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Query: UMLS:C0546837 (esophageal cancer)
 8,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitrosamines and precursor secondary amines were assayed in foods from families in four villages of the esophageal cancer high incidence area of Linxian, Henan Province, People's Republic of China. Amines (as tosylamides) and nitrosamines were readily detected at p.p.m. and p.p.b. levels, respectively, in all samples. In this small preliminary survey (25 families, four villages), however, there were no strong correlation between the levels of the carcinogenic nitrosamines or the precursor secondary amines with the incidence of esophageal cancer in the individual families. The success of the analytical procedures suggests that a more extensive study is warranted.
Carcinogenesis 1986 May
PMID:Nitrosamines and nitrosamine precursors in foods from Linxian, China, a high incidence area for esophageal cancer. 369 1

The properties of N-nitroso compounds (NNC) and of vitamins C and E are briefly described. The author reviews the ability of vitamins C and E to inhibit NNC formation in chemical systems, in nitrite-preserved meat, in experimental animals and in humans. Dietary vitamins C and E both produced 30% to 60% inhibitions in most carcinogenesis experiments employing preformed carcinogens. Vitamin C reversed transformation in an in vitro system. Carcinogenicity tests of the vitamins are reviewed (vitamin C can promote bladder carcinogenesis). Intake of fresh fruits and vegetables (which contain vitamin C) is negatively correlated with cancer of the stomach, esophagus, larynx, mouth and cervix. For gastric and esophageal cancer, there is evidence that this association is due to an inhibition of in vivo NNC formation. Vitamin C is apparently not a useful treatment for cancer. The author supports the recommendation that fresh fruit and vegetable intake be increased to lower the risk of cancer.
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PMID:Effects of vitamins C and E on N-nitroso compound formation, carcinogenesis, and cancer. 375 8

Fusarin C, a fungal metabolite, was recently isolated and identified from corn meal inoculated with Fusarium moniliforme which was one of the most common fungi associated with corn in Linxian county, a high-incidence area of esophageal cancer. In the presence of S-9 mix, fusarin C significantly increased the number of revertants in Salmonella typhimurium TA 100, and induced SCE, micronuclei, chromosome aberrations and 6-TG resistant mutants in V79 cells. The toxic action of fusarin C on V79 cells was much stronger in the absence of S-9 mix. However, fusarin C did not show, at the largest concentration used, any significant mutagenic or clastogenic effect on the cells without the addition of S-9 mix. The possible relationship between the consumption of corn contaminated with F. moniliforme and the cause of esophageal cancer was discussed.
Carcinogenesis 1985 Jun
PMID:A mutagenic metabolite produced by Fusarium moniliforme isolated from Linxian county, China. 400 77

One of the most advanced experimental models for investigations of the metabolic fate and of mechanisms of action of initiators and promoters at the cell and/or the molecular level is the three-stage initiation/promotion/progression model of carcinogenesis in mouse skin. In etiologic investigation by experimental analyses of local lifestyle-associated esophageal cancer on the Caribbean island of Curacao, based on this model initiators of the solitary carcinogenic PAH type and promoters of the cocarcinogenic diterpene ester (tigliane) type were suggested as putative principal risk factors. In metabolic investigations it was shown that 7,12-dimethylbenz(a)anthracene (DMBA) requires metabolic activation to yield "ultimate initiator(s)," whereas TPA and its diterpene ester congeners are "ultimate promoters" themselves. Yet naturally occurring "cryptic" forms of diterpene ester irritants and promoters require metabolic activation. To show structure/activity relationships, selected new diterpene structures of the tigliane, ingenane, and daphnane types and their irritant and promoting activities in mouse skin are presented in this paper. Common structural features of the diterpene moieties relevant for interaction with cellular receptors are identified. Synthetic modification of the ester moieties reveals highly unsaturated analogs of 12-O-tetradecanoylphorbol-13-acetate (TPA) allowing for dissection of the promotional stage in the mouse skin model in two operationally defined substages, PI and PII. In many tissues and cells, TPA and congeners induce various different biological effects, e.g., phospholipid synthesis is stimulated in epidermis, virus synthesis is stimulated in human lymphoblastoid cell lines carrying latent genomes of Epstein-Barr virus (EBV), and prostaglandin E2 is rapidly released from mouse peritoneal macrophages. Altogether a remarkable biological and biochemical pleiotropism of diterpene ester promoters is indicated. In investigations of the molecular mechanism of action of diterpene esters, non-promoting short chain phorbol esters, such as phorbol-12,13-dipropionate (PDPr) were shown to inhibit diterpene ester-induced promotion in vivo. In radioligand assays employing (20-3H)PDPr as well as (20-3H)TPA, specific binding to the particulate fractions of mouse skin and other mouse organs, including the brain, is seen. Inhibition of specific binding by a series of diterpene esters is correlated with their irritant and promoting activities.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Irritant diterpene ester promoters of mouse skin: contributions to etiologies of environmental cancer and to biochemical mechanisms of carcinogenesis. 609 81

