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

A possible protective effect of selenium against lung cancer has been indicated in recent studies. Workers in copper smelters are exposed to a combination of airborne selenium and carcinogens. In this study lung tissue concentrations of selenium, antimony, arsenic, cadmium, chromium, cobalt, lanthanum, and lead from 76 dead copper smelter workers were compared with those of 15 controls from a rural area and 10 controls from an urban area. The mean exposure time for the dead workers was 31.2 years, and the mean retirement time after the end of exposure 7.2 years. Lung cancer appeared in the workers with the lowest selenium lung tissue levels (selenium median value 71 micrograms/kg wet weight), as compared with both the controls (rural group, median value 110; urban group, median value 136) and other causes of death among the workers (median value 158). The quotient between the metals and selenium was used for comparison: a high quotient indicating a low protective effect of selenium and vice versa. The median values of the quotients between antimony, arsenic, cadmium, lanthanum, lead, chromium, and cobalt versus selenium were all numerically higher among the cases of lung cancer, the first five significantly higher (p less than 0.05) in 28 of the 35 comparisons between the lung cancer group and all other groups of smelter workers and controls. The different lung metal concentrations for each person were weighted according to their carcinogenic potency (Crx4 + Asx3 + Cdx2 + Sbx1 + Cox1 + Lax1 + Pbx1) against their corresponding selenium concentrations. From these calculations the protective effect of selenium was even more pronounced.
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PMID:Protective effect of selenium on lung cancer in smelter workers. 404 90

A narrow band of counties extending along the southeastern Atlantic coast from Jacksonville, Florida to Charleston, South Carolina were found to have excessively high incidence rates for esophageal cancer in non-white males. White males in the same areas have a 30% higher incidence rate for lung cancer but only average incidence rates were found for non-white males. Selenium is considered to decrease cancer risk in the animal model. In this coastal region, a study of 130 cancer patients who developed a malignancy 2-12 years after baseline examination showed no dose response relationship between baseline serum selenium levels and risk of subsequent cancer.
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PMID:Is serum selenium a risk factor for cancer? 406 2

Fifteen tumor-containing specimens were obtained directly from patients with small cell carcinoma of the lung and tested for their ability to grow in serum-supplemented medium and in serum-free medium supplemented with hydrocortisone, insulin, transferrin, estrogen, and selenium (HITES). The tumor cells replicated in 14 of 15 cases (93%) in the HITES medium and in 10 of 15 cases (67%) in the serum-supplemented medium. The neoplastic origin of the cells growing in the HITES medium was confirmed by standard cytologic criteria, by DNA content analysis using flow cytometry, and by their ability to form colonies in agarose and tumors in athymic nude mice. While the tumor cells had very similar morphologies in both media, the serum-free medium did not support the growth of nonmalignant stromal cells, and essentially pure cultures of replicating tumor cells were obtained 7-10 days after plating. The selectivity of the HITES medium was demonstrated by the failure of cells to grow in 20 specimens cytologically negative for small cell carcinoma and in 9 of 10 specimens containing other tumor types (including other types of lung cancer). The results demonstrate that a chemically defined medium, determined by work on tissue culture-adapted human tumor lines, can support the selective growth of tumor specimens obtained directly from patients. Such selective formulas are probably specific for different tumor types and thus could be used for diagnosis, drug sensitivity testing in vitro, and identification of factors regulating tumor growth. All of these have direct application to patient treatment.
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PMID:Selective growth in serum-free hormone-supplemented medium of tumor cells obtained by biopsy from patients with small cell carcinoma of the lung. 626 40

