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

A cohort of 5,080 men living in a retirement community in California (United States) and initially free from lung cancer were followed from June 1981 to December 1989. At recruitment, each study participant completed a mailed questionnaire which requested information on the subject's medical history, use of cigarettes, and usual consumption frequencies during the preceding 12 months of 44 vegetable and fruit items. Men who had never smoked had the highest mean daily intake of beta-carotene (8,505 micrograms), followed by past smokers (7,761 micrograms) and then by current smokers (6,178 micrograms). beta-Carotene intake of the subject's wife was correlated significantly with that of the husband in the 4,018 spouse pairs (r = 0.46; P = 0.0001). Among men with similar smoking habits, dietary beta-carotene intake significantly decreased with the spouse's smoking habit: never, past, and current smokers (P = 0.004; test for linear trend). During 31,477 person-years of follow-up, 125 incident cases of lung cancer were observed among the cohort of 5,080 men. Age-adjusted relative risks for lung cancer were below unity (i.e., demonstrating a reduced risk) for higher relative to lower consumption of beta-carotene, of all vegetables and fruits, and of yellow vegetables alone. However, these relative risks approached or crossed the null value when adjusted for personal smoking.
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PMID:Dietary beta-carotene, cigarette smoking, and lung cancer in men. 161 Sep 67

Of 600 carotenoids from natural sources that have been characterized, fewer than 10% serve as precursors of vitamin A. Many dietary carotenoids, both with and without provitamin A activity, are found in the blood and tissues of humans. beta-Carotene, the most nutritionally active carotenoid, comprises 15-30% of total serum carotenoids. Vitamin A is formed primarily by the oxygen-dependent central cleavage of beta-carotene and other provitamin A carotenoids. Several carotenoids show enhancement of the immune response, inhibition of mutagenesis, reduction of induced nuclear damage, and protection from various neoplastic events in cells, tissues, and whole animals. Carotenoids also protect against photo-induced tissue damage. Some carotenoids, including beta-carotene, quench highly reactive singlet oxygen under certain conditions and can block free radical-mediated reactions. In epidemiological studies, the intake of carotenoid-rich fruits and vegetables has been correlated with protection from some forms of cancer, particularly lung cancer. Similarly, serum beta-carotene levels have been associated with a decreased chance of developing lung cancer. It must be stressed, however, that these epidemiological associations do not show cause and effect. In this regard, long-term intervention trials with beta-carotene supplements are in progress. Whatever the results of these trials, carotenoids clearly show biological actions in animals distinct from their function as precursors of vitamin A.
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PMID:Biological actions of carotenoids. 265 56

We reviewed the human epidemiologic studies of the possible protective effect against lung cancer of various dietary constituents, including preformed vitamin A, carotene, vitamin E, selenium, and vitamin C. Beta carotene has strong potential as a protective agent, though constituents of green and yellow vegetables other than carotene may account for the reduced cancer incidence observed in many studies. Selenium also deserves attention as a potential chemopreventive nutrient, though data are limited. Data on vitamin E are sparse and inconclusive, and there is little evidence that vitamin C provides protection against human lung cancer. It is likely that cessation of cigarette smoking would have a far greater influence on reducing lung cancer incidence than any known dietary modification.
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PMID:Diet and lung cancer. A review of the epidemiologic evidence in humans. 354 20

The Alpha-Tocopherol Beta-Carotene (ATBC) Cancer Prevention Study was a placebo-controlled, randomized intervention trial testing the hypothesis that beta-carotene and alpha-tocopherol (vitamin E) supplements prevent lung and other cancers. The study is predicated on a substantial body of evidence supporting a role in cancer prevention for these micronutrients. Based on the 2 x 2 factorial study design, 29,133 eligible male cigarette smokers aged 50-69 y were randomly assigned to receive beta-carotene (20 mg), alpha-tocopherol (50 mg), beta-carotene and alpha-tocopherol, or placebo daily for 5-8 y. Capsule compliance was high (median = 99%). beta-Carotene treatment did not result in a decrease in cancer at any of the major sites but rather in an increase at several sites, most notably lung, prostate, and stomach (number of cases 474 compared with 402, 138 compared with 112, and 70 compared with 56, respectively). The vitamin E group had fewer incident cancers of the prostate and colorectum compared with the group not receiving vitamin E (number of cases 99 compared with 151 and 68 compared with 81, respectively), but more cancers of the stomach (70 compared with 56). In contrast to these intervention-based findings for beta-carotene and vitamin E supplements, we observed lower lung cancer rates in men with higher amounts of both serum and dietary beta-carotene and vitamin E at baseline.
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PMID:Effects of alpha-tocopherol and beta-carotene supplements on cancer incidence in the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study. 749 43

