Cancer Causes & Control

, Volume 24, Issue 10, pp 1885–1891 | Cite as

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

  • Mahboobeh Safaeian
  • Preetha Rajaraman
  • Patricia Hartge
  • Meredith Yeager
  • Martha Linet
  • Mary Ann Butler
  • Avima M. Ruder
  • Mark P. Purdue
  • Ann Hsing
  • Laura Beane-Freeman
  • Jane A. Hoppin
  • Demetrius Albanes
  • Stephanie J. Weinstein
  • Peter D. Inskip
  • Alina Brenner
  • Nathaniel Rothman
  • Nilanjan Chatterjee
  • Elizabeth M. Gillanders
  • Stephen J. Chanock
  • Sophia S. Wang
Brief report

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.

Keywords

Single-nucleotide polymorphisms Glioma Allergies Autoimmune conditions Gene–environment interaction 

Notes

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.

Supplementary material

10552_2013_244_MOESM1_ESM.docx (144 kb)
Supplementary material 1 (DOCX 143 kb)

References

  1. 1.
    Central Brain Tumor Registry of the United States (CBTRU) (2010) CBTRUS Statistical Report: Primary Brain and Central Nervous System Tumors Diagnosed in the United States in 2004–2006: Central Brain Tumor Registry of the United States (CBTRUS); 2010Google Scholar
  2. 2.
    Bondy ML, Scheurer ME, Malmer B et al (2008) Brain tumor epidemiology: consensus from the Brain Tumor Epidemiology Consortium. Cancer 113(7 Suppl):1953–1968PubMedCrossRefGoogle Scholar
  3. 3.
    Scheurer ME, Etzel CJ, Liu M et al (2007) Aggregation of cancer in first-degree relatives of patients with glioma. Cancer Epidemiol Biomarkers Prev 16(11):2491–2495PubMedCrossRefGoogle Scholar
  4. 4.
    Malmer B, Henriksson R, Gronberg H (2003) Familial brain tumours-genetics or environment? A nationwide cohort study of cancer risk in spouses and first-degree relatives of brain tumour patients. Int J Cancer 106(2):260–263PubMedCrossRefGoogle Scholar
  5. 5.
    Wrensch M, Lee M, Miike R et al (1997) Familial and personal medical history of cancer and nervous system conditions among adults with glioma and controls. Am J Epidemiol 145(7):581–593PubMedCrossRefGoogle Scholar
  6. 6.
    Hill DA, Inskip PD, Shapiro WR et al (2003) Cancer in first-degree relatives and risk of glioma in adults. Cancer Epidemiol Biomarkers Prev 12(12):1443–1448PubMedGoogle Scholar
  7. 7.
    Shete S, Hosking FJ, Robertson LB et al (2009) Genome-wide association study identifies five susceptibility loci for glioma. Nat Genet 41(8):899–904PubMedCrossRefGoogle Scholar
  8. 8.
    Wrensch M, Jenkins RB, Chang JS et al (2009) Variants in the CDKN2B and RTEL1 regions are associated with high-grade glioma susceptibility. Nat Genet 41(8):905–908PubMedCrossRefGoogle Scholar
  9. 9.
    Linos E, Raine T, Alonso A, Michaud D (2007) Atopy and risk of brain tumors: a meta-analysis. J Natl Cancer Inst 99(20):1544–1550PubMedCrossRefGoogle Scholar
  10. 10.
    Brenner AV, Linet MS, Fine HA et al (2002) History of allergies and autoimmune diseases and risk of brain tumors in adults. Int J Cancer 99(2):252–259PubMedCrossRefGoogle Scholar
  11. 11.
    Wiemels JL, Wilson D, Patil C et al (2009) IgE, allergy, and risk of glioma: update from the San Francisco Bay Area Adult Glioma Study in the temozolomide era. Int J Cancer 125(3):680–687PubMedCrossRefGoogle Scholar
  12. 12.
    Wigertz A, Lonn S, Schwartzbaum J et al (2007) Allergic conditions and brain tumor risk. Am J Epidemiol 166(8):941–950PubMedCrossRefGoogle Scholar
  13. 13.
    Schoemaker MJ, Robertson L, Wigertz A et al (2010) Interaction between 5 genetic variants and allergy in glioma risk. Am J Epidemiol 171(11):1165–1173PubMedCrossRefGoogle Scholar
  14. 14.
    LaChance DH, Yang P, Johnson DR et al (2011) Associations of high-grade glioma with glioma risk alleles and histories of allergy and smoking. Am J Epidemiol 174(5):574–581PubMedCrossRefGoogle Scholar
  15. 15.
    Inskip PD, Tarone RE, Hatch EE et al (2001) Cellular-telephone use and brain tumors. N Engl J Med 344(2):79–86PubMedCrossRefGoogle Scholar
  16. 16.
    Ruder AM, Waters MA, Carreon T et al (2006) The Upper Midwest Health Study: a case-control study of primary intracranial gliomas in farm and rural residents. J Agric Saf Health 12(4):255–274PubMedGoogle Scholar
  17. 17.
    Gohagan JK, Prorok PC, Hayes RB, Kramer BS (2000) The Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial of the National Cancer Institute: history, organization, and status. Control Clin Trials 21(6 Suppl):251S–272SPubMedCrossRefGoogle Scholar
  18. 18.
    The ATBC Cancer Prevention Study Group (1994) The alpha-tocopherol, beta-carotene lung cancer prevention study: design, methods, participant characteristics, and compliance. Ann Epidemiol 4(1):1–10Google Scholar
  19. 19.
    Alavanja MC, Sandler DP, McMaster SB et al (1996) The agricultural health study. Environ Health Perspect 104(4):362–369PubMedCrossRefGoogle Scholar
  20. 20.
    Petersen GM, Amundadottir L, Fuchs CS et al (2010) A genome-wide association study identifies pancreatic cancer susceptibility loci on chromosomes 13q22.1, 1q32.1 and 5p15.33. Nat Genet 42(3):224–228PubMedCrossRefGoogle Scholar
  21. 21.
    Thomas G, Jacobs KB, Yeager M et al (2008) Multiple loci identified in a genome-wide association study of prostate cancer. Nat Genet 40(3):310–315PubMedCrossRefGoogle Scholar
  22. 22.
    Marchini J, Howie B, Myers S, McVean G, Donnelly P (2007) A new multipoint method for genome-wide association studies by imputation of genotypes. Nat Genet 39(7):906–913PubMedCrossRefGoogle Scholar
  23. 23.
    Kleihues P, Louis DN, Scheithauer BW et al (2002) The WHO classification of tumors of the nervous system. J Neuropathol Exp Neurol 61(3):215–225PubMedGoogle Scholar
  24. 24.
    Burney PG, Laitinen LA, Perdrizet S et al (1989) Validity and repeatability of the IUATLD (1984) Bronchial Symptoms Questionnaire: an international comparison. Eur Respir J 2(10):940–945PubMedGoogle Scholar
  25. 25.
    De Roos AJ, Cooper GS, Alavanja MC, Sandler DP (2005) Rheumatoid arthritis among women in the Agricultural Health Study: risk associated with farming activities and exposures. Ann Epidemiol 15(10):762–770PubMedCrossRefGoogle Scholar
  26. 26.
    Centers for Disease Control and Prevention (2011) National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011Google Scholar
  27. 27.
    Arbes SJ Jr, Gergen PJ, Vaughn B, Zeldin DC (2007) Asthma cases attributable to atopy: results from the Third National Health and Nutrition Examination Survey. J Allergy Clin Immunol 120(5):1139–1145PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media Dordrecht (outside the USA) 2013

