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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were made on the effect of mucin on the induction of gastric carcinomas by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), with or without sodium chloride, in male Wistar rats. Seven groups of rats were treated as follows: Group 4 was given continuously 50 mg MNNG/liter solution to drink and 1 ml of saturated sodium chloride once a week and fed on stock diet supplemented with 4% mucin. Group 2 was given 50 mg MNNG/liter solution and fed on stock diet supplemented with 4% mucin. Group 3 received 1 ml of saturated sodium chloride once a week and 50 mg MNNG/liter solution to drink. Group 1 was treated with MNNG only. Group 5 was fed on stock diet supplemented with 4% mucin. Group 6 was given sodium chloride only. Group 7 was untreated. The incidence of gastric cancer in Group 3 was significantly higher than that in Group 4 (P less than 0.05) or in Group 1 (P less than 0.05). The difference in the incidence of gastric cancer in Groups 2 and 4, and of intestinal tumors in Groups 1 to 4 were not statistically significant. No malignant tumors were seen in Groups 5, 6, and 7. Thus mucin reduced the high incidence of gastric cancer induced by MNNG and sodium chloride to the level induced by MNNG alone, but it had no effect on the incidence of intestinal tumors. The effect of mucin in preventing destruction of the gastric mucosal barrier by sodium chloride and so reducing the induction of gastric cancer is discussed.
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PMID:Protective effect of mucin on experimental gastric cancer induced by N-methyl-N'-nitro-N-nitrosoguanidine plus sodium chloride in rats. 96 54

Methods have been established to produce gastric cancer in rats and dogs by administration of N-methyl-N'-nitro-N-nitrosoguanidine or of the ethyl derivate. The agent is administered in drinking water or by a pellet diet soaked in the carcinogen. Histologically well differentiated and poorly differentiated types of adenocarcinoma and signet-ring cell tumors are induced in several months with greath reliability. Metastases were observed in both rats and dogs with gastric carcinoma. The carcinogenic effect could be enhanced by surface active agents, sodium chloride, iodoacetamide, insertion of plastic beads into the stomach and gastroenteroanastomosis. Follow-up studies by radiologic, endoscopic and bioptic examinations are possible in the dog. There are similarities in these experimental tumors to those in man and thus they provide means for the investigation of histogenesis, prevention, and chemotherapy of gastric cancer. An adenocarcinoma of the glandular stomach of a Wistar rat was successively transplanted to new born rats of the same strain.
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PMID:[Experimental gastric cancer (author's transl)]. 96 36

Catechol and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) are gastric carcinogens in rats. Catechol, sodium chloride and bile salts have enhancing effects on gastric carcinogenesis induced by MNNG in rats. The effects of these compounds on proliferation of pyloric mucosa cells in male F344 rats were examined immunohistochemically using bromodeoxyuridine (BrdU) and anti-BrdU monoclonal antibody. Rats were given MNNG (83 micrograms/ml in their drinking water), catechol (0.8% in their diet), sodium taurocholate (0.3% in their diet), sodium taurodeoxycholate (0.3% in their diet), or sodium chloride (10% in their diet or by intragastric administration of 1 ml of saturated solution once a week) for 4 weeks. All these treatments markedly enhanced cell proliferation of the pyloric epithelium, suggesting the importance of enhanced cell proliferation in the development of gastric cancer.
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PMID:Effects of 4-week treatment with gastric carcinogens and enhancing agents on proliferation of gastric mucosa cells in rats. 275 82

In a series of extensive studies on gastric carcinogenesis, we have used Sprague-Dawley rats to examine the morphologic, histochemical, and biochemical effects of risk and protective factors on N-methyl-N'-nitro-N-nitroso guanidine (MNNG)-induced tumors in an attempt to link early observations with the end-point lesion, gastric cancer. We have observed that the putative risk factors sodium chloride (NaCl); a mixture of bile acids; aspirin; alcohol; and nitrite enhance MNNG-induced neoplasia of the gastric mucosa. On the other hand butylated hydroxyanisol (BHA), Se and difluromethylornithine (DFMO) were protective and inhibited the induction of gastric mucosal neoplasia. In most cases, early changes detected by a number of criteria correlated with the end-point, gastric neoplasia. This model appears to be useful in screening and evaluating chemicals for risk for or protection against gastric cancer.
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PMID:Gastric carcinogenesis: a model for the identification of risk factors. 312 Nov 66

Atrophic gastritis with intestinal metaplasia cannot be regarded as a form of precancerous change, but it is of profound significance in the development of gastric carcinoma. It would be reasonable to infer that those subjects who have atrophic gastritis with intestinal metaplasia to any great extent represent a high-risk population for gastric cancer. Environmental factors, especially dietary habits, are implicated in the etiology of gastric carcinoma. Intake of high concentrations of sodium chloride is assumed to promote the development of carcinoma of the stomach. Cigarette smoking is also one of the risk factors in the pathogenesis of gastric cancer, supposedly acting as an initiator in gastric tumorigenesis. Although a controversy exists as to whether gastric resection for benign ulcers enhances the subsequent development of gastric carcinoma, it appears likely that an increased amount of long-term duodenogastric reflux after partial gastrectomy results in a higher incidence of carcinoma in the stomach remnant.
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PMID:[High-risk population of gastric cancer patients]. 363 68