The identification of so-called co-carcinogens i.e. "per se essentially non-carcinogenic amplifiers" of carcinogenesis - especially promoters of initiation(or tumors) - as a new, non-classical group of risk factors has added a new dimension to the etiology of cancer in man. Indeed, in real human life, multifactorial causation of cancer may be considered the rule and classical unifactorial causation the exception. This comprehensive and current concept of the etiology of cancer in man and certain prototype experimental models of multifactorial carcinogenesis allow for proposals of a standardized terminology which may be adequate for common use in both, experimental and epidemiological oncology. On the background of a recent experimental analysis of life style esophageal cancer the current situation regarding the scientific basis of classification and grading of carcinogenic risk factors will be reviewed. It may be helpful in legislation aiming at more environmental safety.
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PMID:Co-carcinogens of the initiation-(or tumor)promoter type as environmental risk factors of cancer in man, experimental analysis of an etiologic model situation of life style cancer and current problems of assessment of cancer risk in multifactorial carcinogenesis. 638 18

Biochemical analyses were conducted to evaluate the nutritional status of a high esophageal cancer risk population in Linxian, People's Republic of China. A study was conducted in September 1980 in which plasma levels of vitamins A, B2, and C were analyzed. In a second study in 1983, the plasma fat-soluble vitamins were analyzed with a newly developed high-performance liquid chromatography method that allowed the simultaneous determination of retinol, alpha-tocopherol, beta-carotene, alpha-carotene, and lycopene in 0.1 ml of plasma sample. The average plasma retinol levels ranged from 24 to 27 micrograms/dl among the population groups, with 20-35% of the individuals having levels under 20 micrograms/dl. Low plasma beta-carotene levels averaging 8-12 micrograms/dl were observed among the population groups. Low plasma alpha-tocopherol levels with average values around 700 micrograms/dl were also observed; about half the individuals were either low or deficient in vitamin E. After 4 months of supplementation with daily multivitamin tablets, the plasma contents of retinol and alpha-tocopherol were significantly increased. The plasma alpha-carotene and beta-carotene were also increased, possibly as a reflection of seasonal changes in the diet or a sparing effect of vitamins A and E on these carotenes. Low plasma ascorbate levels with an average of 567 micrograms/dl were observed, and about 23% of the individuals had values under 200 micrograms/dl. Riboflavin deficiency was prevalent, with about 90% of the subjects having an erythrocyte glutathione activation coefficient over 1.2. The study establishes the low nutritional status in vitamins of the population in Linxian and provides the background for further studies on the effects of nutritional deficiency on carcinogenesis.
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PMID:Vitamin A and other deficiencies in Linxian, a high esophageal cancer incidence area in northern China. 659 53

