Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
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

Peripheral blood lymphocytes from patients with protein calorie malnutrition, atopic eczema, systemic lupus erythematosus and in three groups of patients with liver disease, were characterized by reactivity with monoclonal antibodies to the surface antigens of helper-inducer (OKT4) and suppressor-cytotoxic (OKT8) T cell subsets and to a common T cell antigen (OKT3). The protein calorie malnutrition group showed a considerable decrease in all subsets while patients with atopic eczema displayed an increase in the total number of OKT3+ cells, attributable primarily to an increase in the OKT4+ cell population with the OKT8+ cells remaining within normal values. In the SLE group, only 3 of the 16 patients had OKT8+ numbers below that of normal controls, whereas the mean number of OKT4+ cells in the group was less than normal controls. The striking feature of patients with liver disease, was the altered ratio of OKT4+ to OKT8+ cells in the hepatocellular carcinoma and amebic liver abscess groups due primarily to decreased OKT4+ and raised OKT8+ cell subpopulations.
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PMID:Lymphocyte subtypes in patients with atopic eczema, protein calorie malnutrition, SLE and liver disease. 630 60

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

The control of communicable diseases, malnutrition and birth complications has been the main preoccupation of the Member States of the African Region of WHO. As a result of these control measures, death rates, particularly among infants and young children, have continued to decline. This has increased life expectancy to the extent that we are now witnessing the emergence of the diseases prevalent in the industrial world: they have already become a major public health problem in Africa. Carcinoma of the cervix and hepatocellular carcinoma are the commonest forms of cancer afflicting the people of this Region. Others include cancers of the breast, skin, prostate, oesophagus, stomach and bladder. Burkitt's lymphoma is the commonest childhood malignancy. The causal factors of some of these tumours are known, and can therefore be eliminated by primary prevention. This is shown by the almost total absence of carcinoma of the penis in those communities that practise male circumcision, and the decrease in the incidence of squamous-cell carcinoma of the skin that resulted from the prevention of tropical ulcer, thanks to effective care of injuries and wounds. The priorities of the WHO cancer programme are therefore primary prevention, early detection and the provision of adequate pain relief. The success of the programme will depend mainly on whether the services provided will benefit the majority of the population.
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PMID:WHO cancer control programme in the African region. 653 17

Management of protein-calorie malnutrition found in 32 patients with severe liver diseases such as fulminant hepatitis and cirrhosis of the liver was carried out using 2 types of synthetic amino acid solution (Hep-OU and Fischer solution) for intravenous and enteral alimentations with rapid monitoring of serum aminogram. Intravenous hyperalimentation of these cases resulted in maintenance of nutritional status with improvement of nitrogen balance and normalization of impaired serum aminogram. During this study, however, nutritional support was initiated only when intractable ascites, upper gastrointestinal bleeding and hepatic encephalopathy were observed. In 2 cases of fulminant hepatitis with sepsis and 3 hepatoma patients with ascites, elemental diet containing maltose and amino acids was used to supply sufficient amounts of nutrients in a minimum volume of water. These techniques with simultaneous monitoring of urinary excretion of 3-methylhistidine and creatinine height index as nutritional parameters make nutritional management easy for patients with liver disease.
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PMID:Nutritional management of patients with severe liver disease by using intravenous hyperalimentation and elemental diet. 676 41

