Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0546837 (esophageal cancer)
 8,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum spermidine was assayed by radioimmunoassay in different stages of esophageal carcinogenesis in the population from high risk area of esophageal cancer, Linxian County. The serum spermidine values were 76.94 +/- 74.38 ng/ml in 36 normal individuals; 115.71 +/- 113.45 ng/ml in 35 patients with marked epithelial hyperplasia (MEH) and 294.48 +/- 135.36 ng/ml in 31 patients with early esophageal cancer. Patients with MEH were given intervention treatment by Aminoretinoic Ester or Anticancer B or placebo (Starch) as controls. One year later, samples from the population were collected again for serum spermidine measurement. The values were 95.8 +/- 68.2 ng/ml in 27 normals; 125.1 +/- 72.9 ng/ml in 62 patients with MEH treated by Anticancer B; 125.6 +/- 117.2 ng/ml in 64 patients with MEH by Aminoretinoic Ester; 162.4 +/- 76.6 ng/ml in 62 controls and 210.5 +/- 182.9 ng/ml in 44 patients with early esophageal cancer. The results showed that spermidine radioimmunoassay could reflect the tendency of esophageal precancerous changes toward cancer or back to normal. They can be taken as a mid-way monitor indicator for tumor-blocking drugs. Also, it could be of value in the early diagnosis of esophageal cancer.
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PMID:[Spermidine radioimmunoassay in monitor of precancerous lesions of esophagus]. 325 Aug 30

The effects of 12-O-tetradecanoylphorbol-13-acetate (TPA), a tumor-promoting phorbol diester, were determined with regard to the induction of esophageal cancer in Wistar rats following a low-dose initial administration of the esophageal carcinogen N-amyl-N-methylnitrosamine [(AMN) CAS: 13256-07-0]. The induction of esophageal cancer was enhanced by TPA given in drinking water after AMN administration; i.e., the incidence of developing esophageal cancers and the multiplicity (number of esophageal cancers per rat) were significantly higher in groups given TPA solution orally after an oral administration of AMN than in those given the AMN solution alone. The enhancement of carcinogenesis with TPA was not affected by the interval between the administration of AMN and the administration of TPA. However, pretreatment with TPA before AMN administration did not enhance the induction of esophageal cancer. Neoplasms were not detected in groups given only TPA or tap water. Because this approach is similar to the phenomenon of two-stage carcinogenesis in the skin, it should provide a meaningful experimental model for studying two-stage carcinogenesis in the esophagus.
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PMID:Enhancement of esophageal carcinogenesis induced in rats by N-amyl-N-methylnitrosamine in the presence of 12-O-tetradecanoylphorbol-13-acetate. 347 38

Although no absolute certainty exists about the role of nutrition in the etiology of cancer, many facts in favor of the relationship became available during the last decades. Correlation studies, experimental work and to a lesser extent case-control studies made it possible to clarify the role of certain nutrients and foods in carcinogenesis. The most important cancer sites where nutrition could play a role are esophagus, stomach, colon, rectum, prostate and breast. Esophageal cancer is of a very complex etiology, in which alcohol intake plays an important role, at least in western countries. The cancer-promoting properties of alcohol intake are enhanced by smoking. Three factors from nutrition are probably related to stomach cancer, namely salt, nitrate/nitrite and vitamin C. Salt is caustic to the stomach mucosa, resulting in atrophic gastritis. Salt is also co-carcinogenic and stomach cancer-promoting in experimental animals. Nitrate is probably important at the stage of atrophic gastritis, where bacterial overgrowth, due to the high pH, converts nitrates in nitrites, making the loco synthesis possible of potent nitrosocarcinogens. Vitamin C inhibits the latter step. The epidemiological evidence for the role of those factors is provided. The most important among them is the strong and consistent association of stomach cancer mortality with stroke. Rectum, colon, prostate and breast cancer are related in some way to fat intake. They all seem positively related to saturated fat intake, whereas breast cancer is probably also promoted by polyunsaturated fat intake. However, polyunsaturated fat seems to be without effect on rectum cancer. Colon and prostate cancer are probably also influenced by polyunsaturated fat but to a lesser degree than breast cancer. An important argument for this are the positive ecological correlations between changes in rectum, colon and breast cancer mortality from 1968 on, and changes occurring in coronary heart diseases, stroke and diabetes mortality. Those six types of mortality are decreasing, or only slightly increasing in the USA, Belgium, France, the Netherlands, etc. They are strongly increasing in East European countries. The intake of saturated fat has generally decreased in the first group of countries, and has markedly increased in the second group.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutrition and cancer. 353 16

