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

Superoxide dismutase (SOD) activity and content of lipid peroxides (LPO) in human hepatocellular carcinoma (HCC) tissue were studied. It was observed that SOD activity and LPO content in HCC tissue were lower than those in normal liver tissue (P less than 0.001 respectively). The contents of copper, zinc and manganese in HCC tissue were also lower than those in normal liver tissue (P less than 0.001, P less than 0.05). Furthermore, LPO content in necrotic HCC tissue was higher than that in non-necrotic HCC tissue (P less than 0.05). The results suggest that deficiency of copper, zinc and manganese in HCC tissue may be a contributing factor that leads to impairment of SOD activity. Decreased SOD activity in liver cancer cells was a negative feedback of the multiplication of cancer cells loss of lipid peroxidation explains the malignancy of HCC, and enhanced lipid peroxidation in liver cancer cells may cause the necrosis of cancer cells.
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PMID:[Impaired superoxide dismutase activity and decreased content of lipid peroxides in hepatocellular carcinoma tissue]. 165 38

To provide clues to the causes of liver cancer in China, we studied the correlation of certain dietary and biochemical markers with liver cancer mortality across 65 Chinese counties. Mortality rates were significantly linked to the county-wide prevalence of hepatitis-B surface antigen positivity. Rates were also higher in counties with high plasma levels of total cholesterol and high consumption of liquor, rapeseed oil, and mouldy corn, while inverse associations were observed for wheat consumption. All of the observed associations, except those with cholesterol and rapeseed oil, were more pronounced in men than in women. No significant correlations with liver cancer mortality were found for consumption of several other foods; plasma levels of retinol, beta-carotene, alpha-tocopherol, selenium, zinc and ferritin; or urine levels of aflatoxin B1. Although causal inferences cannot be derived, this ecological study suggests that chronic infection with hepatitis-B virus contributes to the substantial variation in liver cancer mortality in China, and provides leads for further studies into the role of dietary and nutritional determinants.
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PMID:Correlates of liver cancer mortality in China. 206 44

We have measured zinc levels in serum and urine of healthy controls, patients with liver cirrhosis and patients with cirrhosis and hepatic cancer. In patients with ascitic fluid, we also measured zinc, total protein, albumin and alpha 2-globulin. Basal measurements were performed in blood drawn at 8.00, before the intravenous administration of 8 mg zinc in the form of zinc sulphate. Serum levels were measured at various intervals to a total time of 24 h after overload, and total urine was collected for zinc determinations 24 h before and 24 h after overload. Under basal conditions, cirrhotic patients had lower serum levels and higher rates of urinary excretion of zinc than controls. After overload, blood levels of zinc fell more rapidly in cirrhotic patients than in controls, the former group showing no concomitant rise in urinary zinc excretion, thus suggesting an organic deficit in this trace element. In ascitic fluid, the concentration of zinc was positively correlated with protein content.
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PMID:Zinc and liver cirrhosis. 207 94

Serum and urinary zinc were assessed in 53 patients with a variety of chronic liver diseases (CLD) and 59 healthy volunteers using atomic absorption spectrophotometry. Liver zinc was also assessed in 18 patients and 10 controls. All patients had significantly lower serum zinc (mean = 36.3 +/- 2.9 ug/dl) than controls (79.3 +/- 4.0 ug/dl) and higher urinary excretion (651.0 +/- 53 ug/24 hrs) than controls (316.0 +/- 26 ug/24 hrs). Mean liver zinc was also lower in cirrhotic patients (85.10 +/- 21.31 ug/g) than control values (112.40 +/- 31.72 ug/g) but patients with schistosomiasis had identical values with controls. Decreasing levels were noted from chronic hepatitis through cirrhosis to primary liver cancer and decompensated patients had lower levels than well-compensated disease. No difference was seen between alcoholic and non-alcoholic cirrhotics. This study indicates that hyperzincuria occurs in association with zinc deficiency in CLD, an abnormality which may be important in the genesis of some features of the disease.
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PMID:Zinc status in chronic liver disease; studies in Nigerian patients. 208

Superoxide dismutase (SOD) activity in hepatocellular carcinoma (HCC) tissue was studied. It was observed that activities of total SOD, Cu, Zn-SOD and Mn-SOD in HCC tissue were lower than those in normal liver tissues respectively (P less than 0.001 & 0.01 less than P less than 0.05). SOD activity in poorly differentiated HCC tissue was lower than that in well differentiated HCC tissue. Contents of copper, zinc and manganese in HCC tissues were lower than those in normal liver tissues respectively (P less than 0.001 & P less than 0.01). This study suggests that decreased content of copper, zinc and manganese may be one of the factors that lead to impairment of SOD activity. The characteristic of lower SOD activity in HCC tissue and poorly differentiated HCC tissue may be a negative regulation to limitless proliferation and poor differentiation of liver cancer cells.
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PMID:[Superoxide dismutase activity in tissues from 19 cases of hepatocellular carcinoma]. 216 38

