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)

Rat alpha-macrofetoprotein (AMF) and alpha-fetoprotein (AFP) are secreted by the fetal liver and become elevated in serum during hepatocarcinogenesis and in animals bearing hepatocellular carcinomas. It has been suggested that these fetal plasma proteins may be influenced by related control mechanisms. The experiments presented herein examined the early responses of these plasma proteins during hepatocarcinogenesis using the hepatocarcinogens acetylaminofluorene and diethylnitrosamine. Under these conditions, AFP serum concentrations were elevated within a few days of exposure to acetylaminofluorene, whereas AMF serum concentrations remained essentially normal. AFP became elevated after a number of weeks of exposure to diethylnitrosamine. In either regimen, AMF became elevated only later when large primary hepatocellular carcinomas were found. The time of appearance of AMF after transfer of an AFP-secreting Morris hepatoma indicated that AMF was elevated only in animals with extremely large, necrotic tumors. Thus, it appears that elevation of serum AFP resulted from either exposure to hepatocarcinogens or production by hepatocellular carcinomas, but that the elevations of serum AMF levels resulted from inflammatory injury or necrosis of tumor tissues.
Cancer Res 1979 Sep
PMID:Rat alpha-macrofetoprotein (acute-phase alpha 2-macroglobulin) during hepatocarcinogenesis. 8 3

Ataxia-telangiectasia (AT) is a multi-system disease involving the cerebellum, cutaneous blood vessels and the immune system including both cellular and humoral components. It also involves hematological, endocrine and peripheral nervous systems. This disease is often associated with abnormal liver function tests, such as, raised alkaline phosphatase and various nonspecific histological changes in the liver. High incidence of various malignancies involving lymphoreticular, gastrointestinal and mesenchymal organs have reported in ataxia-telangiectasia. Elevated levels of alpha fetoprotein have been noted commonly in this disorder. In spite of the hepatic histological and biochemical changes associated with elevated alpha fetoprotein, to our knowledge, development of hepatocellular carcinoma has not been reported in patients with ataxia-telangiectasia. A case of a young white female with AT who developed hepatocellular carcinoma along with significantly elevated levels of alpha fetoprotein is presented.
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PMID:Ataxia-telangiectasia and hepatocellular carcinoma. 9 92

The presence of hepatitis B virus (HBV) antigens was examined in specimens of liver tissue obtained at necropsy from black Senegalese patients suffering from primary hepatocellular carcinoma (PHC). The results were correlated with markers of hepatitis B infection in serum. Hepatitis B surface antigen (HBsAg) and core antigen (HBcAg) were sought for in 15 liver extracts. HBsAg was found in the liver in 10 of 12 cases with HBsAg-positive serum. HBcAg was detected in three livers. The HBsAg was detected in seven of eight livers by immunofluorescence and orcein staining. HBsAg-positive cells were mainly located in the peri-tumoral cirrhotic tissue, although positive hepatocytes were also found in tumour nodules in liver from one of the patients. HBcAg was found in five of seven cases by immunofluorescence in hepatocytes of the cirrhotic areas. HBcAg fluorescence was primarily nuclear but, in some lobules, a patchy cytoplasmic fluorescence was observed. This suggests a cytoplasm-nucleus pathway in the synthesis of the HBV core antigen. Electron microscopy was performed on two HBsAg- and HBcAg-positive cases. Fibrillar and crystalline cytoplasmic inclusions were observed in tumour cells. In the same cells, 20-25 nm virus-like particles were present in swollen cisternae of the endoplasmic reticulum.
Int J Cancer 1979 Oct 15
PMID:Hepatitis B virus antigens in human primary hepatocellular carcinoma tissues. 9 79

Mice fed a diet containing 0.3 or 0.03% triethanolamine developed malignant tumors. Females showed a high incidence of tumors in lymphoid tissues, while this type was absent in males. Tumors in other tissues were produced at a considerable rate in both sexes, but no hepatoma was found. Triethanolamine was not mutagenic to Bacillus subtilis by itself, but it became mutagenic after reacting with sodium nitrite under acidic conditions or when the mixture was heated. Although N-nitrosodiethanolamine, a known carcinogen and mutagen, was detected in the reaction mixture by thin-layer chromatography, it may not be the main mutagenic product, because the product was a stable and direct mutagen and its mutagenic activity was destroyed by liver enzymes, unlike N-nitrosodiethanolamine. The lethal and mutagenic DNA damages produced by this unidentified product were susceptible to some extent to the repair functions of the bacteria.
Cancer Res 1978 Nov
PMID:Carcinogenicity of triethanolamine in mice and its mutagenicity after reaction with sodium nitrite in bacteria. 10 Feb 10

