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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The transplantable MC-29 virus-derived hepatoma is a suitable model for studying the influence of immune status on virus-derived hepatomas in chickens. It was found that both humoral and cellular immunologic reactions have a role in the pathogenesis of virus-derived hepatomas and that virus-derived hepatomas can be influenced by nonspecific immunostimulation. The lymphoid system was profoundly altered in hepatoma-bearing chickens; this cannot be neglected when studying correlations between immune reactions and carcinogenesis. Profound changes were also observed in protein synthesis and the steroid receptor system of hepatoma-bearing chickens compared to healthy birds; this also complicates the understanding of the role of immune mechanisms in carcinogenesis.
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PMID:Influence of immune status on virus-derived transplantable hepatoma in chickens. 3 44

Areas of hyperplastic livers that acquire hyperbasophilic properties at advanced stages of carcinogenesis apparently represent the sites of neoplastic trasnformation, and hyperstaining of cytoplasmic RNA with basic dyes also characterizes the cancer cells. Estimations of the RNA content of cell fractions from normal rat liver and solid Novikoff hepatoma provided no evidence that the intense staining of cancer cells could be explained on the basis of an increase in cytoplasmic RNA content. The possibility that cytoplasmic fractions of Novikoff hepatoma show greater affinity for basic dyes than corresponding normal fractions has been examined by means of a test-tube toluidine blue-binding assay. The results revealed that the dye-binding capacity of total cytoplasmic fractions from tumors is 75% higher than normal after Carnoy fixation which retains mostly ribosomal RNA. Assays on fresh ribosomes indicated that tumor ribosomes bind 71% more toluidine blue per mg of RNA than the ribosomal preparation from normal liver. This study thus demonstrates a greater affinity of tumor RNA for basic dyes, and a comparison of biochemical and cytophotometric analyses suggests that an increase in basophilia by a factor OF ABOUT 2 WOULD BE DUE TO A qualitative alteration in robosomal RNA molecules and/or ribosome structure in cnacer cells.
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PMID:Biochemical estimation of the basic dye-binding capacity of RNA from rat hepatoma. 4 92

(1) Passive hemagglutination and radioimmunoassay are suitable methods for the detection of AFP in the low concentration range. (2) In 3.72% of the cases a clinically unknown carcinoma was found in an unselected group of patients with liver cirrhosis. (3) 21.9% of the patients showed AFP elevations up to 2000 ng/ml. In 10.6% of this group, increasing titers demonstrated a primary liver cell carcinoma. In 89.4% a transitory rise of AFP was not associated with tumor growth. Levels return to normal values within three months in 90% of the cases. (4) Transitory AFP elevations are not correlated to clinical conditions (praecoma, coma, delirium, bleeding, ascites, shunt) or to biochemical parameters (GOT, GPT, bilirubin, prothrombin complex time, gamma-globulin). (5) A temporary rise in AFP is more frequently observed in groups with high hepatoma incidence than in groups with low hepatoma incidence. (6) Therefore, it may be suggested that a transitory rise of AFP could reflect a "primary reaction" of carcinogenesis. (7) Primary liver cell carcinoma is found to be more frequent in posthepatitic than in postalcoholic, cryptogenic, and other cirrhosis and to be more frequent in australia-antigen positive than in australia-antigen negative cases. (8) Routine serological tumor antigen screening of patients with a precancerous disease is useful.
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PMID:Early detection of hepatoma: prospective study in liver cirrhosis using passive hemagglutination and the radioimmunoassay. 5 21