Although protein-energy malnutrition is common in the cancer patient, the efficacy of aggressive nutritional therapy is unclear. This study evaluates the effects of protein deficiency on tumor growth, response, and chemotherapy complications in primary and metastatic rat hepatoma. Seventy-two ACI rats (200-250 g) with implanted Morris hepatoma were divided into four groups (N = 18 for each group): 1, regular diet; 2, regular diet plus cyclophosphamide (CPM) (100 mg/kg/ip); 3, protein-free diet; and 4, protein-free diet + CPM. Forty additional rats in similar groups (5-8, ten in each group) underwent intravenous injection of 6 X 10(3) tumor cells to produce pulmonary metastases. Animals were assessed for survival, tumor size, serum albumin, number of pulmonary metastases, and hemorrhagic cystitis at 2 weeks. Survival was 50% in groups 4 and 8, and 100% in the others. Serum albumin was significantly lower in rats on protein free diets (2.59 +/- 0.37 vs 3.35 +/- 0.40 g%, P less than 0.01). Tumor volume was significantly reduced by CPM (26.0 +/- 4.2 cm3 vs 1.2 +/- 0.4 cm3, P less than 0.01). Protein-free diets resulted in lower total body weight, and reduced tumor volume without, but not with CPM (14 +/- 1.6 cm3 P less than 0.05, 1.1 +/- 0.3 cm3, P less than 0.05 vs above controls). CPM reduced the number of pulmonary metastases in regular diet groups (307.2 +/- 108.3 vs 36 +/- 11, P less than 0.01), while protein free diets did not significantly affect metastases, without or with CPM (251.7 +/- 71.4 and 22.3 +/- 12.4, P greater than 0.05 vs controls). Hemorrhagic cystitis was much more common in protein free groups compared to rats on regular diets (55 vs 11%, P less than 0.01). These data indicate that protein deficiency did not affect response to chemotherapy in a primary or metastatic rat hepatoma model. However, protein deficiency results in a significantly increased rate of mortality, weight loss, and hemorrhagic cystitis which may lead to delay or cessation of cancer therapy.
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PMID:The effect of protein deficiency on growth and response of primary and metastatic hepatoma. 684 9

Rats fed a choline deficient diet develop foci of enzyme-altered hepatocytes with subsequent formation of hepatic tumors. This is the only nutritional deficiency that, in itself, causes cancer. We suggested that carcinogenesis is triggered, in part, because of abnormalities in cell signals which regulate cell proliferation and cell death. Because choline deficient rats develop fatty liver (choline is needed for hepatic secretion of certain lipoproteins), we examined whether an important lipid second messenger involved in proliferative signaling, 1,2-sn-diacylglycerol, accumulated in liver and resulted in the prolonged activation of protein kinase C. We observed that 1,2-sn-diacylglycerol accumulated in the plasma membrane from the non-tumor portion of livers of rats fed a choline deficient diet, and that unsaturated free fatty acids, another activator of protein kinase C, also accumulated in deficient livers. Protein kinase C in the hepatic plasma membrane and nucleus of choline deficient rats was elevated for months; this is the only model system which exhibits such prolonged activation of protein kinase C. Premalignant, abnormal hepatic foci were detected only in the deficient rats, and 15% of deficient rats (none of the controls) had hepatocellular carcinoma at 1 year on the diet. In rats, an early event in choline deficiency is an increase in the rate of cell death. In liver from choline deficient rats, we observed an increase in the numbers of liver cells with fragmented DNA (characteristic of programmed cell death; apoptosis). We used a cell culture model (immortalized rat hepatocytes) to study the effects of choline deficiency on apoptosis. Liver cells grown in a choline deficient medium became depleted of choline, accumulated triacylglycerol and 1,2-sn-diacylglycerol, and had increased DNA fragmentation and other morphologic and biochemical changes associated with apoptosis. This model has great potential as a tool for studying the underlying link between choline deficiency and the regulation of the balance between cell proliferation and cell death. We suggest that choline deficiency altered the cell proliferation signals mediated by protein kinase C within liver, and altered cell apoptosis. These changes in cell signaling may be the triggering events which result in hepatic carcinogenesis.
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PMID:Choline and hepatocarcinogenesis in the rat. 764 29