Parenteral and enteral nutrition are being used as adjuncts to cancer therapy. A liquid diet formulation containing a 27% solution of glucose and 3.9% crystalline amino acids with electrolytes and vitamins was given continuously for a week via parenteral (iv), and via intragastric (ig) routes and also was given ad libitum via the oral or per os (po) route to groups of Buffalo rats with and without a Morris No. 7777 transplantable hepatoma to find out how these feeding procedures affect tumor-host interactions. Other groups of rats with and without the hepatoma were given solid food ad libitum. The following parameters were examined: mortality, carcass and organ weights, body and tumor growth, nitrogen balance, energy intake, fluid balance, urinalysis, hematology values, and serum protein levels. The results are considered with respect to the influence of the tumor on the host and the influence of the feeding procedure on the animal with and without a tumor. The presence of the hepatoma was associated with: higher mortality, a decrease in carcass mass, leucocytosis, anemia, a decrease in serum IgG, transferrin and albumin, and an increase in serum alpha fetoprotein. The iv and ig feeding procedures alone resulted in some mortality which was exacerbated by the presence of the tumor. Mortality was especially high in the tumorous rats on the ig feeding procedure. The degree of positive nitrogen balance and carcass mass was similar in non-tumorous rats fed the same liquid diet formula when given iv, ig, or po. Tumorous rats fed the liquid diet ad libitum showed anorexia and a significantly lower nitrogen balance. The iv and ig feeding of tumorous rats at a level which was well above those of the tumorous rats given solid or liquid diet ad libitum maintained the same degree of positive nitrogen balance as non-tumorous rats. Even though the iv feeding of tumorous rats maintained about the same degree of positive nitrogen balance as non-tumorous rats, these tumorous rats still suffered loss of carcass mass. It appears that the large rapidly growing hepatoma has priority for available nutrition over the host. It is further suggested that the rapidly growing hepatoma places an ever increasing demand on the available nutrients. Thus, a point is eventually reached where even supplemental nutritional support can no longer meet the needs of the growing hepatoma and the host.
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PMID:Tumor-host responses to various nutritional feeding procedures in rats. 10 99

gamma-Irradiated rat hepatoma cells are immunogenic in syngeneic WAB/Not rats, so that immunized animals are protected against tumour-cell challenge and circulating tumour-specific antibody is produced. Treatment of the immunizing cells with glutaraldehyde at concentrations of 0.001% or greater for 30 min rendered these cells non-protective in tumour-rejection tests and no longer able to induce significant formation of specific antibody. However, tumour-specific antigens were shown to be expressed upon treated cells; they specifically bound tumour-specific antibody from syngeneic immune sera assessed in indirect membrane-immunofluorescence tests. Also, these cells specifically absorbed antibody from immune or tumour-bearer sera, as demonstrated in the indirect membrane-immunofluorescence test or a complement-dependent 51Cr-release test. Alloantigen expression was not influenced by glutaraldehyde treatment, although glutaraldehyde-treated hepatoma cells failed to induce alloantibody formation in KX/Not rats. Polyacrylamide-gel electrophoresis of treated cells, surface-labelled with 125I, indicated that extensive cross-linking of the surface protein occurred as a result of glutaraldehyde treatment. The present findings establish that although the expression of a tumour-specific antigen is necessary for the induction of immuno-protection against tumour-cell challenge, this alone is not a sufficient condition for eliciting tumour immunity.
Br J Cancer 1979 Jun
PMID:Modification of the immunogenicity and antigenicity of rat hepatoma cells. I. Cell-surface stabilization with glutaraldehyde. 10 10

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.
Br J Cancer 1979 Jun
PMID:Lipid peroxidation of the microsomal fraction and extracted microsomal lipids from DAB-induced hepatomas. 10 13

Rats bearing the Morris hepatoma No. 7777 were randomized into three treatment groups. Two of the groups received a nutritionally complete liquid formula diet per os ad libitum. One of these two groups received hydrazine sulfate (HS; an inhibitor of gluconeogenesis) twice daily (15 mg/kg) for 5 days. A third group of tumorous rats received the HS therapy and was given the liquid diet parenterally for 5 days. Tumorous rats fed per os, especially with HS therapy demonstrated inhibition of tumor growth, reduction of body and carcass weight, anorexia and decreased nitrogen retention. The combination of parenteral feeding and HS therapy sustained body and carcass weight with high nitrogen retention but stimulated tumor growth and was associated with liver toxicity. These results support the concept that cancer cachexia involves 'a systemic energy-losing cycle dependent on an interplay of tumor glycolysis and gluconeogenesis'.
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PMID:Total parenteral nutrition and inhibition of gluconeogenesis on tumor-host responses. 11 15

When the effects of 7,12-dimethylbenz(a)anthracene (DMBA) on normal and malignant rat liver epithelial cells were compared in a colony inhibition assay, this carcinogen showed a preferential cytotoxic action on the normal cells. In investigations of the biochemical basis of this selective toxicity, it was found that both cell lines were similarly effective in binding DMBA to DNA and that both cell lines had the capacity to metabolize this carcinogen. However, the hepatoma cells were more efficient than were the normal cells in generating very polar metabolites (not organic solvent extractable). These studies suggest that the basis of the resistance of the hepatoma cells to the toxicity induced by DMBA lies in their ability to detoxify biologically active metabolites. Several phenols were examined as possible toxic metabolites of DMBA, but these were not toxic at dose levels at which DMBA kills most of the normal cells.
Cancer Res 1979 Dec
PMID:Biochemical basis for cytotoxicity of 7,12-dimethylbenz(a)anthracene in rat liver epithelial cells. 11 85

Bovine pineal polypeptide extract (PPE) exerted an anti-tumor effect on mouse-transplantable tumors: mammary cancer (RSM), squamous cell cervical carcinoma (SCC), hepatoma-22a and lympholeukemia LIO-1, and had no effect on Harding-Passey melanoma and leukemia L-1210. It was shown that PPE possessed the ability to decrease the incidence of DMBA-induced mammary adenocarcinomas in rats. The daily administration of 0.5 mg PPE prolonged the life span of rats by 25% and failed to influence spontaneous tumor development. The arguments in favor of a possible mechanism of anti-tumor action of the pineal gland are submitted. It is suggested that the anti-tumor effect of PPE may occur when the syndrome of cancrophilia is induced by tumor transplantation or chemical carcinogens.
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PMID:Study of the anti-tumor effect of polypeptide pineal extract. 11 14


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