In studies in this and other laboratories, induction of hepatocardinoma by several different chemical carcinogens was enhanced in rats fed diets deficient in lipotropes (choline, methionine, folic acid), amino acids, and niacin, and high in fat. In some cases, specific supplementation with lipotropes blocked carcinogenesis. In studies reported here, specific supplementation of a marginally deficient diet that enhanced carcinogenesis in rats, with the amino acids or lipotropes in which it was deficient, significantly decreased induction of hepatocarcinoma by N-nitrosodiethylamine. Niacin supplementation decreased hepatocarcinoma incidence only slight; the addition of beef fat to an adequate diet did not enhance tumor induction. Rats fed the amino acid- or lipotrope-supplemented diets had an increased incidence of hepatic hemangioendothelial sarcomas, compared to deficient rats or to rats fed the adequate control diet. Methionine was contained in both the amino acid and the lipotrope supplement and probably was responsible for reducing hepatocarcinoma incidence. Methionine has been found to have an anticarcinogenic effect in other studies and also to block the depletion of hepatic folate stores that is induced by N-nitrosodiethylamine. Interactions between carcinogens, S-adenosylmethionine, and folate may be significant in hepatic or other tissue carcinogenesis. One of more hepatic microsomal oxidases were depressed in rats fed any of the high-fat diets but were not correlated with tumor incidence.
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PMID:Reduction of N-nitrosodiethylamine carcinogenesis in rats by lipotrope or amino acid supplementation of a marginally deficient diet. 6 28

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

Carcinogen-induced experimental hepatomas are often characterized by new individually distinct antigens capable of inducing tumor immunity in syngeneic hosts. These antigens arise as a consequence of cell-carcinogen interaction and may result from modification or replacement of normal cell-surface components. Their role in immunosurveillance is not established, but they offer a target for tumor immunotherapy. Reexpressed fetal antigens have also been detected, either as secretory products (alpha 1-fetoprotein) or as common cell-surface components on hepatoma cells. The role of fetal antigens in therapy is doubtful, but they may be important diagnostic indicators of neoplastic change. Possibly associated with these are common antigens initiated early after carcinogen treatment, before malignant cells are detected. Together, the antigens associated with liver carcinogenesis may prove to be powerful tools in understanding the process of liver neoplasia.
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PMID:Antigenic changes associated with liver carcinogenesis. 8

A single injection of dimethylnitrosamine (DMN), 12.0-15.6 mg-kg, given to 100 g female rats 24 h after partial hepatectomy, induced hepatocellular carcinoma. No animals receiving DMN without partial hepatectomy developed liver carcinomas. Previous evidence had suggested that the incidence of tumours was highest when DMN was administered during the wave of DNA replication which follows partial hepatectomy. The present experiments made this suggestive evidence statistically significant. A single treatment with diethylnitrosamine (DEN) induced liver cell cancer when given to intact or to partially hepatectomised rats. No tumors developed when another alkylating carcinogen, methyl methanesulphonate (MMS), was administered after partial hepatectomy. The significance of these results in relation to the mechanism of initiation of carcinogenesis is discussed.
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PMID:Effect of a single treatment with the alkylating carcinogens dimethynitrosamine, diethylnitrosamine and methyl methanesulphonate, on liver regenerating after partial hepatectomy. I. Test for induction of liver carcinomas. 16 61

DNA synthesis in a transplanted hepatoma induced by 3'-methyl-4-dimethylaminoazobenzene was significantly reduced (P less than 0.01) in rats maintained on diets low (0.4 mug/g) or high (greater than or equal to 500 mug/g) in zinc when compared with control animals given 60 mug zinc/g. 3-Methylcholanthrene-induced carcinogenesis was considerably lowered in mice receiving the same low or high zinc diets during the induction periods.
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PMID:Zinc intake, neoplastic DNA synthesis, and chemical carcinogenesis in rats and mice. 16 62

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 biosynthesis of aldolase A and B subunits has been studied in rat liver during the administration of carcinogen AAF4. Transition from a predominance of aldolase B to A was observed during carcinogenesis in rat liver. Changes in isozymic pattern and FDP to F-1-P cleavage activity ratio were observed before histological alterations typical of hepatoma could be detected. Our data support the hypothesis of dedifferentiation during hepatocarcinogenesis which in an early stage results in switching on of the gene for aldolase A with simultaneous continuation of biosynthesis of aldolase B within single cells.
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PMID:Isozyme pattern of fructose diphosphate aldolase during hepatocarcinogenesis induced by 2-acetylaminofluorene in rat liver. 17 Feb 26


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