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

We studied the selenium (Se) concentration in whole blood and plasma, glutathione peroxidase (GSH-Px) activity in red blood cells and plasma, as well as both of these parameters in cancerous and tumor-free lung tissue of lung cancer patients. Blood samples were taken from 84 cancer patients and 61 healthy controls. Normal and neoplastic lung tissues were obtained from 57 patients at the time of surgery. Se concentrations in whole blood and plasma were lower by 23% (p < 0.001) in patients compared with controls. GSH-Px activity in red cells was lower by 20.2% (p < 0.004) and in plasma by 11.7% (p < 0.05) in patients than in the control group. On the other hand, the tumor Se level was higher by 66.6% (p < 0.0001) and GSH Px activity by 49.5% (p < 0.0001) than in adjacent tumor-free tissue. No differences in Se concentrations and GSH-Px activities were found between squamous cell carcinoma and adenocarcinoma nor among the clinical stages of the disease. In the whole blood and plasma of cancer patients significantly lower Se concentrations were found in smokers than in nonsmokers. Significantly lower Se concentrations were also found among cancer patients who were smokers compared with controls. These findings show that in the blood of cancer the antioxidant ability, as measured by Se and GSH-Px, is reduced significantly. The cause of increased Se and GSH-Px in the malignant part of the lung is not understood and requires further studies.
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PMID:Decreased selenium concentration and glutathione peroxidase activity in blood and increase of these parameters in malignant tissue of lung cancer patients. 927 Sep 89

The hypothesis that a dietary supplement of selenium (Se) may reduce cancer risk was tested experimentally in humans. Patients with histories of basal/squamous cell carcinomas of the skin were assigned randomly in double-blind fashion to daily oral supplements of either Se-enriched yeast (200 micrograms Se/day), or a low-Se yeast placebo. A total of 1312 patients recruited in 1983-1990 were followed with regular dermatologic examinations through 1993 for a total of 8269 person-years of observation. Skin cancer diagnoses were confirmed histologically. Plasma Se concentration was determined at 6-12 months intervals. All deaths and patient-reported illnesses were recorded; reported cancers were confirmed and documented by consultation with the patient medical care providers. The results indicate that Se did not significantly affect the primary endpoints: incidences of recurrent basal/squamous cell carcinomas of the skin. However, Se-treatment was associated with reductions in several secondary endpoints: total mortality, mortality from all cancers combined, as well as the incidence of all cancers combined, lung cancer, colorectal cancer and prostate cancer. The consistencies of these associations over time, between study clinics and for the leading cancer sites strongly suggests benefits of Se-supplementation for this cohort of patients, supporting the hypothesis that supplemental Se can reduce cancer risk. Although Se did not shown protective effects against non-melanoma skin cancers, the suggested reductions in risks to other frequent cancers demand further evaluation in well controlled clinical intervention trials.
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PMID:Reduction of cancer risk with an oral supplement of selenium. 931 15

In this review, large-scale randomized intervention trials evaluating the effects of vitamin and mineral supplementation on cancer rates are summarized. The trials enrolled up to 30,000 adults who were followed for up to 12 years, and included assessments of multiple vitamin and mineral combinations in an area of China with limited micronutrient intake and one of the world's highest cancer rates; and of beta carotene, vitamin E, or selenium in several more well nourished western populations, some at very high risk of lung cancer. Results to date have been mixed. Significantly lower cancer mortality has been found among those supplemented with a combination of beta carotene, vitamin E, and selenium in the China trial and with selenium in the United States, but risks of lung cancer were increased in Finnish and American trials provided with high-dose beta carotene supplementation. In combination, the trials indicate that the relation between specific micronutrient intake and cancer risk is complex, but have provided information to target further research on the potential benefits of selenium, vitamin E, and combinations of vitamins and minerals.
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PMID:Vitamin/mineral supplementation and cancer risk: international chemoprevention trials. 934 99