Tobaccos from countries with high and low incidences of lung cancer were analyzed. Tobacco concentrations of polonium-210 were similar in cigarettes from high- and low-incidence countries, as were levels of cigarette smoke tar and nicotine. Tobaccos from low-incidence countries had significantly lower Alternaria spore counts. Mean selenium concentrations of tobaccos from the high-incidence countries (0.16 +/- 0.05 micrograms/g) were significantly lower than those of tobaccos from the low-incidence countries (0.49 +/- 0.22 micrograms/g).
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PMID:Composition of tobaccos from countries with high and low incidences of lung cancer. I. Selenium, polonium-210, Alternaria, tar, and nicotine. 693 62

Tissue concentrations of antimony in lung, liver, and kidney tissue from a group of deceased smelter workers from northern Sweden have been compared with those of a group of persons without occupational exposure from a nearby area. Neutron activation analysis was used to determine the antimony concentration of lung tissue from exposed workers; these concentrations were 12-fold higher than those of referents (p less than 0.001). For lung tissue there was no tendency towards decreased antimony concentrations with time (up to 20 a) after the cessation of exposure, and this result indicates a long biological half-time. The highest values were found for workers who had worked for many years at the roasters and in the arsenic and selenium departments. There was no significant difference between the antimony concentration of the lung tissue from workers who had died of lung cancer and those of persons who died of other malignancies, cardiovascular disease, or other causes. This finding does not however rule out the possibility of a role for antimony in the etiology of lung cancer among smelter workers since multiple factors may have been operating. The antimony concentration of the liver tissue and the kidney cortex did not differ from the corresponding values of the reference group; this finding indicates either a short biological half-time or insignificance for the systemic distribution of antimony.
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PMID:Antimony in lung, liver and kidney tissue from deceased smelter workers. 715 39

Concentrations of arsenic and selenium in lung, liver, and kidney tissue from dead smelter workers and from a control group have been determined with the aid of neutron activation analysis. A sevenfold increase of arsenic was found in lung tissue from the exposed workers compared with the control group. The median value of arsenic in lung tissue from workers dead from respiratory cancer was not higher than corresponding values from workers dead from other malignancies or from cardiovascular or other diseases. With increasing period of retirement the malignancies or from cardiovascular or other diseases. With increasing period of retirement the arsenic content diminished in liver tissue but not in lung tissue, indicating a long biological half life of arsenic in lung tissue. The workers dead from malignancies had a higher As/Se quotient than workers dead from other diseases, which does not contradict the protective theory of selenium. Accumulation of antimony, cadmium, lead and lanthanum was observed in lung tissue from the exposed workers. Six of the workers died from lung cancer and the highest concentrations of any of the elements were always observed in the lung tissue from these six cases. This observation speaks in favour of a multifactorial cause behind the excess mortality from lung cancer in smelter workers.
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PMID:Arsenic and selenium in lung, liver, and kidney tissue from dead smelter workers. 723 43

Polymorphisms in inherited metabolic traits and intake of dietary antioxidants have been reported to be associated with risk for the development of lung cancer in smokers. This increased risk of lung cancer is presumably attributable to the accumulation of DNA damage. We conducted a study to investigate whether genetic metabolic variants and antioxidant consumption affected the sister chromatid exchange (SCE) level in lymphocytes. Study subjects were 78 friends and spouses of cases from a case-control study of lung cancer designed to investigate the association of metabolic polymorphisms with lung cancer. The metabolic traits studied included glutathione S-transferase class mu and variants of P-450 isoenzymes CYP1A1 and CYP2D6. Intake of antioxidants including vitamins A, C, and E and selenium was determined through the administration of a validated, semiquantitative food frequency questionnaire. Detailed information on smoking, family history of cancer, medical history, and environmental and occupational exposures was also obtained in an interviewer-administered questionnaire. Smoking status was found to be significantly associated with SCE frequency. In addition SCE frequency decreased with the period of time since quitting smoking. The presence of one or more glutathione S-transferase class mu alleles was associated with significantly lower SCE. Higher intake of vitamin A and selenium was also inversely associated with SCE level. Thus, the results suggest that glutathione S-transferase class mu and the intake of vitamin A and selenium may modulate the accumulation of chromosomal damage in lymphocytes.
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PMID:Glutathione S-transferase mu genotype, diet, and smoking as determinants of sister chromatid exchange frequency in lymphocytes. 754 11

