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Query: UMLS:C0242379 (lung cancer)
 71,905 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antioxidant micronutrients are one of the body's primary defenses against free radicals and reactive oxygen molecules. Carotenoids, vitamin C, and vitamin E trap these molecules, and selenium is an essential component of an antioxidant enzyme. There is considerable support from animal studies for a protective effect of antioxidant micronutrients on cancer. However, the role of these micronutrients in cancer prevention in humans is less clear. Diet studies suggest protective effects of fruits and vegetables on risk of cancer at several sites. Inverse associations between dietary carotenoids and serum beta-carotene and lung cancer have been observed repeatedly. Vitamin C has also been consistently inversely associated with risk of oral and esophageal cancer in diet studies and with stomach cancer in both diet and plasma studies. It remains unknown, however, whether carotenoids and vitamin C or some other component of fruits and vegetables, the primary sources of these micronutrients, prevent cancer in humans. Selenium has been inversely correlated with cancers at numerous sites in ecologic studies, but observational studies do not provide strong support for a protective effect of selenium on cancer at any site. There also is not strong support for a protective effect of vitamin E on cancer in humans. Results of studies on the association of antioxidant micronutrients with cancer at many sites are inconsistent. This could be due to lack of a true protective effect or could be related to methodologic problems in assessing dietary intake in epidemiologic studies.
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PMID:Antioxidant micronutrients in cancer prevention. 202 68

The combined effect of Vit. A and E, selenium, cysteine and BHA on 3MC-induced lung cancer in Wistar rats was investigated. The supplementation of these compounds at their safe doses reduced the incidence of lung cancer from 47.2% to 31.6% (P less than 0.05). The total superoxide dismutase (SOD) and Mn-SOD activities in the lung cancer tissue were much lower than those in the normal tissue (P less than 0.001). It is possible that in the early stage of carcinogenesis, this change occurs only in the limited focus and does not affect the enzyme level as a whole, so SOD assay of peripheral blood can not reflect the carcinogenesis status in the lung.
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PMID:[Inhibitory effect of micronutrients and BHA on lung cancer induced in rats]. 207 36

Several factors are known to promote the development of a lung cancer. Smoking, occupation, environment, chronic bronchitis, and scars in the lung are all risk factors. Many studies have stressed the importance of nutrition, in particular vitamins. Vitamin A is necessary for cell differentiation. Retrospective and prospective studies have proven the inverse relation between provitamin A, beta-carotene, and lung cancer of the squamous and oat cell types. Studies in which beta-carotene or natural vitamin A are supplied to smokers, controls, and patients after resection for lung cancer are in progress. The study of other vitamins such as vitamin C and vitamin E has not led to definitive conclusions. The trace element selenium may also exert a beneficial effect.
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PMID:Vitamins and lung cancer. 211 8

The association between the serum selenium level and the subsequent incidence of cancer was investigated in a longitudinal study of 39,268 men and women participating in the Social Insurance Institution's Mobile Clinic Health Examination Survey in Finland. The baseline examinations, including the collection of blood samples, were performed in 1968-1972. During a median follow-up of 10 years, 1,096 new cancer cases were identified from the files of the Finnish Cancer Registry. Selenium concentrations were measured from the stored serum samples collected from these cancer cases and from two controls per case, matched for sex, municipality, and age. The mean serum selenium level was 59.1 micrograms/L among all male cancer cases and 62.5 micrograms/L among controls. The difference was statistically significant (P less than .001). Corresponding values among women were 63.6 and 63.9 micrograms/L, respectively. Low serum selenium levels were associated with an increased risk of developing cancer at several sites, especially cancers of the stomach and lung among men. The relative risk of lung cancer between the highest and lowest decile of serum selenium was 0.11, and it differed significantly from unity (P less than .001). These findings are in agreement with the hypothesis that low selenium intake may increase the risk of some cancers among men.
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PMID:Serum selenium and subsequent risk of cancer among Finnish men and women. 233 4

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

A self-administered food use questionnaire which included 276 food items and mixed dishes and a portion size picture booklet with 122 photographs was developed for a large lung cancer intervention trial among approximately 27,000 Finnish men aged 50-69 years. The reproducibility and validity of this questionnaire were studied from March to October 1984. In the reproducibility study, 121 men aged 55-69 years completed the questionnaire three times, at three-month intervals. The intraclass correlations varied from 0.56 for vitamin A to 0.88 for alcohol, with most falling between 0.60 and 0.70. In the validity study, 190 men of similar age kept food consumption records for 12 two-day periods, distributed evenly over a period of six months, and filled in the questionnaire both before and after this period. Correlations between nutrient intake values from the food records and the food use questionnaires ranged from 0.40 for selenium to 0.80 for alcohol. Among subjects who belonged to the lowest quintile on the basis of the food record measurement, an average of 51 per cent fell into the same quintile and 76 per cent fell into the lowest two quintiles when they were categorized on the basis of the food use questionnaire. Findings were similar for the upper tail of the distribution. These data indicate that the self-administered food use questionnaire is useful for measuring individual or group intakes for a variety of nutrients.
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PMID:Reproducibility and validity of dietary assessment instruments. I. A self-administered food use questionnaire with a portion size picture booklet. 245 36

