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Query: UMLS:C0345904 (liver cancer)
 15,188 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Food samples collected in Murang'a district, Kenya are known to be contaminated with a mycotoxin, aflatoxin B1 (AFB), and a positive correlation exists between the dietary intake of AFB and the incidence of liver cancer. When urine samples collected in this district were analyzed for the presence of 2,3-dihydro-2-(7'-guanyl)-3-hydroxyaflatoxin B1 (AFB-GuaI) by h.p.l.c., 6 of 81 samples had a detectable level of a compound whose fluorescence spectrum was identical to chemically synthesized AFB-GuaI as confirmed by photoncounting fluorescence spectrophotometry. These results are an indication of interaction between the ultimate carcinogenic form of AFB and cellular nucleic acids in vivo and further support the hypothesis that AFB may play an important role in the etiology of human liver cancer.
Carcinogenesis 1983 Sep
PMID:Detection of putative adduct with fluorescence characteristics identical to 2,3-dihydro-2-(7'-guanyl)-3-hydroxyaflatoxin B1 in human urine collected in Murang'a district, Kenya. 641 78

A vitamin A (retinyl acetate)-deficient diet enhanced liver cancer in rats exposed to aflatoxin B1 (AFB1) and also caused a 29% incidence of colon cancer. The following factors were considered in attempts to define conditions under which vitamin-A-deprived rats were more susceptible to colon cancer induced by AFB1: liver morphology, enterohepatic recirculation, level of reduced glutathione (GSH) in liver, and differing capacities for conjugation of aflatoxin to GSH. Enzyme concentrations in liver, in intestinal and colon mucosa, and in intestinal and colon contents suggested that AFB1 may have different metabolites and that there may be differing susceptibilities of colon mucosa to carcinogenesis. Binding studies supported this hypothesis. Previous studies have shown that colon epithelium from vitamin-A-deficient rats binds more AFB1 than colon epithelium from normal, vitamin-A-supplemented animals. In the present study, vitamin A supplementation to the vitamin-A-deficient rats before oral administration of 3H-AFB1 significantly decreased the binding capacity at 12 and 15 hours after dosing with the carcinogen. These results suggest that the effect of vitamin A on the metabolism of the carcinogen, particularly on binding of AFB1 to cellular macromolecules, may be the mechanism by which vitamin A modifies aflatoxin's carcinogenic potential, influenced in part through enzymatic mechanisms.
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PMID:Vitamin A and aflatoxin: effect on liver and colon cancer. 641 17

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.
Carcinogenesis 1984 Oct
PMID:The induction of liver cancer by dietary deficiency of choline and methionine without added carcinogens. 648 58

In order to confirm the close association between chronic hepatitis B virus (HBV) infection and primary hepatocellular carcinoma (PHC) in Japan, 8,646 male hepatitis B surface antigen (HBs Ag)-positive blood donors (GPT less than or equal to 35 Karmen units) were followed up. Twenty liver cancer cases were observed during the follow-up period (average 6.2 years), the expected number calculated on the basis of age-specific incidence rates among the general population being 3.03. Therefore, the observed to expected ratio of liver cancer was 6.60, that is significantly higher than 1.0. During the same follow-up period, a total of 76 deaths were observed, of which 20 were due to liver cancers and 9 to liver cirrhoses, meaning that nearly 40% of deaths among the study subjects due to chronic liver diseases. Drinking and smoking habits in the liver cancer cases were compared with those observed in healthy male HBV carriers. A strong positive association between drinking habits and liver cancer was observed and there was a significant dose-response relationship after adjustment for cigarette smoking habits. A high risk of liver cancer was also observed among heavy smokers, but a significant dose-response relationship could not be found between smoking habits and liver cancer, partly because of the limited number of the study subjects. These findings suggest that HBV is a major etiologic agent of PHC in Japan where the HBs Ag prevalence rate is about 2%, and alcohol drinking and cigarette smoking may promote the process of HB viral hepato-carcinogenesis.
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PMID:Follow-up study of HBs Ag-positive blood donors with special reference to effect of drinking and smoking on development of liver cancer. 651 Nov 24

Unlike the great heterogeneity and diversity in the initial interactions of a chemical carcinogen with DNA and in the phenotypes of the late malignant neoplasms, the intermediate steps in liver carcinogenesis, the hepatocyte nodules, are remarkably similar. This commonality is seen in six different models of liver cancer development using carcinogens and promoters of quite different chemical structure and properties. The hepatocytes in the nodules show a similar arrangement and architecture, cytology and cytochemistry, blood supply, biological behavior, and biochemical pattern. These observations, coupled with the program nature of the remodeling of the hepatocyte nodules, strongly suggest that at least some of the earlier steps in carcinogenesis are of a physiological adaptive nature.
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PMID:Chemical carcinogenesis: hepatocyte nodules with a special phenotype as a common step at the crossroads. 651 81