Radioimmunoassay of monoclonal antibodies against O6-methyldeoxyguanosine (O6-MedG) was used to detect the presence of these DNA adducts in the human esophageal epithelium. The analysis comprised 48 adjacent epithelial specimens of the esophageal and cardiac cancer resected in Linxian County and 30 specimens of the fetal esophageal epithelium and 4 of the normal esophageal epithelium from autopsy as collected from the hospital in Beijing. The results show that O6-MedG was detected in all the specimens from the esophageal and cardiac cancer patients. In 7 samples in the adjacent epithelium of esophageal cancer, the level of O6-MedG ranged from 0.5 to 1.0 pmol/mgDNA. 19 showed higher levels up to 37.4 pmol/mgDNA with a mean of 4.72 +/- 6.08 pmol/mgDNA. 5 samples of gastric mucosa showed the level of O6-MedG ranging 0.3-1.0 pmol/mgDNA and the remaining 6 showed a higher level of 1.2-13.4 pmol/mgDNA. The mean was 3.31 +/- 3.97. In all the 11 patients, O6-MedG was detected in the para-cancerous gastric mucosa of the cardiac cancer. 4 normal autopsied esophageal epithelial samples were too low for detection. Samples from the fetal esophageal epithelium showed lower level of O6-MedG, the mean was 0.4 +/- 0.57 pmol/mgDNA. The results mentioned above give us the new evidence that the effect of N-nitrosamines is most likely a causative factor in the carcinogenesis of human esophageal cancer.
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PMID:[O6-methyldeoxyguanosine in DNA of the adjacent epithelium in human esophageal cancer in Linxian County]. 356 84

Zinc and vitamin A are known to interact, and deficiencies have been associated with carcinogenesis in experimental animals and humans. Since we previously have demonstrated decreased plasma zinc and vitamin A levels in patients with esophageal cancer, we wished to examine endoscopically obtained epithelial tissue for vitamin A and zinc content. This was not feasible for vitamin A, but using newly developed techniques for zinc analysis of small tissue samples, we measured esophageal epithelial zinc as well as plasma zinc and plasma vitamin A in 21 patients with esophageal cancer, 17 patients with esophagitis, and 12 normals. Mean plasma zinc in the esophageal cancer group (56 +/- 3 micrograms/dl) (mean +/- SEM) was significantly less than in the esophagitis group (72 +/- 5 micrograms/dl) and the normals (78 +/- 5 micrograms/dl). Mean plasma vitamin A in the esophageal cancer group (32 +/- 3 micrograms/dl) was significantly less than the esophagitis group (57 +/- 4 micrograms/dl) or the normals (58 +/- 5 micrograms/dl). There was no significant difference in tissue zinc content (measured as micrograms zinc/g wet weight of tissue, mean +/- SEM) among cancerous tissue (57 +/- 5 micrograms/g) and adjacent normal tissue (61 +/- 4 micrograms/g), esophagitis tissue (66 +/- 6 micrograms/g) and adjacent normal tissue (61 +/- 6 micrograms/g), or normal esophageal tissue (59 +/- 6 micrograms/g). We conclude that deficiencies of zinc or vitamin A may be cofactors in the induction of human esophageal cancer, but a mechanism cannot be accounted for by differences in epithelial zinc content.
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PMID:Esophageal zinc content in human squamous esophageal cancer. 358 28

Epidemiologic studies of the relationships between vitamins and 3 types of cancer are reviewed. First, the widely reported association between vitamin A and beta-carotene and risk of lung cancer is considered. In a large population-based case-control study of lung cancer among white males in New Jersey, increased intake of vegetables, dark green vegetables, dark yellow-orange vegetables, and carotenoids were each associated with reduced risk, but intake of retinol or total vitamin A was not related. The protective effect of vegetables was limited to current and recent cigarette smokers, which suggests that vegetable intake prevents a late-stage event in carcinogenesis. Consumption of dark yellow-orange vegetables was consistently more predictive of reduced risk than either the total carotenoid index or consumption of any other food group, possible because of the high content of beta-carotene in this food group. The results and limitations of other epidemiologic studies of diet and lung cancer are reviewed. Second, the evolving relationship between multiple micronutrient deficiencies and esophageal cancer is discussed. In a death certificate-based case-control study of esophageal cancer in black males in Washington, D.C., several indicators of general nutritional status, including consumption of fresh or frozen meat and fish, dairy products and eggs, and fruit and vegetables, and the number of meals eaten per day, were inversely and independently correlated with the risk of esophageal cancer. Estimates of intake of micronutrients, such as carotenoids, vitamin C, thiamin, and riboflavin, were less strongly associated with reduced risk than were the broad food groups that provide most of each micronutrient. Thus no single micronutrient deficiency was identified. Other studies suggest that generally poor nutrition may partially explain the susceptibility of urban black men to esophageal cancer. Finally, the postulated association between low folacin levels and risk of cervical cancer is examined. Among women who use oral contraceptives, serum and red blood cell folacin levels were reported to be lower among those with cervical dysplasia. In a clinical trial involving oral contraceptive users, cervical dysplasia gradually decreased in the group supplemented with oral folate but remained unchanged in the group given the placebo. Other epidemiologic studies of diet and cervical cancer are discussed.
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PMID:Epidemiologic studies of vitamins and cancer of the lung, esophagus, and cervix. 359 17

