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

Flavonoids are effective antioxidants and, in theory, may provide protection against cancer, although direct human evidence of this is scarce. The relation between the intake of antioxidant flavonoids and subsequent risk of cancer was studied among 9,959 Finnish men and women aged 15-99 years and initially cancer free. Food consumption was estimated by the dietary history method, covering the total habitual diet during the previous year. During a follow-up in 1967-1991, 997 cancer cases and 151 lung cancer cases were diagnosed. An inverse association was observed between the intake of flavonoids and incidence of all sites of cancer combined. The sex- and age-adjusted relative risk of all sites of cancer combined between the highest and lowest quartiles of flavonoid intake was 0.80 (95% confidence interval 0.67-0.96). This association was mainly a result of lung cancer, which presented a corresponding relative risk of 0.54 (95% confidence interval 0.34-0.87). The association between flavonoid intake and lung cancer incidence was not due to the intake of antioxidant vitamins or other potential confounding factors, as adjustment for factors such as smoking and intakes of energy, vitamin E, vitamin C, and beta-carotene did not materially alter the results. The association was strongest in persons under 50 years of age and in nonsmokers with relative risks of 0.33 (95% confidence interval 0.15-0.77) and 0.13 (95% confidence interval 0.03-0.58), respectively. Of the major dietary flavonoid sources, the consumption of apples showed an inverse association with lung cancer incidence, with a relative risk of 0.42 (95% confidence interval 0.23-0.76) after adjustment for the intake of other fruits and vegetables. The results are in line with the hypothesis that flavonoid intake in some circumstances may be involved in the cancer process, resulting in lowered risks.
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PMID:Dietary flavonoids and the risk of lung cancer and other malignant neoplasms. 924 6

The relation between the dietary intake of vitamins E, C, and A (estimated by a 24-hour recall) and lung cancer incidence was examined in the First National Health and Nutrition Examination Survey Epidemiologic Followup Study cohort of 3,968 men and 6,100 women, aged 25-74 years. During a median follow-up period of 19 years (from 1971-1975 to 1992), 248 persons developed lung cancer. Adjusted for potential confounders using Cox proportional hazards regression methods with age as the underlying time variable, the relative risk of lung cancer for subjects in the highest quartile of vitamin C intake compared with those in the lowest quartile was 0.66 (95% confidence interval (CI) 0.45-0.96). For vitamin A intake, a protective effect was observed only for its fruit and vegetable component (carotenoids) among current smokers (relative risk = 0.49, 95% CI 0.29-0.84), but this was modified by the intensity of smoking (a statistically significant effect (relative risk = 0.33, 95% CI 0.13-0.84) was observed only for those in the lowest tertile of pack-years of smoking). The vitamin E intake-lung cancer relation was modified by the intensity of smoking with a significant protective effect confined to current smokers in the lowest tertile of pack-years of smoking (relative risk = 0.36, 95% CI 0.16-0.83). Overall, there was no additional protective effect of supplements of vitamins E, C, and A beyond that provided through dietary intake. When vitamin E, vitamin C, and carotenoid intakes were examined in combination, a strong protective effect was observed for those in the highest compared with those in the lowest quartile of all three intakes (relative risk = 0.32, 95% CI 0.14-0.74). These data provide support for a protective role of dietary vitamins E and C and of carotenoids against lung cancer risk but with a modification in effects by the intensity of cigarette exposure. While smoking avoidance is the most important behavior to reduce lung cancer risk, the daily consumption of a variety of fruits and vegetables that provides a combination of these nutrients and other potential protective factors may offer the best dietary protection against lung cancer.
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PMID:Intake of vitamins E, C, and A and risk of lung cancer. The NHANES I epidemiologic followup study. First National Health and Nutrition Examination Survey. 924 7

The relationship between diet and alcohol and lung cancer was evaluated among participants of the New York State Cohort (United States), comprising 27,544 men (395 cases) and 20,456 women (130 cases) who completed a brief mailed questionnaire in 1980. Participants were followed up through 1987 with the assistance of the New York State Department of Health's Vital Statistics Section and Cancer Registry. Among men, inverse relationships with vitamin C, folate, and carotenoids, and positive associations with total fat, monounsaturated and saturated fat were observed after adjusting for age, education, cigarettes/day, years smoking, and total energy intake. The relationships observed with folate and saturated fat were stronger for heavy smokers. Also, the effect of folate, total fat, and monounsaturated fat seemed to be limited to squamous cell carcinomas. We found no indication that cholesterol or polyunsaturated fat was associated with lung cancer. Diet did not appear to exert a major role on lung cancer risk among women. Although diet modification should never be considered a substitute for smoking cessation, its role as an additional strategy in lung cancer prevention deserves attention.
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PMID:Diet and alcohol consumption and lung cancer risk in the New York State Cohort (United States) 942 23