It has been suggested that protective factors might explain the differential incidence of lung cancer within a given population. Changes in diet, for example, might modulate neoplastic cell formation, since food contains many modifiers of carcinogenesis. The number of studies carried out so far does not permit to draw final conclusions yet. Interesting topics to be discussed include substances which doubtlessly play no role whatsoever for the prevention of lung cancer, like vitamin C, and those which seemingly do, like selenium. Still others consist in cholesterol, vitamins A and E, for which data are either controversial or, at present, still scanty. Moreover, the paper reviews the importance of interactions among nutrients for their effects on cancer risk. Considering major studies in this field, the review puts into evidence the principal results of research carried out so far.
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PMID:Nutrition and lung cancer. 248 50

38 subjects were randomly divided into 2 groups of 19 each. Group 1 consumed a selenium supplement (150 micrograms/d X 21) and Group 2 received only placebo(glucose). After supplementation, blood Se levels and plasma GSH-Px activities in Group 1 increased from 76 to 100 ng/ml (P less than 0.05) and 0.082 to 0.122 e.u./ml (P less than 0.01) respectively. All measured Se, GSH-Px values in Group 2, and high concentrations of lipid peroxides (greater than 4 nmol/ml as malonaldehyde) in both groups remained approximately the same. Se supplementation resulted in a marked decrease of RBC cadmium (Cd) from 32.3 to 25.4 micrograms/g Hb (P less than 0.001). Urinary and fecal Cd in 5 subjects of each group were analyzed every 4 days, and the results demonstrated that Cd was mainly excreted in feces after Se supplementation. One week after discontinuing of Se treatment, Cd content in urine and feces decreased to control levels. Theoretical evidence for chemoprevention of lung cancer with Se in this area was thus provided.
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PMID:[Influence of selenium supplement on cadmium metabolism in human]. 252 86

An increased chromosomal aberration and micronuclei rate of cultured lymphocytes among smelter workers in Yunnan Tin Corporation has been associated with exposure to arsenic which might be involved in carcinogenesis of lung cancer in this area. Selenium, as an essential trace element for life, antagonizes the toxic effects of arsenic. The low intake of selenium among workers in this area might increase injurious effects of arsenic in the tissues. The preliminary results showed that the chromosomal aberration rate of cultured lymphocytes in smelter workers was lowered about 46.1% after treatment with selenium 150 micrograms/d for 21 days. It will provide clues for further study on the elimination of toxicity of arsenic among workers who are exposed to arsenic by supplementation of selenium.
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PMID:[Investigation of protective effect of selenium on genetic materials among workers exposed to arsenic]. 262 64

Evidence pertaining to the role of dietary factors in carcinogenesis comes from both epidemiological studies and laboratory experiments. In 1982, the Committee on Diet, Nutrition, and Cancer of the National Research Council conducted a comprehensive evaluation of this evidence. That assessment as well as recent epidemiological and laboratory investigations suggest that a high fat diet is associated with increased susceptibility to cancer of different sites, particularly the breast and colon, and to a lesser extent, the prostate. Current data permit no definitive conclusions about other dietary macroconstituents including cholesterol, total caloric intake, protein, carbohydrates and total dietary fiber. Specific components of fiber, however, may have a protective effect against colon cancer. In epidemiological studies, frequent consumption of certain fruits and vegetables, especially citrus fruits and carotene-rich and cruciferous vegetables, is associated with a lower incidence of cancers at various sites. The specific components responsible for these effects are not clearly identified, although the epidemiological evidence appears to be most consistent for a protective effect of carotene on lung cancer and less so for vitamins A and C and various cancer sites. The laboratory evidence is most consistent for vitamin A deficiency and enhanced tumorigenesis, and for the ability of various nonnutritive components in cruciferous vegetables to block in-vivo carcinogenesis. The data for minerals and carcinogenesis are extremely limited, although preliminary evidence from both epidemiological and laboratory studies suggests that selenium may protect against overall cancer risk. Frequent consumption of cured, pickled, or smoked foods, possibly because they may contain nitrosamines or polycyclic aromatic hydrocarbons, appears to increase the risk of esophageal or stomach cancer, however, the specific causative agents in these foods are not clearly identified. Excessive alcohol consumption among smokers appears to be associated with an elevated risk of cancers of the oral cavity, esophagus, larynx, and respiratory tract. The mechanisms of action of dietary factors on carcinogenesis are poorly understood. The NRC committee, and more recently, the National Cancer Institute and the American Cancer Society have proposed interim dietary guidelines to lower the risk of cancer. These guidelines are consistent with general dietary recommendations proposed by U.S. government agencies for maintenance of good health.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Diet, nutrition, and cancer. 301 Mar 79


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