Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sex-specific mortality rates for selected cancer sites (including oesophagus, stomach, liver, lung, colorectum, breast and cervix) and a variety of biochemical indicators of antioxidant status, enzyme activity and oxidative stress (including plasma levels of beta-carotene, alpha-tocopherol, ascorbic acid, selenium, glutathione peroxidase, catalase, superoxide dismutase, iron, copper, zinc, total cholesterol and lipid peroxide) were examined in an ecological study of 65 mostly rural counties in the People's Republic of China. The wide range of both mortality rates and biochemical values and the measurement of a comprehensive set of biochemical indicators permitted both simple correlational and multivariate analyses of the joint and relative effects of each factor on site-specific cancer mortality. Plasma levels of dietary antioxidants were consistently negatively correlated with cancer mortality rates. Ascorbic acid was most strongly negatively associated with most cancers and selenium with oesophageal and stomach cancers. beta-carotene was found to have a protective effect independent of retinol, particularly for stomach cancer.
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PMID:Antioxidant status and cancer mortality in China. 152 64

The influence of dietary selenium on the incidence of stomach carcinoma induced by N-methyl-N'-nitro-N-nitrosoguanidine was studied in 108 rats that survived for over 10 wk. The incidence of glandular stomach cancer in the high-selenium (4.0 ppm) diet group (20 carcinomas in 54 rats) was lower than in the low-selenium (0.1 ppm) diet group (33 carcinomas in 54 rats). The selenium level and glutathione peroxidase activity in the blood, liver, and stomach mucosa were significantly higher in the high-selenium diet group than in the low-selenium diet group. Glutathione peroxidase activity as well as the concentration of selenium in the glandular stomach was increased significantly in the high-selenium diet group.
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PMID:Inhibitory effect of dietary selenium on carcinogenesis in rat glandular stomach induced by N-methyl-N'-nitro-N-nitrosoguanidine. 369 71

Selenium (Se) compounds have shown an inhibitory effect on chemically induced tumours in several laboratory models and there is an inverse epidemiological relationship between Se status and certain types of cancer. Little is known about the influence of Se on the development of stomach cancer. Three different forms of dietary Se, selenomethionine, sodium selenite, and high-selenium yeast were investigated as possible inhibitors of benzo(a)pyrene-induced forestomach tumours in mice. The effects of sodium selenite in combination with vitamin E, and of Se-deficiency were also studied. None of the dietary modifications had any effect on tumour incidence or number. Marked elevations of whole-blood glutathione peroxidase (GSH-Px) activities were observed in animals supplemented with all Se-compounds. High-selenium yeast caused the largest increase of GSH-Px activity followed by sodium selenite and selenomethionine. The results indicate that the inhibitory effect of Se on carcinogenesis may be specific with respect to organ site or tumour cell examined.
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PMID:Effects of dietary selenium compounds on benzo (a)-pyrene-induced forestomach tumours and whole-blood glutathione peroxidase activities in C3H mice. 375 57

In 68 subjects the activities of Cu/Zn-superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were investigated in gastric mucosa. The patients were classified according to the histological finding into following groups: 12 with normal finding (N), 16 with superficial gastritis (SG), 13 with mild atrophic gastritis (MAG), 19 with severe atrophic gastritis (SAG) and 8 with gastritis after partial gastrectomy (PGG). The comparison of groups SG, MAG, SAG and PGG with the group N revealed the following changes: in SG increased SOD and GSH-Px, in MAG and SAG no significant changes, and in PGG increase in SOD, CAT and GSH-Px were observed. It was supposed that increased enzymatic activities were caused by higher concentration of active oxygen species produced by phagocytizing leukocytes in inflamed gastric mucosa. Administration of vitamin E resulted in significant reduction of SOD and CAT activities, on the other hand GSH-Px activity significantly increased. The explanation of this effect of vitamin E requires further studies. A prolonged interaction of active oxygen species with chemical carcinogens (N-nitroso- or diazonium compounds, PAH) can exhibit a significant promoting effect on the development of intestinal type of gastric cancer from its precancerous conditions, above all after partial gastrectomy.
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PMID:Gastric mucosal antioxidant activity in patients at increased risk of gastric cancer. 827 61