Previous evidence suggests that malignant tumors cause an oxidative burden to human antioxidative defense systems. We followed the plasma total radical-trapping antioxidant parameters (TRAP) and their main antioxidant components (alpha-tocopherol, uric acid, protein sulfhydryl groups, and unidentified antioxidant proportions) in 13 lung cancer patients and 7 control patients scheduled for thoracotomy. Plasma samples were collected 9 times during a 5 month follow-up period in the cancer patients. The objective of the study was to evaluate the effects of surgical removal of lung cancer on human plasma total antioxidant capacity. A significant reduction of plasma TRAP (period effect of ANOVA, p = 0.0006) and its components appeared in both groups during the first postoperative day. This decrease was due to reduction of ascorbate (p = 0.002) alpha-tocopherol (p = 0.0001) and urate (p = 0.05) concentrations. At 3 and 5 months after the surgical removal of the tumor there was an augmentation in plasma TRAP concentrations (p = 0.02, 3 months; p = 0.07, 5 months). This was mainly due to the increases in plasma yet as unidentified antioxidant components (UNID) and protein SH-groups. The data indicates that, first, thoracotomy itself causes a reduction in plasma TRAP during the early hours after operation, and secondly surgical removal of lung cancer increases plasma TRAP concentrations compared to the baseline values possibly reflecting the relief of oxidative stress caused by malignant tumors.
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PMID:Effects of surgical removal of lung cancer on total plasma antioxidant capacity in lung cancer patients. 970 May 84

To examine whether dietary sugar modifies lung cancer risk, a case-control study involving 463 cases with lung cancer and 465 hospitalized controls was conducted in Uruguay in the period 1993-1996. Dietary patterns were assessed in detail using a 64-item food-frequency questionnaire, which allowed the calculation of total energy intake. After adjustment for potential confounders through a model that included tobacco smoking and total energy, total fat, vitamin C, and alpha-carotene intakes, an increased risk for sugar-rich foods, total sucrose intake, sucrose to dietary fiber ratio, and glycemic index for lung cancer was observed (odds ratio for highest category of total sucrose intake = 1.55, 95% confidence interval = 0.99-2.44). When lung cancer was analyzed separately by cell type, odds ratios for small cell and large cell undifferentiated carcinoma were higher than those observed for squamous cell and adenocarcinoma of the lung. The joint effect of pack-years, total fat intake, and sucrose intake was associated with an increased risk of 28.3 (95% confidence interval = 13.4-59.7) for high values of the three variables. The study suggests that high sucrose intake could be an important risk factor in lung carcinogenesis. Further studies, both epidemiological and experimental, are needed to replicate the present findings and to clarify the mechanism(s) of sucrose intake in lung carcinogenesis.
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PMID:Dietary sugar and lung cancer: a case-control study in Uruguay. 977 Jul 25

This paper assesses critically the science base that underpins the argument that oxidative damage is a significant causative factor in the development of human diseases and that antioxidants are capable of preventing or ameliorating these disease processes. The assessment has been carried out under a number of headings, and some recommendations for future research are made based on the present day knowledge base. The knowledge database (1) Consideration of the basic science that underlies understanding of the role of free radicals in causing cellular pathologies, and the role of antioxidants in preventing this, shows that an imbalance of reactive oxygen species and antioxidant defence systems may lead to chemical modifications of biologically relevant macromolecules. This imbalance provides a logical pathobiochemical mechanism for the initiation and development of several disease states. Experimental data obtained in vivo provide evidence that antioxidants function in systems that scavenge reactive oxygen species and that these are relevant to what occurs in vivo. The relevance in vivo of these observations depends inter alia on knowledge of the uptake and distribution of the antioxidant within the human body, and on what tissue levels of the antioxidant may be expected in relation to dietary levels. (2) There is some way to go until validated precise methods are available for measuring biomarkers of oxidative damage in human subjects in vivo under minimally invasive conditions. With respect to oxidative damage in DNa, HPLC and GC-mass spectrophotometry methods have both merits and limitations. Lipid oxidation products in plasma are best measured as isoprostanes or as lipid hydroperoxides using specific HPLC techniques. Development of isoprostane measurement will advance specificity and precision. The measurement of oxidative damage to proteins has some potential but such methods have not been effectively exploited. (3) Epidemiological studies support the hypothesis that the major antioxidant nutrients vitamin E and vitamin C, and beta-carotene (which may or may not be acting as an antioxidant in vivo), may play a beneficial role in prevention of several chronic disorders. More research is needed on the impact of other non-nutrient compounds, such as other carotenoids and flavonoids, on human health. In general, human intervention studies using hard end-points are the gold standard. Trials are restricted mainly to the major antioxidants and do not allow firm conclusions because of inconsistent findings, an insufficient number of studies and the use of varying doses. There is evidence that large doses of beta-carotene may be deleterious to the health of certain subgroups of the population such as heavy habitual smokers. (4) With respect to the safety of administration of supplementary vitamins, vitamin C is safe at levels of supplementation up to 600 mg/d, and higher levels, up to 2000 mg/d, are without risk. Vitamin E has a very low human toxicity and an intake of 1000 mg/d is without risk; 3200 mg/d has been shown to be without any consistent risk. Large intakes of beta-carotene must be viewed with caution because they have been shown to confer detriment to a population at high risk of lung cancer when administered after many years of high risk (smoking) behaviour. Until further work clarifies the situation in heavy smokers with respect to taking supplements, larger doses should be avoided by such individuals. There is little reliable information about the human toxicology of flavonoids and related non-nutrient antioxidant constituents of the diet. (5) The food industry has long experience in the control of oxidative damage in foods and this experience can be used to advantage for the protection of food antioxidants which are beneficial. Some of these, such as vitamins C and E and beta-carotene, are well known, and strategies for their protection in foods are already exploited by food technologies. (ABSTRACT TRUNCATED)
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PMID:Functional food science and defence against reactive oxidative species. 984 55

