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

The etiologic relationship of parasitic liver disease to primary liver cancer has long been debated. For this reason, a review of 4611 necropsies was carried out to determine the frequency with which hepatocellular carcinoma occurred in association with schistosomiasis. Of 227 cases of hepatocellular carcinoma, 24 (10.6%) were associated with schistosomiasis japonica. This was significantly higher than the incidence of this carcinoma without schistosomiasis (2.78%). The majority of the 24 cases exhibited the features of a mixed macronodular and micronodular cirrhosis (Gall's posthepatitic cirrhosis); this was super-imposed upon and caused a masking of schistosomiasis fibrosis. By radioimmunoassay hepatitis B antigen was positive in 27% of these cases. A review of the literature indicated that chronic schistosomiasis, on its own, is unlikely to be the cause of primary liver cell carcinoma. Histologic features resembling post-hepatitic cirrhosis combined with a high frequency of hepatitis B antigen suggest that viral hepatitis rather than S. japonicum is the more likely etiologic factor involved, or has a synergistic effect on carcinogenesis.
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PMID:Primary liver cancer coincident with Schistosomiasis japonica. A study of 24 necropsies. 16 89

The history of chemical carcinogenesis is a record of the observations of physicians and epidemiologists of the relation between the occurrence of uncommon cancers in humans and the exposures of those people to certain chemical agents. In parallel with some of these findings, experimental animal models were developed to imitate the findings in humans. From these experimental studies has been obtained most of the information we have about the mechanisms of chemical carcinogenesis. Many of the biochemical studies have focused on liver cancer which might be an inappropriate general model for chemically induced cancer, liver cancer being comparatively rare in humans. It is not known to what extent exposures to any particular chemical carcinogens are responsible for the major human cancers, and the agents responsible for most of them are not known. It is probable that many noncarcinogenic chemicals act as promotors of carcinogenesis, and among these alcohol can be included as in important contributor.
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PMID:Current status of experimental chemical carcinogenesis and its applications to human cancer risk. 37 27

Alcohol combined with tobacco smoking is an established risk factor for cancers of the oropharynx, esophagus, and larynx. It should be possible to clarify further the role of alcohol itself, the modifying effects of tobacco, dose-response relationships, and nutritional cofactors. Studies are also needed to delineate the steps by which alcohol consumption leads to liver cancer and to resolve the suggestion that certain beverages may predispose to other cancers including those of the pancreas and rectum. Epidemiological investigations should be combined with experimental work to identify hazardous fractions in alcoholic beverages and to delineate the mechanisms by which alcohol promotes carcinogenesis. Epidemiologists and biometricians may also contribute toward the development of programs aimed at primary prevention and early detection of cancers related to alcohol and tobacco. Incorporation of research questions into data collection systems deserves serious questions into data collection systems deserves serious consideration as a means of obtaining additional valuable information for etiological studies.
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PMID:Epidemiological opportunities in alcohol-related cancer. 44 91

A new hypothesis leading to a new model of liver carcinogenesis is described; it is based on the acquisition by carcinogen-altered hepatocytes during initiation of a new functional handle--resistance to the cytotoxicity of a carcinogen--and on the ability of such cells to proliferate in an environment that prevents proliferation of normal hepatocytes. The creation of such a differential environment now enables a quantitative analysis for initiation, the beginning synchronization of the putative premalignant hepatocytes for about 15 cell cycles, the study of the pattern of growth of such resistant cells to form nodules that have some resemblance to the organizational pattern of fetal liver, the analysis of the appearance of distinctive positive and negative markers for these cells, and the further investigation of the development of liver cancer from such cells. The remarkable similarity in overall pattern betweeen the development of cancer in the skin and in the liver with chemicals and the possible role of both somatic mutation and neodifferentiation in carcinogenesis are briefly discussed.
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PMID:Newer insights into the pathogenesis of liver cancer. 92 Jul 80

The insulin-like growth factor II (IGF-II) is involved in embryonic growth. Modifications of its expression might play a role in the development of primary liver cancer in humans and woodchucks. In the liver, little information is available on the cell types involved in its synthesis. We have investigated the expression of IGF-II as well as IGF-II, IGF-I and insulin receptor mRNAs in non parenchymal liver cell preparations in rats of various ages. The results indicate that Kupffer cells, endothelial cells and fat-storing cells express both IGF-II and the three different receptor mRNAs. Furthermore, a switch from a fetal to an adult IGF-II mRNA profile was obtained in the different cell preparations. Therefore, our results indicate that regulation of IGF-II gene expression can be analyzed through these isolated liver cell preparations. These results might also be important in investigating the potential role of IGF-II in liver carcinogenesis.
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PMID:Expression of insulin-like growth factor II (IGF-II) and IGF-II, IGF-I and insulin receptors mRNAs in isolated non-parenchymal rat liver cells. 131 Jul 5