Risk factors for gastric cancer are receiving renewed attention in light of the recent positive association of Helicobacter pylori infection with gastric cancer. The effect of H.pylori on the balance between oxidants and antioxidants in the stomach is not well known. In this study, we investigated if exposure of gastric cells to H. pylori increases oxidant-associated gastric epithelial cell injury. A human gastric epithelial cell line (AGS) was grown on 96-well clusters, then exposed overnight to either live H.pylori (four cagA(+) and four cagA(-)) or broth culture supernatant from an isogenic H.pylori cagA(+) strain with and without vacA activity. Incubation of AGS cells with cagA(+) and cagA(-) H.pylori strains before exposure to reactive oxygen species (ROS) reduced cell viability on average to 73.7% and 39.5% of controls, respectively. The percent viability of cells exposed to ROS after incubation with control broth, vacA(-) broth and vacA(+) broth was 97.7%, 70.5% and 63.5%, respectively. Experiments were then performed to evaluate the effects of H.pylori exposure on the activities of ROS-scavenging enzymes [catalase, glutathione peroxidase and superoxide dismutase (SOD)] and formation of 8-hydroxy-2-deoxyguanosine (8-OH-dG) adducts in AGS cells. Overnight exposure to cagA(-) strains reduced catalase activity by 42%; in contrast, exposure to cagA(+) H.pylori strains increased catalase activity by 51%. Glutathione peroxidase activity increased with exposure to both cagA(-) and cagA(+) strains by 95% and 240%, respectively. Total SOD activity increased 156% after exposure to cagA(+) strains and was marginally increased (52%) with exposure to cagA(-) strains. CuZn-SOD protein levels, assayed by enzyme-linked immunosorbent assay, were not significantly altered by exposure to H.pylori strains; however, Mn-SOD concentrations were significantly increased (P: < 0.02) after exposure to both cagA(-) and cagA(+) H.pylori strains. Exposure of AGS cells to cagA(+) and cagA(-) H.pylori was associated with, on average, 44.5 and 99.0 8-OH-dG/10(6) dG, respectively. The increase in catalase, glutathione peroxidase and SOD activity is associated with fewer 8-OH-dG DNA adducts and reduced susceptibility of AGS cells to lethal injury from ROS after exposure to cagA(+) H.pylori strains when compared with exposure to cagA(-) H.pylori strains. Alteration in the activity of ROS-scavenging enzymes by the presence of H. pylori may in part be responsible for the increased risk of gastric cancer in persons infected with H.pylori.
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PMID:Influence of Helicobacter pylori on reactive oxygen-induced gastric epithelial cell injury. 1106 73

Helicobacter pylori infection stimulates several intracellular signaling pathways and is accompanied by increased gene expression in gastric epithelial cells. High-density cDNA microarray was used to characterize the mRNA expression profile of genes in human gastric cancer cells (MKN45, AGS) cocultured with H. pylori. Coculture with cag pathogenicity island (PAI)-positive H. pylori (wild-type) significantly up-regulated mRNA expression in 8 of 2304 genes tested. In 6 (interleukin-8, I(kappaB)alpha, A20, ERF-1, keratin K7, glutathione peroxidase) of the 8 genes, up-regulation was confirmed by RT-PCR. In coculture with isogenic cagE-negative mutant ((Delta)cagE), which encodes a type IV secretion system with other genes in the cag PAI, no significant up-regulation was found. We further analyzed the role of A20. Transfection of expression vector encoding A20 resulted in an inhibition of H. pylori-mediated NF-kappaB activation, indicating that H. pylori-mediated A20 expression could be a negative regulator of NF-kappaB activation. Taken together, these results indicate the importance of microarray technology as a tool for analyzing the complex interplay between H. pylori and the host.
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PMID:cDNA microarray analysis of Helicobacter pylori-mediated alteration of gene expression in gastric cancer cells. 1139 99