A 1:1 case-control study of lung cancer incidence among women in Shenyang was conducted to explore the relationship between diet and the risk of lung cancer, with emphasis on the potential effects of a list of specific dietary constituents on modifying lung cancer risks. Dietary information on 290 cases and population-matched controls was obtained by personal interviews. Multiple logistic regression models were used for the statistical analysis and summarization of the data. A significant difference was found between cases and controls with respect to intake of beta-carotene, vitamin C and fibers, all of which reduced the risk for lung cancer in a dose-dependent manner; yielding calculated odds ratio (OR) of 0.84, 0.75, and 0.46, respectively. The apparent effects of these nutrients persisted after adjusting for cigarette smoking;suggesting that they may function as protective factors to reduce the risk for lung cancer in Chinese women.
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PMID:A case-control study of the relationship between dietary factors and risk of lung cancer in women of Shenyang, China. 986 17

Even though it is well established that oxygen-free radicals are the main mechanism responsible for the cytotoxicity produced during radiotherapy, the role of the human antioxidant defense system in clinical radiation oncology is still to be clarified. Changes in the human plasma total peroxyl radical trapping capacity (TRAP) and its individual components were followed during clinical radiotherapy for lung cancer. Sixteen patients receiving radical-aimed radiotherapy provided blood samples nine times during the treatment. Our hypothesis was that oxygen-free radical production increased by irradiation should decrease the plasma TRAP as a consequence of oxidative stress. Only a moderate reduction of the plasma TRAP was found during the therapy in the study group taken as a whole, but the development pattern of TRAP and its unidentified components were clearly different in those patients showing complete or partial response to the treatment and those in which the disease progressed unabated. Plasma ascorbate levels showed no significant changes during radiotherapy. A decrease in vitamin E concentrations was seen after 6 Gy (p=0.05). Uric acid concentrations increased towards the end of the radiotherapy in both response groups (p=0.02 at 50 Gy). In this study, 26.6% of the plasma TRAP was due to unidentified antioxidants (UNID).
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PMID:Human plasma antioxidant capacity during radiotherapy for lung cancer: a clinical study. 989 70

Newly available data of a case-control study of lung cancer in women in Spain were analyzed to assess the relationship with the intake of specific carotenoids (alpha-carotene, beta-carotene, lutein, and lycopene) and flavonoids (quercetin, kaempferol, myricetin, and luteolin). The study included 103 cases and 206 hospital controls, matched by age and residence. Usual food intake was estimated through a food-frequency questionnaire. With adjustment for smoking habit and vitamin E, vitamin C, and total flavonoid intake, no association was found for the intake of alpha-carotene, beta-carotene, or lutein. The odds ratio (95% confidence interval) for women in the highest tertile of lycopene intake with respect to the lowest was 0.56 (0.26-1.24), with p for trend = 0.15. A nonsignificant association was observed for the highest vs. lowest tertile intake of kaempferol (odds ratio = 0.51, 95% confidence interval = 0.22-1.17), with p for trend = 0.10, after adjustment for smoking and vitamin E, vitamin C, and total carotenoid intake. No protective effect was observed for quercetin or luteolin or for total flavonoid intake.
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PMID:Intake of specific carotenoids and flavonoids and the risk of lung cancer in women in Barcelona, Spain. 1005 Feb 65

Cyclin D1 antisense (D1AS)-transfected lung epithelial cell lines were serum deprived and then analyzed for three hallmarks of apoptosis: appearance of single-strand DNA breaks, alteration of apoptosis-related protein expression, and induction of chromatin condensation. Single-strand DNA breaks appeared at significant levels 24 h after serum deprivation, whereas induction of chromatin condensation was observed after 72 h. The antioxidants dimethyl sulfoxide, ascorbate, and glutathione, as well as insulin-like growth factor-I, inhibited induction of DNA damage in this assay. Additionally, proliferating cell nuclear antigen expression is completely suppressed in the D1AS cells, indicating a mechanism to explain the reduced capacity for DNA repair. Increased expression of cyclin D1, which is a common lesion in lung cancer, may thus prevent induction of apoptosis in an oxidizing and growth factor-poor environment. Reducing cyclin D1 expression in lung cancer cells by expression of D1AS RNA disrupted these protective pathways.
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PMID:Abrogation of cyclin D1 expression predisposes lung cancer cells to serum deprivation-induced apoptosis. 1019 66


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