Selenium is an essential trace element, the deficiency of which is associated with an increased incidence of some human cancers. Dietary supplementation with selenium has been reported to produce a decrease in the incidence of some cancers in humans. Thioredoxin reductase (TR) is a newly discovered homodimeric selenocysteine (SeCys)-containing protein that catalyzes the NADPH-dependent reduction of the redox protein thioredoxin (Trx). Trx is overexpressed by a number of human tumors, and experimental studies have shown that Trx contributes to the growth and to the transformed phenotype of some human cancer cells. Thus, TR, by reducing Trx, could play a role in regulating the growth of normal and cancer cells. We have investigated mechanisms by which selenium, in the form of sodium selenite, added to serum-free growth medium regulates TR activity in cancer cell lines. Selenium caused a dose-dependent increase in cellular TR activity. The increase in TR activity produced by 1 microM Se compared to medium with no added selenium was: for MCF-7 breast cancer cells, 37-fold; for HT-29 colon cancer cells, 19-fold; and for A549 lung cancer cells, 8-fold. In contrast, Jurkat and HL-60 leukemia cells showed no increase in TR activity. The half-life of the time course of induction of TR in HT-29 cells after adding selenium was 10 h. The increase in TR activity was accompanied by an increase in TR protein levels up to 3-fold and an increase in the specific activity of the enzyme of 5-32-fold, depending on the cell line. Studies using 75Se showed that the amount of selenium incorporated into TR increased with increasing selenium concentration up to a ratio of 1 selenium per TR monomer. There was an increase in TR mRNA levels of 2-5-fold at 1 microM selenium and an increase in the stability of TR mRNA with a half-life for degradation of 21 h compared to 10 h in the absence of selenium. Trx mRNA and protein levels and Trx mRNA stability were not affected by selenium. The results of the study show that the increase in TR activity caused by selenium is specific and due to several effects, including an increase in the stability of TR mRNA leading to increased TR mRNA levels, an increase in TR protein, but predominantly to an increase in the specific activity of TR associated with increased incorporation of selenium into the enzyme.
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PMID:Mechanisms of the regulation of thioredoxin reductase activity in cancer cells by the chemopreventive agent selenium. 935 64

Lung cancer cases diagnosed during the period 1975 through 1993 and matched controls were identified in the rosters of Washington County, Maryland residents who had donated blood for a serum bank in 1974 or 1989. Plasma from participants in the 1989 project was assayed for ascorbic acid; serum or plasma was assayed for participants in either project for alpha- and beta-carotene, cryptoxanthin, lutein/zeaxanthin, lycopene, alpha-tocopherol, selenium, and peroxyl radical absorption capacity. Among the total group of 258 cases and 515 controls, serum/plasma concentrations were significantly lower among cases than controls for cryptoxanthin, beta-carotene, and lutein/zeaxanthin with case-control differences of -25.5, -17.1, and -10.1%, respectively. Modest nonsignificant case-control differences in a protective direction were noted for alpha-carotene and ascorbic acid. There were only trivial differences for lycopene, alpha-tocopherol, selenium, and peroxyl radical absorption capacity. Findings are reported for males and females and for persons who had never smoked cigarettes, former smokers, and current smokers at baseline. These results and those from previous studies suggest that beta-carotene is a marker for some protective factor(s) against lung cancer; that cryptoxanthin, alpha-carotene, and ascorbic acid need to be investigated further as potentially protective factors or associates of a protective factor; and that lycopene, alpha-tocopherol, selenium, and peroxyl radical absorption capacity are unlikely to be associated with lung cancer risk. Until specific preventive factors are identified, the best protection against lung cancer is still the avoidance of airborne carcinogens, especially tobacco smoke; second best is the consumption of a diet rich in fruits and vegetables.
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PMID:The risk of developing lung cancer associated with antioxidants in the blood: ascorbic acid, carotenoids, alpha-tocopherol, selenium, and total peroxyl radical absorbing capacity. 1882 Feb 77

Selenium, zinc and copper were measured in plasma, hair and tissue of patients affected by either breast or lung cancer and their controls. A decrease in plasma Se and Zn in women affected by breast cancer was observed, whereas plasma Cu was increased in lung cancer. No significant modification was found in hair trace element levels adjusted for the main confounders, in particular for hair treatment which altered Se content. The examined elements were highly concentrated in cancerous vs normal tissue, but results changed according to the unit used to express results. The usefulness and significance of these biomarkers of trace element status are discussed in the light of the most recent literature data.
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PMID:Observations on the use of plasma, hair and tissue to evaluate trace element status in cancer. 944 63

The hypothesis that low selenium may in some circumstances be a risk factor for lung cancer was investigated in a case-control study nested within a longitudinal study. Serum samples from 9,101 cancer-free individuals were collected and stored at -20 degrees C by the Finnish Mobile Clinic in 1968-1971 and 1973-1976. During follow-up until the end of 1991, 95 cases of lung cancer were diagnosed. Selenium concentrations were determined from the serum samples of the cases and 190 controls, individually matched for sex, age, and place of residence. Mean levels of serum selenium in cases and controls were 53.2 microg/liter and 57.8 microg/liter, respectively. The relative risk of lung cancer between the highest and lowest tertiles of serum selenium, adjusted for smoking, serum alpha-tocopherol, serum cholesterol, serum copper, serum orosomucoid, and body mass index (kg/m2), was 0.41 (95% confidence interval (CI) 0.17-0.94). The association was stronger at lower levels (<5.9 mg/liter) of alpha-tocopherol (relative risk=0.24, 95% CI 0.07-0.85). The association was also pronounced among current smokers and at higher levels of serum orosomucoid and serum copper. The relative risk for smokers who were twice ranked in higher selenium tertiles, at an interval of 4-7 years, in comparison with smokers who remained in the lowest tertile was 0.16 (95% CI 0.04-0.74). In accordance with the hypothesis, the findings suggest that very low selenium status may contribute to the risk of lung cancer.
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PMID:Is low selenium status a risk factor for lung cancer? 982 69

