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Selenium, selenoenzymes, oxidative stress and risk of neoplastic progression from Barrett's esophagus: results from biomarkers and genetic variants.

Abstract

Clinical trials have suggested a protective effect of selenium supplementation on the risk of esophageal cancer, which may be mediated through the antioxidant activity of selenoenzymes. We investigated whether serum selenium concentrations, selenoenzyme activity, oxidative stress and genetic variation in selenoenzymes were associated with the risk of neoplastic progression to esophageal adenocarcinoma (EA) and two intermediate endpoints, aneuploidy and tetraploidy. In this prospective cohort study, during an average follow-up of 7.3 years, 47 EA cases, 41 aneuploidy cases and 51 tetraploidy cases accrued among 361 participants from the Seattle Barrett's Esophagus Research Study who were free of EA at the time of blood draw and had at least one follow-up visit. Development to EA was assessed histologically and aneuploidy and tetraploidy by DNA content flow cytometry. Serum selenium concentrations were measured using atomic absorption spectrometry, activity of glutathione peroxidase (GPX) 1 and GPX3 by substrate-specific coupled test procedures, selenoprotein P (SEPP1) concentrations and protein carbonyl content by ELISA method and malondialdehyde concentrations by HPLC. Genetic variants in GPX1-4 and SEPP1 were genotyped. Serum selenium was not associated with the risk of neoplastic progression to EA, aneuploidy or tetraploidy (P for trend = 0.25 to 0.85). SEPP1 concentrations were positively associated with the risk of EA [hazard ratio (HR) = 3.95, 95% confidence intervals (CI) = 1.42-10.97 comparing the third tertile with the first] and with aneuploidy (HR = 6.53, 95% CI = 1.31-32.58), but not selenoenzyme activity or oxidative stress markers. No genetic variants, overall, were associated with the risk of neoplastic progression to EA (global p = 0.12-0.69). Our results do not support a protective effect of selenium on risk of neoplastic progression to EA. Our study is the first to report positive associations of plasma SEPP1 concentrations with the risk of EA and aneuploidy, which warrants further investigation.

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  • Authors+Show Affiliations

    ,

    Public Health Science Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.

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    Source

    PloS one 7:6 2012 pg e38612

    MeSH

    Adenocarcinoma
    Aged
    Aged, 80 and over
    Aneuploidy
    Barrett Esophagus
    Biomarkers, Tumor
    Esophageal Neoplasms
    Female
    Follow-Up Studies
    Glutathione Peroxidase
    Humans
    Male
    Middle Aged
    Neoplasm Proteins
    Oxidative Stress
    Prospective Studies
    Retrospective Studies
    Selenium
    Selenoproteins

    Pub Type(s)

    Clinical Trial
    Journal Article
    Research Support, N.I.H., Extramural

    Language

    eng

    PubMed ID

    22715394

    Citation

    Takata, Yumie, et al. "Selenium, Selenoenzymes, Oxidative Stress and Risk of Neoplastic Progression From Barrett's Esophagus: Results From Biomarkers and Genetic Variants." PloS One, vol. 7, no. 6, 2012, pp. e38612.
    Takata Y, Kristal AR, Santella RM, et al. Selenium, selenoenzymes, oxidative stress and risk of neoplastic progression from Barrett's esophagus: results from biomarkers and genetic variants. PLoS ONE. 2012;7(6):e38612.
    Takata, Y., Kristal, A. R., Santella, R. M., King, I. B., Duggan, D. J., Lampe, J. W., ... Peters, U. (2012). Selenium, selenoenzymes, oxidative stress and risk of neoplastic progression from Barrett's esophagus: results from biomarkers and genetic variants. PloS One, 7(6), pp. e38612. doi:10.1371/journal.pone.0038612.
    Takata Y, et al. Selenium, Selenoenzymes, Oxidative Stress and Risk of Neoplastic Progression From Barrett's Esophagus: Results From Biomarkers and Genetic Variants. PLoS ONE. 2012;7(6):e38612. PubMed PMID: 22715394.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Selenium, selenoenzymes, oxidative stress and risk of neoplastic progression from Barrett's esophagus: results from biomarkers and genetic variants. AU - Takata,Yumie, AU - Kristal,Alan R, AU - Santella,Regina M, AU - King,Irena B, AU - Duggan,David J, AU - Lampe,Johanna W, AU - Rayman,Margaret P, AU - Blount,Patricia L, AU - Reid,Brian J, AU - Vaughan,Thomas L, AU - Peters,Ulrike, Y1 - 2012/06/08/ PY - 2012/02/02/received PY - 2012/05/07/accepted PY - 2012/6/21/entrez PY - 2012/6/21/pubmed PY - 2015/2/13/medline SP - e38612 EP - e38612 JF - PloS one JO - PLoS ONE VL - 7 IS - 6 N2 - Clinical trials have suggested a protective effect of selenium supplementation on the risk of esophageal cancer, which may be mediated through the antioxidant activity of selenoenzymes. We investigated whether serum selenium concentrations, selenoenzyme activity, oxidative stress and genetic variation in selenoenzymes were associated with the risk of neoplastic progression to esophageal adenocarcinoma (EA) and two intermediate endpoints, aneuploidy and tetraploidy. In this prospective cohort study, during an average follow-up of 7.3 years, 47 EA cases, 41 aneuploidy cases and 51 tetraploidy cases accrued among 361 participants from the Seattle Barrett's Esophagus Research Study who were free of EA at the time of blood draw and had at least one follow-up visit. Development to EA was assessed histologically and aneuploidy and tetraploidy by DNA content flow cytometry. Serum selenium concentrations were measured using atomic absorption spectrometry, activity of glutathione peroxidase (GPX) 1 and GPX3 by substrate-specific coupled test procedures, selenoprotein P (SEPP1) concentrations and protein carbonyl content by ELISA method and malondialdehyde concentrations by HPLC. Genetic variants in GPX1-4 and SEPP1 were genotyped. Serum selenium was not associated with the risk of neoplastic progression to EA, aneuploidy or tetraploidy (P for trend = 0.25 to 0.85). SEPP1 concentrations were positively associated with the risk of EA [hazard ratio (HR) = 3.95, 95% confidence intervals (CI) = 1.42-10.97 comparing the third tertile with the first] and with aneuploidy (HR = 6.53, 95% CI = 1.31-32.58), but not selenoenzyme activity or oxidative stress markers. No genetic variants, overall, were associated with the risk of neoplastic progression to EA (global p = 0.12-0.69). Our results do not support a protective effect of selenium on risk of neoplastic progression to EA. Our study is the first to report positive associations of plasma SEPP1 concentrations with the risk of EA and aneuploidy, which warrants further investigation. SN - 1932-6203 UR - https://www.unboundmedicine.com/medline/citation/22715394/Selenium_selenoenzymes_oxidative_stress_and_risk_of_neoplastic_progression_from_Barrett's_esophagus:_results_from_biomarkers_and_genetic_variants_ L2 - http://dx.plos.org/10.1371/journal.pone.0038612 DB - PRIME DP - Unbound Medicine ER -