The potential role of antioxidant vitamins (ascorbic acid, beta-carotene, alpha-tocopherol), minerals (selenium) and non-vitamin natural antioxidants (e.g. glutathione) in the prevention of cancer diseases is reviewed. Free oxygen radicals, especially the hydroxyl radical .OH modify nitrogen bases, split DNA, stimulate oncogene activators and probably in many other ways participate in carcinogenesis. In a great number of experimental and epidemiological studies a significant increase of cancer risk in laboratory animals and in humans with low antioxidant status was found. Significant protective effects of ascorbic acid, beta-carotene, alpha-tocopherol and selenium against the incidence of gastrointestinal and lung cancer were achieved in most, but not in all prospective and intervention studies. It is probable that extremely high premature cancer mortality in postcommunist countries of Central and East Europe is caused by high consumption of cigarettes, spirits and saturated fats, by pollution, and by very low consumption of the chief sources of natural antioxidants (fruits, vegetables). (Fig. 13, Ref. 29).
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PMID:[The role of antioxidants in the prevention of tumors]. 755 84

Serum samples were collected in Hiroshima and Nagasaki, Japan, from 1970 to 1972 for 208 persons who in 1973-1983 developed stomach cancer; for 77 who in 1973-1983 developed lung cancer; and for controls matched for age, sex, city, and season of blood collection. Average serum levels of selenium and zinc were slightly (< 5%) but not significantly lower among the cancer cases than among controls. Smoking-adjusted risks of lung cancer were elevated only among those in the lowest quartiles of serum selenium [odds ratio (OR) = 1.8] and zinc (OR = 1.3); the trends in risk of this cancer with decreasing serum levels were neither linear nor significant. Little or no excess risk of stomach cancer was observed among those with lowest levels of selenium (OR = 1.0) or zinc (OR = 1.2). These exploratory findings add to limited data available from other reports showing slightly increased risks of lung cancer associated with low blood levels of selenium, but suggest little association with either lung or stomach cancer across normal selenium or zinc ranges in this Japanese population.
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PMID:Prediagnostic serum selenium and zinc levels and subsequent risk of lung and stomach cancer in Japan. 800 Feb 96

The consistent deletion of 3p21 in lung cancer has led to intensive efforts to identify a lung tumor suppressor gene at this locus. We recently mapped the gene for the selenium-dependent drug-detoxifying enzyme glutathione peroxidase 1 (GPX1) to this location by in situ hybridization. We developed a polymerase chain reaction-based assay which demonstrated the existence of three GPX1 alleles characterized by the number of alanines in a polyalanine coding sequence in exon 1. These three alleles produced a heterozygote frequency of 70% in two separate populations: normal tissue DNA taken from Centre d'Etude du Polmorphisme Humain (CEPH) parents and normal tissue taken from cancer patients. In contrast, 10 heterozygote tumors were detected out of 64 lung cancer specimens. Linkage analysis of GPX1 to Genethon 3p markers in CEPH pedigrees demonstrated that GPX1 was located between the two microsatellite markers believed to flank the lung cancer deletion site. Nucleotide sequence analysis of GPX1 alleles did not reveal any mutations of this gene in lung tumors. However, sequence analysis did reveal that the three GPX1 alleles were characterized by three nucleotide substitutions in addition to the polyalanine polymorphism, including a substitution at codon 198 which results in either a proline or leucine at that position. Therefore, the different GPX1 alleles encode structurally different hGPx1 subunits. In addition, analysis of allele frequency suggests that the GPX1*ALA7 allele may occur less frequently in tumors with 3p21 deletions.
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PMID:Loss of heterozygosity of the human cytosolic glutathione peroxidase I gene in lung cancer. 800 Dec 33


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