The carotenoid, beta-carotene, has been examined in human trials as a possible lung cancer chemopreventive agent, but initial results indicate that the compound is ineffective. Here we have considered whether beta-carotene could enhance gap junctional intercellular communication (GJIC) and affect the growth of lung epithelial cells, since these effects may be involved in the carotenoid's chemopreventive actions. In accordance with its lack of lung cancer chemopreventive activity, beta-carotene (1-10 microM; 1-5 days treatment durations) did not affect GJIC, gap junction protein (connexin43; Cx43) expression, or growth in vitro of non-transformed (C10) or neoplastic (E9 and 82-132) murine lung epithelial cells. beta-Carotene enhanced GJIC and Cx43 expression and reduced the growth of C3H10T1/2 murine fibroblasts, however. These data indicate that the effects of beta-carotene on GJIC and growth are cell-specific which may partly explain why the carotenoid is an ineffective lung cancer chemopreventive agent.
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PMID:Lack of growth inhibition or enhancement of gap junctional intercellular communication and connexin43 expression by beta-carotene in murine lung epithelial cells in vitro. 895 Feb 6

beta-Carotene and alpha-tocopherol have been thought to reduce risk of lung cancer. Whether beta-carotene and alpha-tocopherol influence human DNA adducts, indicators of biologically effective doses of carcinogens, has been seldom studied. In this cross-sectional study, we measured plasma beta-carotene and alpha-tocopherol in 192 healthy men and DNA adducts in lymphocytes in 104 of the subjects. Because genetic polymorphism of cytochrome P-4501A1 (CYP1A1) and glutathione S-transferase M1 (GSTM1) has been associated with interference in formation of reactive intermediates and detoxification of polycyclic aromatic hydrocarbons, we also obtained data concerning genetic polymorphism of CYP1A1 and GSTM1. In multiple regression analysis, parameters such as alcohol consumed per day, high-density lipoprotein cholesterol, Quetelet index, and cigarettes smoked per day were correlated inversely, whereas age, plasma alpha-tocopherol, and intake frequency of fruits were correlated positively with plasma beta-carotene concentration. DNA adduct levels of high plasma beta-carotene or alpha-tocopherol groups were not significantly different from the DNA adduct levels of low plasma beta-carotene or alpha-tocopherol groups among current smokers or nonsmokers. In variant states of CYP1A1 or GSTM1 polymorphism, after controlling for effect of cigarettes smoked per day, no significant correlation was found between plasma beta-carotene or alpha-tocopherol and DNA adduct levels. These results indicated that alcohol consumption, cigarette smoking, and plasma alpha-tocopherol have a close relationship with plasma beta-carotene. The plasma beta-carotene and alpha-tocopherol were not likely to influence the level of DNA adducts in lymphocytes.
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PMID:Relationship between plasma concentrations of beta-carotene and alpha-tocopherol and life-style factors and levels of DNA adducts in lymphocytes. 897 Jan 85

Lung cancer is the leading cause of cancer death in the United States, and advances in therapy have accounted for an improvement in five-year survival in this disease from 9% to 13% over the last three decades. Molecular genetic evidence has confirmed the epidemiologic link between tobacco and lung cancer causation, and has clarified the etiology of the persistent risk of lung cancer development in former smokers. Retinoids have shown promise in aerodigestive cancer chemoprevention, both in the reversal of preneoplastic lesions and in the prevention of second primary cancers. After initial epidemiologic and dietary studies had linked beta-Carotene with cancer risk reduction, large randomized phase III studies of this compound have shown no evidence of benefit and some evidence of heightened lung cancer risk in active smokers on high dose supplemental beta-Carotene. Therefore, careful clinical, epidemiologic, and basic studies of retinoids using intermediate end point markers are necessary to determine the definitive role of these compounds in the chemoprevention of respiratory tract cancer, with a particular focus on former smokers.
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PMID:Chemoprevention of respiratory tract cancer. 920 2