Riboflavin deficiency diminishes the rate of growth of spontaneous tumors in experimental animals but enhances the carcinogenicity of specific drugs such as the azo dyes, which are degraded by a microsomal hydroxylase system requiring riboflavin. Human esophageal cancer has been epidemiologically associated with riboflavin deficiency, but the precise role of riboflavin in this tumor remains to be defined. Riboflavin nutriture influences epithelial integrity, tissue flavin concentrations, rates of prostaglandin biosynthesis, and glutathione metabolism, each of which may have implications for carcinogenesis.
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PMID:Riboflavin. 359 27

Human fetal esophageal epithelium, after being exposed to NMBzA, was found to contain O6-methyldeoxyguanine (O6-MedG), a NMBzA-modified DNA adduct, in tissue DNA by radioimmunoassay and monoclonal antibody, which is highly specific to O6-MedG. The highest level of O6-MedG was 58.83 pMol/mg DNA after adding 5.0 mM NMBzA in vitro. The level of O6-MedG and the concentration of NMBzA followed the dose-effect relationship. O6-MedG could be eliminated from DNA by normal human fetal esophageal epithelium. About 50% of O6-MedG was cleared away in the first 1-2 hours during the post-treatment incubation, which was followed by a slower phase of elimination with 18% left in 24 hours. The results indicate that the human fetal esophageal epithelium can metabolically activate NMBzA in vitro and form O6-MedG, which, as well known, can cause mutagenesis and carcinogenesis and, hence, may most likely be related to the development of human esophageal cancer.
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PMID:[Modification of esophageal epithelium DNA in the human fetus by N-nitrosomethylbenzylamine (NMBzA)]. 367 12

Consumption by man of cereals contaminated by high levels of Fusaria mycotoxins has caused alimentary toxic aleukia, while chronic consumption at lower levels of contamination has been implicated in esophageal cancer in China and South Africa. Dietary treatment of animals with extracts of Fusaria cultures or with the trichothecene diacetoxyscirpenol (DS) caused esophageal hyperplasia but not cancer. The explanation could be that esophageal cancer is initiated by other factors, possibly by nitrosamines, and that Fusaria mycotoxins act either as co-carcinogens or as promoters as a result of their ability to stimulate cell replication. The effect of DS on replication in esophagus was therefore studied. As squamous stomach has a very similar histological structure to esophagus, the effect of DS on stomach was studied also. A high dose of DS given by gavage was shown by the bromodeoxyuridine-antibody technique to increase DNA replication in the basal cells of the esophagus and of the squamous and glandular stomach. For stomach, this correlated with an increased incorporation of tritiated thymidine into DNA, and an increase in ornithine decarboxylase activity. These effects had returned to normal by 7 days. The increased replication was apparently not a result of cell damage and restorative hyperplasia. It is suggested that, as has been proposed recently for butylated hydroxyanisole, DS may enhance carcinogenesis when exposure is sufficient to stimulate cell replication. This contrasts with the non-threshold action of initiating carcinogens. For man, acute exposure to the critical dose of DS probably occurs only under exceptional circumstances, as during outbreaks of alimentary toxic aleukia. Prolonged exposure to lower dose levels is more likely to be relevant.
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PMID:Stimulation of DNA replication in rat esophagus and stomach by the trichothecene mycotoxin diacetoxyscirpenol. 369 May 8

The fact that the only chemicals known to be potent carcinogens for the esophagus in animals are certain nitrosamines suggests that these environmental carcinogens could be a cause of human esophageal cancer. Epidemiological investigations support this concept. The level of exposure alone is not considered sufficient to account for the very high incidence of the disease in certain regions, but potentiating factors have been shown to have a dramatic effect on nitrosamine-induced esophageal cancer in animal experiments. A likely enhancing factor is consumption of food contaminated by molds, especially by Fusaria spp, a group known to produce trichothecene mycotoxins. The effect of simultaneous treatment with diacetoxyscirpenol (DS) on methyl-benzyl-nitrosamine (NMBzA)-induced esophageal cancer was studied. Feeding a diet containing DS at 10 ppm for 10 weeks caused thickening of the basal cell layer of the esophageal epithelium, but feeding DS (10 ppm) simultaneously with NMBzA (4, 8, 16 ppm) for 10 weeks, or feeding a lower dose of DS with NMBzA for a longer period, or administration of DS per os at intervals during NMBzA treatment, did not potentiate but possibly reduced esophageal tumors. Toxicity, revealed by reduced growth rate of DS-fed animals, may have inhibited carcinogenesis. In contrast to the rapid potentiating effect of zinc deficiency, DS does not appear to cause an early enhancement of esophageal cancer.
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PMID:The effect of the trichothecene mycotoxin diacetoxyscirpenol on nitrosamine-induced esophageal cancer in the rat. 369 63


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