To identify genes whose alterations lead to gastric cancer, gene expression profiles have been obtained from 22 gastric cancer tissues and their surrounding gastric mucosa tissues. A total of 16 genes were differentially expressed in more than 50% of gastric cancer tissues compared with surrounding gastric mucosa tissues. Genes such as HMG-Y, fibroblast collagenase inhibitor, and osteopontin are among those that are overexpressed in over 50% of the gastric cancer tissues. Dihydrodiol dehydrogenase, ribonuclease A, and glutathione peroxidase are among those genes that are underexpressed in over 50% of the gastric cancer tissues. We identified genes that are associated with clinical phenotypes of patients with gastric cancers. Alpha-II spectrin, Na/K-ATPase and KIAA0111 are those that are enhanced in intestinal type of gastric cancer. Gene such as platelet-endothelial tetraspan antigen 3 was enhanced in highly metastatic gastric cancer tissues.
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PMID:Identification of genes differentially expressed between gastric cancers and normal gastric mucosa with cDNA microarrays. 1212 92

In this study, levels of lipid peroxidation and antioxidant enzyme activities were investigated in the erythrocytes of patients with oesophageal and gastric cancers. Erythrocytes were obtained from 17 patients with oesophageal cancer, 37 patients with gastric cancer and 20 healthy controls. Levels of malondialdehyde (MDA), a lipid peroxidation marker, and activities of copper- and zinc-containing superoxide dismutase (CuZn-SOD), catalase (CAT) and glutathione peroxidase (GPx) were determined using spectrophotometric methods. MDA levels and CuZn-SOD activity were significantly higher and GPx and CAT activities significantly lower in patients with oesophageal and gastric cancer than in controls. There were no statistically significant differences in the parameters measured in relation to disease stage in either patient group. These results indicate significant changes in the antioxidant defence system in patients with oesophageal and gastric cancer. It is postulated that this may lead to enhanced action of oxygen radicals, resulting in lipid peroxidation.
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PMID:Antioxidant enzyme activities and lipid peroxidation levels in erythrocytes of patients with oesophageal and gastric cancer. 1674 15

In the present study, total nitrate and nitrite level (as end product of nitric oxide), superoxide dismutase activity, and glutathione peroxidase activity in leukocytes were determined in patients with gastric cancer, and the relationship between measured parameters and tumor grade were evaluated. Leukocyte nitrate and nitrite level was found to be increased and superoxide dismutase activity was found to be decreased in patients compared to controls. When the patient group was categorized, nitrate and nitrite level was found to be higher in patients with a high-grade tumor than in patients with a grade I tumor. We concluded that an increased level of leukocyte nitrate and nitrite is related to tumor grade in patients with gastric cancer; antioxidant activity is also impaired in these patients but it does not seem to be related to grade of tumor.
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PMID:Nitric oxide and antioxidant defense in patients with gastric cancer. 1686 32

Oxidant/antioxidant balance has been suggested as an important factor for initiation and progression of cancer. In order to determine whether the degree of oxidative DNA damage and antioxidant enzyme activities in plasma obtained from patients with gastric and colon cancer who undergo resection can be used as a useful prognostic predictor, plasma level of 8-hydroxydeoxyguanosine (8-OHdG), activities of glutathione peroxidase (G-Px) and superoxide dismutase (SOD) were examined. 19 patients with gastric cancer and 26 patients with colon cancer who were undergoing resection of tumor were included by the study. Venous blood samples were taken just before the surgery. Plasma level of 8-OHdG was determined with ELISA, SOD and G-Px activities in plasma were measured by spectrophotometric kits. 8-OHdG level and activity of G-Px were found to be decreased, SOD activity was found to be increased in both gastric and colon cancer groups as compared to control group. Alpha fetoprotein was found to be correlated with G-Px in the gastric cancer group and correlated with 8-OHdG in the colon cancer group. SOD activity was correlated with CA-15-3 in the gastric cancer group. Low plasma level of 8-OHdG and altered antioxidant activity may implicate the deficient repair of oxidative DNA damage in patients with gastric and colon cancer. Those measured parameters were not found to be related with histopathological data but correlated with some tumor markers.
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PMID:Prognostic significances of oxidative DNA damage evaluated by 8-hydroxy-deoxyguanosine and antioxidant enzymes in patients undergoing resection of gastric and colon carcinoma. 1731 86


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