In an experiment with Wistar rats the question of whether oral vitamin C application has a protective effect in liver carcinogenesis caused by N-nitrosodiethylamine in drinking water (n = 104) was studied. When comparing four groups (without carcinogen, with carcinogen and carcinogen plus vitamin C alternately and concomitantly) significant statistical differences in the linear regression were noted. Ninety per cent of the rats developed hepatocellular carcinomas when only carcinogen was administered whereas the rate with additional administration of vitamin C alternately and concomitantly was 68% and 55%, respectively. Without carcinogen no tumour developed. The results suggest that vitamin C may delay the development of liver cancer upon oral administration of N-nitrosodiethylamine. The explanation for this fact is still hypothetical.
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PMID:Potential protective effect of vitamin C on carcinogenesis caused by nitrosamine in drinking water: an experimental study on Wistar rats. 131 51

Chronic infection by hepatitis B and C viruses is frequently associated to the development of primary liver cancer. Liver cirrhosis, induced by these viral infection, plays an important role in the liver carcinogenesis. In addition, HBV has a direct role in liver cell transformation by a transactivating effect of some viral proteins as well as insertional mutagenesis. The role of hepatitis C virus is not known. The strong association, even in France, of primary liver cancer to these viral infections underline the importance of their prevention by vaccination.
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PMID:[Liver cancer and hepatitis B and C virus]. 133 32

Ames test procedures were used to test 8 natural food extracts for their antimutagenic activity against the mutagenic activity induced in S. typhimurium strains TA98 and TA100 by aflatoxin B1 (AFB1) or metabolic extracts from A. versicolor or A. ochraceus. The tested substances were extracted repeatedly with acetone. The revertants induced by AFB1, metabolic extracts of A. versicolor or A. ochraceus were significantly decreased when extracts of the 8 natural foods were added to the media. The results showed that these extracts had marked inhibitory effects on the mutagenic activity induced by AFB1 or metabolic extracts of the two molds and also suggested that antimutagenic substances were present in these natural foods. These experiments provide a scientific basis for the study of food substances for the prevention of carcinogenesis. It is considered that these 8 natural food extracts produce marked antimutagenic effects and are practically valuable in the field of chemoprophylaxis of liver cancer in humans.
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PMID:Antimutagenic effect of eight natural foods on moldy foods in a high liver cancer incidence area. 137 30

P-Glycoprotein (Pgp) has been shown to mediate multidrug resistance in tumor cell lines. Overexpression of Pgp has been detected in clinical cancer samples of many histological types. The basis and biological significance of such increases in Pgp expression are not well understood. In this study, the expression of Pgp during stepwise progression to rat liver cancer was examined to investigate the possible role of Pgp in carcinogenesis. An immunohistochemical technique was used to detect Pgp at the single-cell level, in a large number of liver nodules, hepatocellular carcinoma, and in distant metastases of the carcinomas. The results showed that distinct changes in Pgp expression occurred during stepwise liver carcinogenesis and that these changes were closely associated with the microscopic anatomy of the lesions. In contrast to gamma-glutamyl transpeptidase and glutathione S-transferase-7.7, whose expression appeared to correlate with the early steps of liver carcinogenesis, Pgp expression was higher in the large hyperplastic nodules and in hepatocellular carcinomas than in the early microscopic lesions. A particularly striking finding was the consistent expression of Pgp in the lung metastases. These findings suggested that Pgp was associated with a more progressed malignant phenotype in liver carcinogenesis.
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PMID:P-glycoprotein expression during tumor progression in the rat liver. 138 36

Cooked food contains a variety of mutagenic heterocyclic amines. All the mutagenic heterocyclic amines tested were carcinogenic in rodents when given in the diet at 0.01-0.08%. Most of them induced cancer in the liver and in other organs. It is noteworthy that the most abundant heterocyclic amine in cooked food, 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, produced colon and mammary carcinomas in rats and lymphomas in mice but no hepatomas in either. 2-Amino-3-methylimidazo[4,5-f]quinoline induced liver cancer in monkeys. Formation of adducts with guanine by heterocyclic amines is presumably involved in their carcinogenesis. Quantification of heterocyclic amines in cooked foods and in human urine indicated that humans are continuously exposed to low levels of them in the diet. These low levels of heterocyclic amines are probably insufficient to produce human cancers by themselves. However, a linear relationship between DNA adduct levels and a wide range of doses of a heterocyclic amine was demonstrated in animals. It suggests that even very low doses of heterocyclic amines form DNA adducts and may be implicated in the development of human cancer under conditions in which many other mutagens-carcinogens, tumor promoters, and factors stimulating cancer progression exist.
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PMID:Food-derived mutagens and carcinogens. 154 46


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