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

Incidence rates of lung cancer have been markedly lower for Fiji than for other South Pacific countries, despite similar rates of smoking. We conducted population-based surveys in several island nations of the South Pacific (Cook Islands, Fiji, Tahiti and New Caledonia) and used data from Caucasian, Japanese, Hawaiian, Filipino and Chinese controls in a case-control study of lung cancer in Hawaii to investigate the role of diet in explaining differences in lung cancer incidence among 20 ethnic-sex groups. In a stepwise linear regression of lung cancer rates on smoking, diet and other variables, smoking, as expected, explained the majority (61%) of the variability in incidence. However, several dietary components also explained significant portions of the variance. Lutein intake explained 14% and vitamin E intake, cholesterol intake and height explained 5-7% each of the remaining variance in incidence. Associations with lutein and vitamin E were inverse, whereas those with cholesterol and height were direct. Dietary beta-carotene intake was not associated with lung cancer incidence. These ecological data provide evidence for a protective effect of lutein against lung cancer. A protective effect of dietary vitamin E and a risk-enhancing effect of dietary cholesterol are also suggested.
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PMID:An ecological study of diet and lung cancer in the South Pacific. 755 46

Sixty-three male cigarette smokers were entered into a cross-sectional study to determine whether inverse associations existed between polycyclic aromatic hydrocarbon (PAH)-DNA adduct levels and intake/serum levels of vitamin A, vitamin C and vitamin E. Associations between PAH-DNA adducts and intakes of carotene, as well as serum levels of beta-carotene, were also determined. Fasting blood samples were collected for assays of PAH-DNA adducts in circulating mononuclear cells, plasma cotinine and serum levels of vitamin A, beta-carotene, vitamin C and vitamin E. Since genetic deficiency in the detoxifying enzyme glutathione S-transferase M1 (GSTM1) has been associated with increased risk of lung cancer, GSTM1 genotype was also determined. Analysis of PAH-DNA adducts by competitive enzyme-linked immunosorbent assay (ELISA) indicated that 70% of the subjects had detectable adducts, with a mean of 4.38 adducts/10(8) nucleotides (range 1.00-24.1/10(8)). Pearson's method was utilized to determine whether any associations existed between the various host variables and PAH-DNA adducts. Previously, no significant associations were found between PAH-DNA adducts and cigarettes smoked/day, pack-years, daily/life-time tar exposures or plasma cotinine levels (Santella et al., Carcinogenesis, 13, 2041-2045, 1992). PAH-DNA adducts were inversely associated with serum cholesterol-adjusted vitamin E levels (r = -0.25, P < or = 0.05) and with smoking-adjusted vitamin C serum levels (r = -0.22, P < or = 0.09). Stratification by GSTM1 genotype indicated that these associations were limited to subjects with the null genotype. The relationship between adducts and serum cholesterol-adjusted vitamin E was significant in those of the null genotype (r = -0.38, P < or = 0.04), but not in those with the gene present (r = -0.12, P = 0.5). Similarly, for smoking-adjusted vitamin C, the relationship with adducts was stronger in subjects with the null genotype (r = -0.35, P < or = 0.06) than in those with GSTM1 present (r = -0.05, P = 0.77). These results are consistent with findings of prior epidemiological studies identifying significant inverse associations between anti-oxidant micronutrient status or GSTM1 genotype and the incidence of lung cancer. Additional studies should be conducted to confirm a possible role for vitamin E in PAH-DNA adduct formation and to explore further the possible roles of vitamin A, beta-carotene and vitamin C in modulating adduct formation and lung cancer risk.
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PMID:Polycyclic aromatic hydrocarbon-DNA adducts in smokers and their relationship to micronutrient levels and the glutathione-S-transferase M1 genotype. 795 90

