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Joint effects between five identified risk variants, allergy, and autoimmune conditions on glioma risk

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Abstract

Common variants in two of the five genetic regions recently identified from genome-wide association studies (GWAS) of risk of glioma were reported to interact with a history of allergic symptoms. In a pooled analysis of five epidemiologic studies, we evaluated the association between the five GWAS implicated gene variants and allergies and autoimmune conditions (AIC) on glioma risk (851 adult glioma cases and 3,977 controls). We further evaluated the joint effects between allergies and AIC and these gene variants on glioma risk. Risk estimates were calculated as odds ratios (OR) and 95 % confidence intervals (95 % CI), adjusted for age, gender, and study. Joint effects were evaluated by conducting stratified analyses whereby the risk associations (OR and 95 % CI) with the allergy or autoimmune conditions for glioma were evaluated by the presence or absence of the ‘at-risk’ variant, and estimated p interaction by fitting models with the main effects of allergy or autoimmune conditions and genotype and an interaction (product) term between them. Four of the five SNPs previously reported by others were statistically significantly associated with increased risk of glioma in our study (rs2736100, rs4295627, rs4977756, and rs6010620); rs498872 was not associated with glioma in our study. Reporting any allergies or AIC was associated with reduced risks of glioma (allergy: adjusted OR = 0.71, 95 % CI 0.55–0.91; AIC: adjusted OR = 0.65, 95 % CI 0.47–0.90). We did not observe differential association between allergic or autoimmune conditions and glioma by genotype, and there were no statistically significant p interactions. Stratified analysis by glioma grade (low and high grade) did not suggest risk differences by disease grade. Our results do not provide evidence that allergies or AIC modulate the association between the four GWAS-identified SNPs examined and risk of glioma.

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Acknowledgments

The study was funded by Intramural Research Program of the National Cancer Institute and the National Institute for Occupational Safety and Health. It was been funded in whole or in part with federal funds from the National Cancer Institute under contract N01-CO-12400. The funding source for AHS is from the Intramural Program of NIEHS.  AHS Data release P1REL0506_02. We are indebted to the scientific and field efforts of Tim Sheehy, Laurie Burdette, Aurelie Vogt, Annelie Landgren, Zhaoming Wang, Arti Aranasi, Michelle Brotzman, Lisa Newman, and Peter Hui.

Conflict of interest

The findings and conclusions in this report are those of the authors and do not necessarily represent the views of the National Institute for Occupational Safety and Health.

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Authors and Affiliations

  1. Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA

    Mahboobeh Safaeian, Preetha Rajaraman, Patricia Hartge, Martha Linet, Mark P. Purdue, Ann Hsing, Laura Beane-Freeman, Demetrius Albanes, Stephanie J. Weinstein, Peter D. Inskip, Alina Brenner, Nathaniel Rothman & Nilanjan Chatterjee

  2. Core Genomics Research, Division of Cancer Epidemiology and Genetics, National Cancer Institute, Bethesda, MD, USA

    Meredith Yeager & Stephen J. Chanock

  3. Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Atlanta, GA, USA

    Mary Ann Butler & Avima M. Ruder

  4. Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle, NC, USA

    Jane A. Hoppin

  5. Division of Cancer Control and Population Sciences, National Cancer Institute, Bethesda, MD, USA

    Elizabeth M. Gillanders

  6. Division of Etiology, Department of Population Sciences, City of Hope, Duarte, CA, USA

    Sophia S. Wang

  7. Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Blvd, Room 7086, Rockville, MD, 20852-7234, USA

    Mahboobeh Safaeian

Authors
  1. Mahboobeh Safaeian
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  2. Preetha Rajaraman
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  3. Patricia Hartge
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  4. Meredith Yeager
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  5. Martha Linet
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  6. Mary Ann Butler
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  7. Avima M. Ruder
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  9. Ann Hsing
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  10. Laura Beane-Freeman
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  11. Jane A. Hoppin
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  12. Demetrius Albanes
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  13. Stephanie J. Weinstein
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  14. Peter D. Inskip
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  15. Alina Brenner
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  16. Nathaniel Rothman
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  17. Nilanjan Chatterjee
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  18. Elizabeth M. Gillanders
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  19. Stephen J. Chanock
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  20. Sophia S. Wang
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Correspondence to Mahboobeh Safaeian.

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Safaeian, M., Rajaraman, P., Hartge, P. et al. Joint effects between five identified risk variants, allergy, and autoimmune conditions on glioma risk. Cancer Causes Control 24, 1885–1891 (2013). https://doi.org/10.1007/s10552-013-0244-7

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  • DOI: https://doi.org/10.1007/s10552-013-0244-7

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