Authors and Affiliations

  • Mahboobeh Safaeian
    • 1
    • 7
  • Preetha Rajaraman
    • 1
  • Patricia Hartge
    • 1
  • Meredith Yeager
    • 2
  • Martha Linet
    • 1
  • Mary Ann Butler
    • 3
  • Avima M. Ruder
    • 3
  • Mark P. Purdue
    • 1
  • Ann Hsing
    • 1
  • Laura Beane-Freeman
    • 1
  • Jane A. Hoppin
    • 4
  • Demetrius Albanes
    • 1
  • Stephanie J. Weinstein
    • 1
  • Peter D. Inskip
    • 1
  • Alina Brenner
    • 1
  • Nathaniel Rothman
    • 1
  • Nilanjan Chatterjee
    • 1
  • Elizabeth M. Gillanders
    • 5
  • Stephen J. Chanock
    • 2
  • Sophia S. Wang
    • 6
  1. 1.Division of Cancer Epidemiology and GeneticsNational Cancer InstituteBethesdaUSA
  2. 2.Core Genomics Research, Division of Cancer Epidemiology and GeneticsNational Cancer InstituteBethesdaUSA
  3. 3.Centers for Disease Control and PreventionNational Institute for Occupational Safety and HealthAtlantaUSA
  4. 4.Epidemiology BranchNational Institute of Environmental Health SciencesResearch TriangleUSA
  5. 5.Division of Cancer Control and Population SciencesNational Cancer InstituteBethesdaUSA
  6. 6.Division of Etiology, Department of Population SciencesCity of HopeDuarteUSA
  7. 7.Infections and Immunoepidemiology Branch, Division of Cancer Epidemiology and GeneticsNational Cancer InstituteRockvilleUSA

Personalised recommendations