The difficulties in the estimation of daily intake of sodium chloride in populations are discussed. Total daily output calculations are hindered by the difficulties investigators encounter in obtaining accurate 24-hour urine collections in field work situations. As an alternative, urinary sodium-to-creatinine ratios were investigated. Such ratios, which do not change significantly with circadian excretion rhythms, are useful indicators of the amount of sodium excreted in the urine. Preliminary observations in Colombian populations at high and low risk of gastric cancer indicated higher sodium excretion in the high-risk group. Loss of sodium by other means, especially perspiration, needs to be estimated in some other way.
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PMID:Urinary sodium-to-creatinine ratio as an indicator of gastric cancer risk. 383 21

To test the hypothesis that excessive intake of sodium chloride is a factor in gastric carcinogenesis, urinary excretion of sodium and creatinine was measured in Colombian subjects. Age, sex, weight, and height regression slopes for creatinine excretion were more similar in Colombia than in other countries. Sodium/creatinine (S/C) ratios correlated with 24-h urinary excretion of sodium revealed higher sodium excretion in populations with higher gastric cancer rates. The S/C ratios were not affected by circadial rhythms, making it possible to use single urine samples to investigate interpopulation differences in sodium excretion.
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PMID:Sodium intake and gastric cancer. 397 84

Dietary sodium chloride has been identified, both experimentally and epidemiologically, as a risk factor for gastric cancer. In order to elucidate the manner in which salt increases gastric tumor incidence in N-methyl-N'-nitro-N-nitrosoguanidine-treated animals, flow cytometric cell cycle analyses were performed on rats which had been treated with 1 ml of a solution of saturated NaCl by gavage and sacrificed 0, 1, 6, 12, 24, or 48 h after treatment. The gastric antra were excised, disaggregated, and stained with propidium iodide for cell cycle analysis. Results showed that there is a reduction in cell yield at early time points due to the toxicity of NaCl, followed by a net increase in the number of cells in the S phase of the cell cycle at 24 h. Treatment of rats with NaCl 24 h prior to a dose of 10 micrograms of 3H-labeled N-methyl-N'-nitro-N-nitrosoguanidine did not lead to an increase in alkylation of DNA isolated from mucosal cells. Therefore, the hypothesis that salt enhances gastric cancer risk from N-methyl-N'-nitro-N-nitrosoguanidine by disruption of the "mucosal barrier" leading to an increased effective dose to target cells is not supported by the results of these experiments. Several studies have shown that cells in S phase are the most susceptible to mutagenesis and that increasing the number of cycling cells in a target organ will increase tumor incidence (e.g., partial hepatectomy). Thus it is possible that NaCl increases gastric cancer risk through the mitogenesis which results from the damage caused to the mucosa by this agent.
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PMID:Flow cytometric analysis of the effect of sodium chloride on gastric cancer risk in the rat. 405 34

The effect of rice and salty rice diets on stomach morphology was investigated in Swiss/ICR mice. Mice were fed rice, salty rice, or standard pellet diets for 3-12 months, starting when the mice were 4 weeks of age. Long-term maintenance on the rice or salty rice diet increased the dimension and wet weight of the forestomach and decreased the same parameters of the glandular stomach. Similar bidirectional changes of the forestomach (hypertrophy) and glandular stomach (atrophy) were produced by hydrocortisone treatment. Histological study showed that a reduction in the parietal cell population accounted for the regression of the glandular stomach in both cases. Evidence is presented to suggest that an excess of carbohydrate and sodium chloride combined with a deficiency of fat and protein produced steroidal disorders that in turn gave rise to hyperplasia of the forestomach and atrophy of the glandular stomach of the mice. Possible impact of the above findings on the genesis of human gastric cancer is discussed in relation to the metabolic competence of the host animals to synthesize vitamin C.
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PMID:Effect of rice and salty rice diets on the structure of mouse stomach. 654 73

The influence of intestinal metaplasia on gastric cancer induction was examined in five-week-old male Wistar:Crj rats. The animals were first treated with two 10 Gy doses of X-rays to the gastric region at a 3-day interval (total 20 Gy) and then, starting two months after the irradiation, received 100 ppm N-methyl-N-nitrosourea (MNU) in their drinking water for 15 weeks. Thereafter they were maintained for 37 weeks with or without a dietary 1% sodium chloride (NaCl) supplement. The incidences of gastric adenocarcinomas in the MNU or MNU plus NaCl groups were significantly higher than in animals receiving X-rays plus MNU with or without NaCl. Intestinal metaplasias and the numbers of alkaline phosphatase (ALP)-positive foci were significantly increased in the X-ray irradiation groups but the numbers of ALP-positive foci were not increased with or without 1% NaCl. An inverse relationship between incidences of gastric tumors and intestinal metaplasias was apparent. The present experiment thus showed that the presence of intestinal metaplasia does not exert a positive influence on induction of gastric neoplasia by MNU in the rat.
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PMID:Lack of any positive effect of intestinal metaplasia on induction of gastric tumors in Wistar rats treated with N-methyl-N-nitrosourea in their drinking water. 796 Nov 16


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