patterns of excretion were different, however, suggesting that the urinary modified nucleosides and bases may be used to differentiate between neoplasms. Although the increase in urinary modified nucleosides and bases by tumor-bearing animals results primarily from more rapid turnover of neoplastic tRNAs, the data indicate that increased turnover of mRNA and possibly rRNA may occur in neoplastic tissue. Preliminary data suggest that increases in urinary modified nucleosides and bases may occur during a precancerous stage. The urinary pattern of modified nucleosides and bases by rats with hepatomas is altered if another primary tumor is present. The results obtained from these studies support the use of modified nucleosides and bases in urine as biochemical markers of cancer.
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PMID:Comparison of urinary modified nucleosides and bases in rats with hepatomas and nephroblastomas. 630 50

This investigation was carried out to evaluate the effects of ginseng in inhibition or prevention of carcinogenesis induced by various chemical carcinogens. Korean red ginseng was administered orally to the newborn mice. 9, 10-Dimethyl-1,2-benzanthracene (DMBA), urethane, and aflatoxin B1 were injected in subscapular region of ICR mice within 24 hr after birth. Controls comprised three groups of ICR newborn mice: normal, (100) ginseng, (200), and vehicle (316). The six experimental groups of ICR newborn mice comprised DMBA (101), DMBA combined with ginseng (103), urethane (94), urethane combined with ginseng (92), aflatoxin B1 (50), and aflatoxin B1 combined with ginseng (47). The mice were autopsied immediately following sacrifice. All major organs were examined grossly and weighed. Histopathological examinations were also made. In the group sacrificed at 48 weeks after the treatment with DMBA (DMBA combined with ginseng extract), the average diameter of the largest lung adenomas decreased by 23%. The incidence of diffuse pulmonary infiltration decreased by 63%, and the average lung weight of male mice decreased by 21%. In the group sacrificed at 28 weeks after the treatment (urethane combined with ginseng), there was a 22% decrease (P less than 0.05) in the incidence of lung adenoma. In the group sacrificed at 56 weeks after birth (aflatoxin B1 combined with ginseng), there were decreases in the incidence of lung adenoma (29%) and hepatoma (75%) (P less than 0.05). These findings indicate that the prolonged administration of Korean red ginseng extract inhibited the incidence and also the proliferation of tumors induced by DMBA, urethane, and aflatoxin B1.
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PMID:Anticarcinogenic effect of long-term oral administration of red ginseng on newborn mice exposed to various chemical carcinogens. 642 59

Fischer 344 male rats fed a choline-methionine deficient diet for from 13 to 24 months developed a 100% incidence of putative preneoplastic hepatocyte nodules and a 51% incidence of hepatocellular carcinoma. The addition of 0.8% choline chloride completely prevented the development of both the nodules and the cancer. The diet contained no added known carcinogen. Analysis of the deficient and supplemented diets revealed no detectable volatile nitrosamines or nitrosamides, nitrite, nitrate or malonaldehyde, less than 0.9 p.p.b. aflatoxin B1 and barely detectable levels of Ames positive material with one strain of Salmonella typhimurium. These findings indicate that a dietary deficiency of choline and methionine can be a major rate limiting factor in the development of liver cancer.
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PMID:The induction of liver cancer by dietary deficiency of choline and methionine without added carcinogens. 648 58

Aflatoxicol (AFL), a metabolite of aflatoxin B1 (AFB1), is formed in vitro by liver preparations from several species including humans. A positive correlation appears to exist between the sensitivity of a species to AFB1 and the species ability to metabolize AFB1 to AFL. Conversion of AFB1 to AFL is, therefore, a questionable detoxification step. The carcinogenicity of a diastereoisomeric mixture of AFL, prepared chemically from AFB1, was compared to AFB1 by tumor incidences being determined in 4 groups of 20 weanling male F344 rats fed either a negative control diet with no aflatoxin, a positive 50-ppb AFB1 control diet, a 50-ppb AFL diet, or a 200-ppb AFL diet for 1 year and then killed at the end of the 2d year. The respective hepatocellular carcinoma incidences were 0, 40, 20, and 70%, demonstrating that AFL is carcinogenic in the rat. The data show that a diastereoisomeric mixture of AFL is one-half as carcinogenic as AFB1, and the dose response appeared nearly linear in that a fourfold increase in dose produced a 3.5-fold increase in tumor incidence. The data did not establish unequivocally that AFL is a proximate carcinogen, but metabolism of AFB1 to AFL should not be considered an efficient detoxification reaction.
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PMID:Carcinogenicity of aflatoxicol in Fischer 344 rats. 678 97

In a study of possible enhancing effects of dimethylnitrosamine (DMN) on aflatoxin B1 (AFB1) hepatocarcinogenesis, male Buffalo strain rats were fed diets containing 1 ppm AFB1, 25 ppm DMN, and a combination of 1 ppm AFB1 and 25 ppm DMN (AFB1 + DMN). The diets were replaced by chow pellets after 6 months, and animals were killed 3, 6, 9 and 12 months after the onset of the experiment. In the untreated control group animals were free of hepatocellular carcinoma but the treated groups fed AFB1, DMN and AFB1 plus DMN developed hepatic lesions ranging from multiple cysts, altered cell foci and neoplastic nodules to hepatocellular carcinomas. Hepatocellular carcinomas developed in 79%, 45% and 5% of rats fed AFB1 plus DMN, AFB1 and DMN respectively at the end of the experiment. Multiple cysts were also found in all periods in animals fed AFB1 plus DMN, whereas rats fed AFB1 and DMN separately developed a few multiple cysts by the end of the experiment. These findings suggest that DMN potentiates the hepatocarcinogenesis induced by AFB1 in rats.
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PMID:Enhancing effects of dimethylnitrosamine on aflatoxin B hepatocarcinogenesis in rats. 679 31


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