This paper (and an extensive supplementary report) considers how far cancer/risk factor associations based on epidemiology have been confirmed by evidence from 226 studies involving interventions other than smoking. Many are small, uncontrolled, of unrepresentative populations, concern cancer markers not cancer, and may involve combinations of agents. Many agents suspected of causing cancer are untested by intervention trials. For seven of 16 agents tested (fibre, folic acid, low-fat diet, riboflavin, zinc, vitamin Bs, and vitamin D), the evidence is clearly inadequate to confirm or deny the epidemiology, while the evidence relating to calcium only concerns biomarkers. For other agents, the evidence relating to cancer itself is weak. In studies where cancer is the endpoint, only three effects have been replicated: (a) selenium supplementation and decreased liver cancer incidence, (b) treatment by the retinoid etretinate and reduced bladder tumours in susceptible individuals, and (c) beta-carotene supplementation and increased lung cancer incidence. Studies involving pre-cancerous conditions as the endpoint, which have a number of practical advantages, more frequently report benefits of intervention. Thus, oral pre-cancerous lesions can certainly be reduced by beta-carotene, vitamin A, and other retinoids, and possibly by vitamin E. It also seems that retinoids can reduce pre-cancerous cervix, skin and lung lesions, that vitamin C and the NSAID sulindac can reduce colonic polyps, and that sunscreens can reduce solar keratoses. Our findings clearly show that the great majority of causal relationships suggested by epidemiology have not been validated by intervention trials. This may be partly due to lack of suitable studies of adequate size or duration, or to using single dietary compounds as agents that are by themselves not responsible for the epidemiologically-observed associations between diet and cancer. However, this lack of validation must cause concern in view of the markedly conflicting evidence on beta-carotene and lung cancer between epidemiological and intervention studies. More intervention studies are needed, but in their absence, caution in interpreting epidemiological findings is warranted.
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PMID:Intervention studies on cancer. 1054 93

Inverse correlations have been found in most studies on the relationship between dietary intake and plasma concentrations of carotenoids on one side and degenerative diseases such as cancer and cardiovascular diseases on the other side. Protective effects of carotenoids have been found for pathologies of the retina and the skin. Concentrations of these molecules in blood are lower in digestive pathologies and HIV. Short- and long-term toxicity of carotenoids was found to be low. In combination with the beneficial effects found for diets rich in carotenoids, this has initiated trials with relatively high doses of carotenoid supplements. In the study in Linxian (China) in a rural population with poor nutritional status, supplementation with beta-carotene, zinc, selenium and vitamin E lowered total mortality and mortality from stomach cancer. Other studies (ATBC, Caret.) on well-fed subjects did not show beneficial effects on mortality from cancer and cardiovascular diseases. On the contrary, higher mortality and lung cancer incidence was found in supplemented subjects that were also exposed to asbestos and cigarette smoke. In these studies, doses of supplemental beta-carotene were high and varied from 20 to 50 mg/day. One still ongoing study, called Suvimax, doses subjects for eight years with a cocktail of vitamins and minerals including 6 mg per day of beta-carotene. This supplementation with physiologically seen more "normal" doses might give clarity on the question if beta-carotene is the protective factor in fruits and vegetables.
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PMID:[Carotenoids: 2. Diseases and supplementation studies]. 1037 77

Cancer chemoprevention is defined as the use of specific chemical compounds to prevent, inhibit or reverse carcinogenesis. Chemopreventive intervention can occur throughout carcinogenesis. Many specific food components (e.g. calcium, selenium, folic acid) may also be suitable for chemopreventive use. Chemopreventive drugs are usually administered chronically and are expected to have low toxicity. A variety of mechanisms explain the actions of chemopreventive compounds including modification of carcinogen activation and cellular uptake, inhibition of aberrant signal transduction, induction of apoptosis and inhibition of angiogenesis. As our understanding of carcinogenesis has developed, more specific pharmacologic targets are being selected, e.g. retinoid receptors or cyclo-oxygenases. Definitive, large-scale placebo-controlled randomized trials are necessary to determine the clinical efficacy of chemopreventive compounds. Recent examples include the striking effectiveness of tamoxifen in reducing the risk of breast cancer in women at high risk. Conversely, beta carotene increased the risk of lung cancer in those who continued to smoke and/or who were exposed to asbestos. The future development of predictive risk models that take into account gene-environment interactions will be of considerable value in deciding on specific chemopreventive interventions in those at increased risk by virtue of life style or occupational exposures.
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PMID:An overview of preventive strategies for pancreatic cancer. 1043 20


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