This study was undertaken to observe whether the administration of reduced glutathione intragastrically to male Fischer 344 rats during the precancerous steps of liver carcinogenesis has any protective effect on the development of hepatocellular carcinoma. Hepatocyte nodules were induced in the liver with a single initiating dose of diethylnitrosamine followed by selection of resistant hepatocytes to generate nodules by a two week exposure to dietary 2-acetylaminofluorene coupled with partial hepatectomy. Animals had hepatocyte ('hyperplastic') nodules when examined by laparotomy at three months. At that time, the animals were divided into two groups. One received daily intragastric glutathione for 8 months while the other received no further treatment. An additional control group received only the selecting (promoting) regimen with no initiator or glutathione. At 12 months, the animals receiving the initiator and promoter regimen had a 65% incidence of hepatocellular carcinoma and those receiving glutathione in addition had a 71% incidence. Under these experimental conditions, the long term administration of glutathione appears to have no observable influence on liver cancer development in this model.
Carcinogenesis 1983
PMID:Failure of glutathione to prevent liver cancer development in rats initiated with diethylnitrosamine in the resistant hepatocyte model. 682 84

This article is a review of the literature on the subject, which has been very little studied. 7 works in Russian and 33 in various Western languages are analyzed, from the point of view of the carcinogenic effects of various types of oral contraceptives on the uterus, cervix, ovaries, and breasts. About 20 instances are mentioned of liver cancer developing in women. The authors note the possibility of transplacental carcinogenesis in view of the fact that the daughters of women who took diethylstilbestrol to prevent spontaneous abortion were in some cases found to be suffering from adenocarcinoma of the vagina 15-20 years later. Other topics discussed are teratogenicity, the effects of OCs on women older than 40, therapeutic uses of OCs, and the need for careful follow-up of women who are using OCs.
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PMID:[Oncological aspects of hormonal contraception]. 701 84

Dietary feedback control (DFC) of hepatic cholesterol synthesis is absent in hepatomas of trout, mouse, rat and man. DFC has also been shown to be defective in rats fed several liver carcinogens, including 2-acetylaminofluorene (AAF). These studies have led to the hypothesis that loss of normal DFC is an early and necessary event in the development of liver cancer. To test this hypothesis, we fed the liver carcinogens benzidine (0.006% in drinking water) or AAF (0.05% in chow) to male Sprague-Dawley rats for either 3 or 6 weeks. We measured cholesterol synthesis as the incorporation of 2-14C-acetate into digitonin-precipitable sterols by liver slices. DFC was tested by adding 2% cholesterol to the diet for 3 days prior to sacrifice. DFC was defective in the AAF-fed rats but was normal in the benzidine-treated rats. These results are at variance with the previously stated hypothesis and, for the first time, suggest that defective DFC is not a consistent finding in the early stages of liver carcinogenesis. Additional research is necessary to explain why DFC is altered by exposure to some liver carcinogens such as AAF but unaffected by exposure to others such as benzidine.
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PMID:Feedback control of cholesterol biosynthesis in rats fed the liver carcinogens benzidine and 2-acetylaminofluorene. 724 21

The administration of either N-nitrosodiethylamine (diethyl-nitrosamine) to intact male F-344 rats or N-methyl-N-nitrosourea to similar animals 18 hr after partial hepatectomy results in the induction of altered resistant hepatocytes that persist for up to 36 weeks with no perceptible decrease in their number. The criterion for resistance was the ability to proliferate rapidly and to develop into foci or nodules when exposed to a level of dietary 2-acetylaminofluorene that inhibits the proliferation of the vast majority of hepatocytes when liver cell proliferation is stimulated by surgical or chemical partial hepatectomy. Since this selection procedure, when coupled with a single dose of diethylnitrosamine, is associated with a high incidence of liver cancer as compared to appropriate controls, and since similar foci and nodules were shown previously to be one site of origin for hepatocellular carcinoma in this model, the induction of resistant hepatocytes is interpreted as initiation. Thus, these results suggest that initiation of liver carcinogenesis in this model is irreversible, at least for a period of 36 weeks.
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PMID:Persistence of resistant putative preneoplastic hepatocytes induced by N-nitrosodiethylamine or N-methyl-N-nitrosourea. 735 42

We studied the relations between glutathione S-transferases (GSTs) from human liver and hepatic cancer and preneoplastic lesions in high risk area of Qidong city and Beijing. A biotin-avidin enzyme-linked immunoassay (BA-ELISA) for serum level of GSTs was developed. The results showed that the GSTs level of normal controls in Qidong city (0.66 +/- 0.54 ng/ml) was higher than that in Beijing (0.37 +/- 0.27 ng/ml). The members of high cancer families, HBVsAg carries and patients having a low level fluctuating pattern of serum AFP were the population with high risk of liver cancer; their serum level of GSTs was 1.25 +/- 1.46, 1.43 +/- 1.44 and 2.81 +/- 1.76 ng/ml respectively, and it was significantly higher than in the normal controls. The content of GSTs of hepatic cancer patients in Qidong city and Beijing was 3.03 +/- 3.35 and 3.60 +/- 3.70 ng/ml respectively, but the positive rate (97%) of GSTs in Qidong city was higher than that (82%) in Beijing. The results suggested that serum expression of GSTs can be used as an enzyme marker for hepatic cancer and preneoplastic lesions. Possible roles of these forms in hepatic carcinogenesis induced by chemical carcinogenesis were discussed.
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PMID:[Glutathione S-transferases in carcinogenesis and diagnosis of liver cancer]. 750 53


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