Head and neck cancer remains a common cause of mortality and morbidity in the United States and throughout the world. In spite of advances in the management of patients with advanced disease, overall survival in this group remains poor. Furthermore, although cancer mortality is lower in patients with early-stage disease, treatment results in significant morbidity, and these patients also face the risk of developing a second primary tumor. Chemoprevention is an innovative approach to decrease overall cancer morbidity and mortality using substances that are capable of preventing cancer progression. Head and neck cancer is an excellent model for chemoprevention, as its biology is consistent with the two concepts important for the development of chemoprevention strategies: field cancerization and multistep carcinogenesis. Several classes of compounds have been evaluated in chemoprevention trials. The most frequently studied agents, the retinoids, were found frequently to induce remissions in patients with oral leukoplakia. Furthermore, retinoids prevented progression to malignancy in one randomized maintenance study. Other agents, including beta-carotene and vitamin E, have been found also to have activity in the management of oral leukoplakia. However, the clinical role of chemopreventive agents in reducing cancer mortality remains to be defined. Two studies, one in head and neck cancer and one in lung cancer, have shown the ability of retinoids to prevent the development of second primary tumors. Current large randomized trials are defining the effectiveness of these agents in reducing the mortality of aerodigestive tract tumors in individuals at high risk.
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PMID:Biology and chemoprevention of head and neck cancer. 805 3

The U.S. National Cancer Institute and the Finnish National Public Institute jointly sponsored a large double-blind, placebo-controlled primary-prevention trial to examine the effects of vitamin E and beta-carotene supplementation on reducing the incidence of lung cancers in male smokers, ages 50-69 years. Supplementation did not result in a significant reduction in lung cancer, and a higher incidence of lung cancer was observed in the group receiving beta-carotene. These results should be examined within the context of the population studied before they are cited as definitive.
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PMID:The Alpha-Tocopherol, Beta-Carotene Cancer Prevention Study in Finland. 809 Mar 76

The Alpha-Tocopherol, Beta-Carotene (ATBC) Lung Cancer Prevention Study was a randomized, double-blind, placebo-controlled, 2 x 2 factorial design, primary prevention trial testing the hypothesis that alpha-tocopherol (50 mg/day) and beta-carotene (20 mg/day) supplements reduce the incidence of lung cancer and possibly other cancers. Total and disease-specific mortality and incidence of various diseases and symptoms were monitored for safety. Between 1985 and 1993, 29,133 eligible male smokers aged 50 to 69 years at entry were randomized to receive daily active supplements or placebo capsules for 5 to 8 years (median 6.1 years), accumulating 169,751 follow-up years. This report describes the study design, methods, and protocol as well as the baseline characteristics and capsule compliance of the participants. The ATBC Study is the largest lung cancer chemoprevention trial conducted to date.
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PMID:The alpha-tocopherol, beta-carotene lung cancer prevention study: design, methods, participant characteristics, and compliance. The ATBC Cancer Prevention Study Group. 820 74

Epidemiological studies have not given sufficient evidence yet for the role of antioxidant nutrients in the prevention of cardiovascular disease. As regards cancer, an inverse association between beta-carotene intake and specific types of cancer, especially lung cancer, has been shown. For other cancer sites and other antioxidants, the association is less clear. The EURAMIC Study, an EC Concerted Action, is a case-control study conducted in 11 countries, in which the combined effect of vitamin E, beta-carotene and selenium, in relation to fatty acid intake, will be examined. The disease endpoints are acute myocardial infarction and early-stage breast cancer. The broad range of antioxidant intake, the use of biomarkers of exposure, and the analysis of pooled data will allow an estimate of the strength of the putative beneficial effect. In this paper the background and design of the study will be introduced.
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PMID:EURAMIC Study: antioxidants, myocardial infarction and breast cancer. Design and main hypotheses. 826 23

The hypotheses that the antioxidant vitamin E provides protection against lung cancer and that this hypothetical protection is modified by smoking status were investigated using two different study designs--a cohort study and a nested case-control study--among Finnish men aged 15 years and over. In the cohort study the association between vitamin E intake and lung cancer risk was studied among 5,254 individuals with 121 lung cancer cases that occurred during a 19-year follow-up, and in the nested case-control study the association between serum vitamin E level and lung cancer risk was studied using 144 lung cancer cases and 270 matched controls as a basis. There was a significant inverse association between vitamin E status and lung cancer occurrence among nonsmokers but not among smokers in both designs. The relative risk of lung cancer between the lowest and highest tertiles of vitamin E intake was 3.3 among nonsmokers and 0.8 among smokers. The corresponding results for serum vitamin E were 6.6 and 0.8, respectively. Nonsmokers with simultaneously low serum levels of vitamin E and other micronutrients (i.e., beta-carotene, retinol and selenium) had a 12-fold greater risk of lung cancer in comparison with men having more satisfactory levels. The corresponding number among smokers was three. The results suggest that vitamin E status is primarily associated with lung cancer risk among nonsmokers. Firm conclusions can, however, be drawn only on the basis of intervention trials.
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PMID:Vitamin E and smoking and the risk of lung cancer. 851 53