The role of nutrients in cancer causation has been a subject of considerable interest, research, and public discussion in recent years. Results from epidemiologic, clinical, and animal studies have suggested that: 1) a reduction in total calories decreases risk for a number of tumor types; 2) dietary protein is directly correlated with liver, prostate, and colon cancer, among others, with increasing dietary protein increasing the risk; 3) increased dietary fat is correlated with increased risk for breast cancer; the evidence for an effect of fat on colon cancer is equivocal in human and animal studies; 4) a deficiency of vitamin A may enhance lung and colon tumors in animal experiments but in human this is equivocal. Increasing vitamin A above normal levels, as an anticarcinogenic effect, has not been satisfactorily demonstrated in animal models. The synthetic retinoid, 13-cis retinoic acid, inhibits both colon and lung cancer in animal models; 5) zinc deficiency is associated with enhanced esophageal cancer in humans and markedly enhances animal tumors; selenium inhibits this form of neoplasia in animals, 6) diets low in lipotropes enhance liver cancer induced by a variety of hepatocarcinogens. Our data from studies in animal models agree in some cases with epidemiological observations, but disagree with others, particularly fat and colon cancer. Overall, some forms of cancer are enhanced by excessive calories, increased dietary protein and fat, and by deficiencies of vitamin A, selenium, zinc, and lipotropes. Decreasing total intake of calories, protein, and fat, and ensuring adequate dietary levels of vitamin A, selenium, zinc, and lipotropes decreases risk for some forms of cancer.
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PMID:The role of nutrients in cancer causation. 243 54

The levels of trace elements in serum of the patients with liver cancer and the normal subjects were determined by the PIXE technique. The significant increase of serum copper level (SCL) and the decrease of serum zinc level (SZL) in the patients with liver cancer, as compared to those of normal, were observed. Cu/Zn ratio in the patients with liver cancer was significantly higher than that of the normal (P less than 0.01). In the Cartesian coordinate graph of SCL + SZL, the liver cancer patients were separated from the normal by a line joining the intersection of abscissa and ordinate and the point of the sum of the mean value and the standard deviation of the Cu/Zn ratio of the normal subjects. The authors believe that the serum Cu/Zn ratio is likely a supplementary target in the diagnosis and prognosis of liver cancer.
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PMID:[Analysis of trace elements by proton induced X-ray emission (PIXE) in serum of patients with liver cancer and normal subjects]. 301 27

HCC occurs in a higher incidence in some subsets of human populations residing in specific geographic areas around the world. These include black populations residing south of the Sahara, particularly in South and East Africa; in populations of Southeast Asia and the Western Pacific; in India, China, and in some other circumscribed areas. These epidemiologic observations strongly suggest that environmental factors are involved in the etiology of HCC. Evidence from human and animal data point toward a multicausal etiology, including dietary or environmental contamination with mycotoxin carcinogens, acting in concert with hepatitis B viral infection and, in some areas, with malnutrition. Dietary factors that appear to influence susceptibility to HCC include fat, protein and amino acids, vitamin A, selenium, and zinc. In addition, alcohol consumption, environmental chemicals that are natural or man made, and genetic predisposition must also be considered. It seems likely that identification of etiologic agents (hepatitis B infection, aflatoxin, malnutrition) and correction or prevention of these are the most promising means for controlling HCC in man.
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PMID:Chemical carcinogenesis: mycotoxins and other chemicals to which humans are exposed. 608 58

A number of biochemical events accompany the development of chronic liver disease and its evolution into hepatic cancer. Low plasma zinc and high plasma copper levels have been observed in individuals with advanced hepatocellular liver disease. Moreover, many investigators have demonstrated an increase in serum estradiol levels in individuals with chronic liver disease and hepatocellular carcinoma (HCC). In the present study, the relationship between these biochemical events and HCC was investigated in an animal model. Specifically, carbon tetrachloride (CCL4) was administered intragastrically to 20 female Sprague Dawley rats for 30 weeks. All 20 animals developed cirrhosis. Six (30%) developed HCC. Significantly higher serum estradiol, zinc and copper levels were observed in the rats developing HCC as compared with those with cirrhosis alone (P < or = 0.05, 0.01 and 0.001, respectively). A trend toward increased serum levels of progesterone, ALT and total bilirubin (0.1 > or = P < or = 0.05) was found in the animals developing HCC. No differences in serum testosterone and alkaline phosphatase levels were noted between animals with and without HCC. These studies demonstrate that in animals with experimental CCL4-induced cirrhosis and HCC serum levels of estradiol, zinc and copper are increased, as is the case in man.
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PMID:CCL4-induced liver cirrhosis and hepatocellular carcinoma in rats: relationship to plasma zinc, copper and estradiol levels. 795 73

Recently we have demonstrated that the human hepatocellular carcinoma-derived cell lines, HepG2 and HuH7, contain gonadotropin-releasing hormone (gonadoliberin) receptors and respond to various molecular forms of gonadoliberin in terms of suppressed proliferation in vitro. This study provides the first demonstration that gonadoliberin inhibits the zinc-induced production of metallothionein mRNA in HepG2 and HuH7 cells. Administration of gonadoliberin agonist (gonadoliberin-A) inhibited the Zn-induced metallothionein mRNA level in a time-related and dose-related manner. The effect of gonadoliberin-A was found to be specific, because concomitant treatment with a gonadoliberin antagonist (gonadoliberin-ANT) blocked gonadoliberin-A inhibition of metallothionein mRNA accumulation. Furthermore, the gonadoliberin-A-induced inhibition of Zn-mediated metallothionein accumulation was found to correlate closely with suppresion of cell proliferation and [3H]thymidine uptake in these cells. It is known that the metal-binding protein metallothionein plays an important role in tumor cell pathobiology and resistance to chemotherapeutic drugs. The present findings may have important implications in the development of an effective chemotherapy for treatment of human liver cancer, in part, by improving the sensitivity of tumor cells through suppression of metallothionein production by gonadoliberin peptides.
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PMID:Inhibition of zinc-induced metallothionein mRNA accumulation by gonadotropin-releasing hormone in human hepatocarcinoma cell line HepG2. 895 50


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