An experimental analysis is described which demonstrates that the epidemiologically established high rate of esophageal cancer among blacks and creoles in Curacao most likely is the result of a multistage process involving initiators and promoters. As part of local lifestyle, the group at risk utilizes for various purposes plant parts of an indigenous bush Croton flavens L. ("Welensali"). Moreover they consume, as an everyday beverage, a "bush tea" made from the leaves of the bush. The roots, leaves and tea are shown to contain a multitude of irritant croton factors which are characterized as diterpene esters of the tigliane type. In mouse skin these exhibit strong promoting activity comparable to that of TPA. As the latter, also the croton factors isolated, show no solitary carcinogenic activity. One cup of Welensali tea contains the equivalent of about 12-times the irritant dose of croton factor F1; in addition, the equivalent of about 1.4-times the irritant dose 50 of the corresponding "cryptic" promoter F1-20-decanoate is present. These amounts are considered sufficient to maintain chronic irritation of the esophagus as an important element of co-carcinogenesis, especially of tumor promotion. Also, persons at risk in Curacao have been exposed at times previously to certain initiators. Mice treated by an initiation/promotion protocol with DMBA (or other initiators) and TPA develop tumors of the forestomach. Therefore, esophageal cancer on Curacao may be considered the first case for cocarcinogens of the tumor promoter type being principal risk factors in a life style cancer.
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PMID:Multistage tumor development in the human esophagus - the first identification of cocarcinogens of the tumor promoter type as principal carcinogenic risk factors in a local life style cancer. 663 57

Zinc deficiency enhances experimental esophageal tumor induction. Vitamin A supplementation inhibits carcinogenesis in animals. Plasma zinc and plasma vitamin A levels are reduced in several human squamous cancers, but have not been studied in a US population with esophageal cancer. Therefore, we measured plasma zinc and vitamin A in patients with newly diagnosed esophageal cancer. In addition, we assessed hepatic and nutritional status and attempted to control for other factors known to influence plasma zinc and vitamin A levels. Plasma zinc and vitamin A were both significantly less in esophageal carcinoma than in age-matched healthy controls (plasma zinc 65.7 +/- 3.3 micrograms/dl [mean +/- SEM] in esophageal cancer versus 80.5 +/- 2.4 micrograms/dl in controls, P less than 0.01; plasma vitamin A 32.6 +/- 3.4 micrograms/dl in esophageal cancer versus 60.2 +/- 4.2 in controls, P less than 0.001). Overall, 15 of 17 patients with esophageal cancer had decreased plasma zinc and/or decreased plasma vitamin A. Our findings are compatible with a hypothesis that zinc or vitamin A deficiency may be co-factors in the induction of human esophageal carcinoma.
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PMID:Plasma zinc and vitamin A in human squamous carcinoma of the esophagus. 683 64

In an area with high incidence of esophageal cancer, Linxian, staple food is heavily contaminated by fungi of the Fusarium genus. We have found that T-2 toxin produced by Fusarium has both direct cytotoxic and proliferative effects on fetal esophageal epithelium. At higher dosage of T-2 toxin (4 ng/ml for 6 days) the cultured epithelium became necrotic. At a lower dosage range of 0.2-1.2 ng/ml, T-2 toxin caused mitogenic effects including focal basal cell hyperplasia, dysplasia, and increased number of mitoses. Atypical mitoses were also seen. These changes are very similar to the premalignant lesions seen in epithelium adjacent to human esophageal carcinoma. These observations suggest that Fusarium mycotoxin can have a role in human esophageal carcinogenesis and should be further investigated.
Carcinogenesis 1983 Sep
PMID:Proliferative and cytotoxic effects of Fusarium T2 toxin on cultured human fetal esophagus. 688 33

Chinese historical records of about 2,000 years ago noted several unique epidemiological features and possible risk factors of esophageal cancer in this country. This paper presents selected recent findings on the epidemiology of esophageal cancer in China with special attention directed to geographical distribution, risk factors, and preventive measures. Some of the major characteristics of this disease in China include: 1) an unusually high mortality, the highest in the world; 2) wide geographical differences in mortality; 3) an irregular concentric belt area of elevated mortality; 4) stability of rates over the years; 5) variations in rate by sex; 6) great ethnic differences in mortality; 7) gullet cancer in chickens comparable to the human disease; and 8) associations with high prevalence of epithelial dysplasia of the esophagus. It has been hypothesized that the prevalence of esophageal cancer in high-risk areas may be associated with fermented and moldy foodstuffs, nitrosamines, deficiencies of molybdenum, nutritional deficiencies, specific living habits, and poor oral hygiene. Accordingly, comprehensive studies are being conducted in Lin County and other areas with elevated risk of this diseases so that the possible function of fungi and nitrosamines in the carcinogenesis of esophageal cancer can be determined.
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PMID:Epidemiology of esophageal cancer in China. 716 71


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