The possible association between lung cancer and a polymorphism of the CYP1A1 gene specific to African-Americans was examined using peripheral blood DNA from 144 incident cases of lung cancer and 230 population controls with detailed data on smoking and other risk factors for the disease. The CYP1A1 variant allele was present in 15.2% of controls and 16.7% of cases. The smoking-adjusted odds ratio for the presence of the variant allele in relation to lung cancer risk overall was 1.3 (95% confidence interval, 0.7-2.4). According to histological type, the strongest association was observed for squamous cell carcinoma (odds ratio, 2.1), but this result was compatible with chance (95% confidence interval, 0.8-5.9). Adenocarcinoma was not materially associated with the presence of the variant allele (odds ratio, 1.3; 95% confidence interval, 0.5-3.2). No important associations were observed upon stratification by several risk factors for lung cancer, including smoking history, occupational exposures to asbestos and motor vehicle exhaust, or low intake of the micronutrient antioxidants beta-carotene, vitamin E, or vitamin C. These results do not confirm an earlier report that this CYP1A1 polymorphism may be an important risk factor for adenocarcinoma of the lung in African-Americans.
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PMID:Lung cancer risk in African-Americans in relation to a race-specific CYP1A1 polymorphism. 879 7

To assess whether antioxidants may reduce the risk of cancer, we reviewed the epidemiologic literature from 1985 through 1993. We assessed the separate relationships of three antioxidants (carotenoids, vitamin C, and vitamin E) with six sites of cancer (lung, upper aerodigestive tract, uterine cervix, colon, breast, prostate). This review was limited to dietary intake or serum nutrient studies that met a predefined set of methodologic standards. We judged the evidence in support of causal relationships based upon consistency of results across studies, strength of association, and evidence of a dose-response relationship. The data concerning carotenoids and lung cancer risk were most consistent (protection found in 4 of 8 diet studies and 5 of 6 serum studies), with strong associations that tended to follow a dose-response pattern. For lung cancer, there was weaker evidence of protection from vitamin C (2 of 6 diet studies) and vitamin E (3 of 4 serum studies). For upper aerodigestive tract cancers (oral cavity, pharynx, or larynx), there was evidence of a protective effect of carotenoids (3 of 4 diet studies) and vitamin C (4 of 5 diet studies). For cancer of the uterine cervix, we found suggestive evidence of protection from vitamin C (4 of 5 diet studies) and perhaps carotenoids (2 of 5 diet studies). For cancers of the colon, breast, and prostate, the current data do not support a protective effect of antioxidants. More definite conclusions about the benefits of antioxidants in cancer prevention will be derived from on-going intervention trials.
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PMID:Epidemiologic studies of antioxidants and cancer in humans. 852 20

Evidence supports the potential role of beta-carotene in cancer prevention. Basic research has demonstrated that beta-carotene can trap organic free radicals and/or deactivate excited oxygen molecules which may have an anticancer effect by preventing tissue damage. Although observational epidemiologic studies are not entirely consistent, many show an inverse association between dietary intake or blood levels of beta-carotene and subsequent cancer risk. Two large-scale randomized trials of beta-carotene have been completed. A Finnish trial demonstrated no benefit of beta-carotene among middle-aged male smokers, with those assigned to this supplement in fact experiencing an increased risk of lung cancer. However, because of the long latency period for cancer, which may be a decade or more, the six-year duration of treatment in this trial may have been inadequate to detect an anticancer effect. A Chinese trial demonstrated a modest reduction in cancer mortality from a combined regimen of beta-carotene, vitamin E, and selenium. The effect of the individual agents could not be assessed, and because the trial was carried out among a nutritionally deficient population, its results may not have direct relevance to well-nourished individuals. Several additional large-scale trials of beta-carotene are ongoing. The Physicians' Health Study, which is testing beta-carotene among 22,071 US male physicians, will have an average duration of treatment of 12.5 years at its scheduled termination in late 1995. Data in women will be available from the Women's Health Study, which began in 1992, and will randomize approximately 40,000 US female health professionals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:beta-carotene and cancer chemoprevention. 853 2


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