Lung cancer chemoprevention continued to make progress in 1997. The incidence of tobacco abuse continues to slowly fall in the United States, and paralleling it, lung cancer incidence. Biomarkers of carcinogenesis and susceptibility continue to be an important area in identifying high-risk patients. The analyses of two major lung cancer prevention trials, beta-Carotene and Retinol Efficacy Trial (CARET) and Alpha-Tocopherol Beta-Carotene (ATBC), were also published this past year. Both found an increased incidence of lung cancer in individuals receiving beta-carotene. In both trials, heavy smokers seem to be the most adversely affected group. The mechanism of this increased incidence of cancer and total deaths still eludes investigators.
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PMID:Prevention of lung cancer. 955 34

Recent intervention trials reported that smokers given dietary beta-carotene supplementation exhibited an increased risk of lung cancer and overall mortality. beta-Carotene has been hypothesized to promote lung carcinogenesis by acting as a prooxidant in the smoke-exposed lung. We have examined the interactions of cigarette smoke with beta-carotene in model systems. Both whole smoke and gas-phase smoke oxidized beta-carotene in toluene to several products, including carbonyl-containing polyene chain cleavage products and beta-carotene epoxides. A major product of the reaction was identified as 4-nitro-beta-carotene, which was formed by nitrogen oxides in smoke. Both cis and all-trans isomers of 4-nitro-beta-carotene were detected. The hypothesis that smoke-driven beta-carotene autoxidation exerts prooxidant effects was tested in a liposome system. Lipid peroxidation in dilinoleoylphosphatidylcholine liposomes exposed to gas-phase smoke was modestly inhibited by the incorporation of 0.1 mol % beta-carotene. Both the lipid soluble antioxidant alpha-tocopherol and the water soluble antioxidant ascorbate were oxidized more slowly by gas-phase smoke exposure in liposomes containing beta-carotene. These data indicate that beta-carotene exerts weak antioxidant effects against smoke-induced oxidative damage in vitro. It is unlikely that a prooxidant effect of beta-carotene occurs under biologically relevant conditions or is responsible for an increased incidence of lung cancer observed in smokers who consume beta-carotene supplements.
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PMID:Reactions of beta-carotene with cigarette smoke oxidants. Identification of carotenoid oxidation products and evaluation of the prooxidant/antioxidant effect. 1036 17

Lung cancer is the most common cancer in the world, and smoking is the major risk factor, accounting for about 90% of the cases. Diet has also been implicated in the development of lung cancer, although the specific nutrients remain to be elucidated. Vitamins with antioxidant activity have received much attention. beta-Carotene, the most efficient provitamin A, was found to be inversely related to the risk of lung cancer in many prospective epidemiological studies, especially in studies measuring serum concentrations of beta-carotene. The findings from controlled trials, however, contradict the hypothesis that beta-carotene could prevent lung cancer, but rather suggest increased risk of lung cancer with supplementary beta-carotene. Data from both prospective studies and a controlled trial suggest no role for vitamin E in lung carcinogenesis. Some prospective epidemiological studies suggest an inverse relationship between dietary vitamin C and the risk of lung cancer, but due to the high correlation between dietary vitamin C and vegetable and fruit intake the independent role of dietary vitamin C is difficult to estimate. Studies using prediagnostic plasma concentrations of ascorbic acid do not support the involvement of vitamin C in lung carcinogenesis, and no controlled trials of vitamin C on lung cancer have been published. Thus, supplementation with antioxidant vitamins cannot be recommended for the prevention of lung cancer. Non-smoking is the most important target in the prevention of lung cancer. High intakes of vegetables and fruits may provide additional protection and are unlikely to be harmful.
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PMID:Vitamins and lung cancer. 1046 74


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