The role of malnutrition in the development of cachexia in rats bearing the Yoshida ascites hepatoma AH-130 was investigated by comparing the changes in tissue protein turnover in these animals with those observed in pair-fed controls. The tumor elicited in rats an early and conspicuous loss of body weight and tissue waste. Protein loss was particularly prominent for the gastrocnemius muscle and the heart and less pronounced for the soleus, while the diaphragm was little affected. Liver, kidneys, and spleen transiently increased in weight then regressed and eventually atrophied, while adrenals were enlarged over the whole experimental period. Protein waste was mainly due to acceleration of tissue protein breakdown, this protein hypercatabolic state being associated with increased cathepsin D activity in liver and gastrocnemius. In pair-fed animals the liver showed a marked protein loss resulting from enhanced catabolism, while the sharp decrease of heart protein content and the less prominent waste of the gastrocnemius were due to a reduction in protein synthesis. The total plasmatic concentration of free amino acids in AH-130-bearing rats was decreased at Day 4, when the tumor was actively proliferating, and returned to control values at Day 10, when the tumor had reached a stationary state. On the contrary, in pair-fed animals total plasma amino acids decreased over the whole experimental period. Plasma branched-chain amino acids were unchanged or even decreased in tumor hosts, while the Gly/Pro ratio was elevated in pair-fed rats. The intracellular concentration of free amino acids was higher in stationary than in exponentially- growing tumors, reflecting the enhanced proteolytic rates observed in stationary tumor cells. On the whole, the results suggest that reduced food uptake and metabolic competition by the tumor are not sufficient to justify the marked hypercatabolism in host tissues during the AH-130 hepatoma growth. The profound differences between tumor-bearing and pair-fed animals suggest that, if malnutrition undoubtedly played a role in this model of cancer cachexia, its effects were overwhelmed and subverted in the frame of the tumor-host interplay that dictated a distinctively peculiar syndrome.
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PMID:Cancer cachexia, malnutrition, and tissue protein turnover in experimental animals. 821 20

Choline deficiency, via deprivation of labile methyl groups, is associated with a greatly increased incidence of hepatocarcinoma in experimental animals. This dietary deficiency also causes fatty liver, because choline is needed for hepatic secretion of lipoproteins. We hypothesized that fatty liver might be associated with the accumulation of 1,2-sn-diradylglycerol and subsequent activation of protein kinase C. Several lines of evidence indicate that cancers might develop secondary to abnormalities in protein kinase C-mediated signal transduction. We observed that rats fed a choline-deficient diet for 1, 6, or 27 weeks had increased hepatic concentrations of 1,2-diradylglycerol. At 1 and 6 weeks, hepatic plasma membrane from choline-deficient rats had increased concentrations of 1,2-sn-diacylglycerol and 1-alkyl, 2-acylglycerol, with the latter accounting for 20-26% of membrane 1,2-sn-diradylglycerol (as compared with only 2-5% in controls). Protein kinase C activity was increased in hepatic plasma membrane at 1 week of choline deficiency. By Western blotting there was an increase in the amount of protein kinase C zeta and a decrease in the amount of protein kinase C delta in liver at 1 week. By 6 weeks of choline deficiency, hepatic plasma membrane and cytosolic protein kinase C (PKC) activities were increased significantly, with increased amounts of hepatic plasma membrane protein kinase C alpha, and delta detected by Western blotting. Glycogen synthase activity in liver was diminished after 1 week of choline deficiency; this enzyme is inhibited by PKC-mediated phosphorylation. We suggest that choline deficiency perturbed PKC-mediated transmembrane signaling within liver and that this contributed to the development of hepatic cancer in these animals.
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PMID:Accumulation of 1,2-sn-diradylglycerol with increased membrane-associated protein kinase C may be the mechanism for spontaneous hepatocarcinogenesis in choline-deficient rats. 842 Sep 80

Primary biliary cirrhosis (PBC) remains one of the commoner indications for orthotopic liver replacement. The two main indications for transplantation are poor quality of life (because of the liver) or end-stage liver disease. A number of prognostic models have identified risk factors indicating poor prognosis, but in practice serum bilirubin greater than 150 mumol/L is used most commonly. Other indications for transplantation include progression of hepatopulmonary syndrome, increasing osteoporosis, evidence of malnutrition, and development of hepatocellular carcinoma. Postoperatively, patients do well. Recurrence of PBC remains controversial, but an increasing number of centers now report that a proportion of patients develop evidence of recurrent disease in the allograft. As yet PBC recurrence remains of little practical importance, although as survival increases beyond 10 years, this may become more relevant.
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PMID:Transplantation for primary biliary cirrhosis. 917 Feb 1


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