Cancer Causes & Control

, Volume 24, Issue 10, pp 1885–1891

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

DOI: 10.1007/s10552-013-0244-7

Cite this article as:
Safaeian, M., Rajaraman, P., Hartge, P. et al. Cancer Causes Control (2013) 24: 1885. doi:10.1007/s10552-013-0244-7

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 polymorphismsGliomaAllergiesAutoimmune conditionsGene–environment interaction

Supplementary material

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

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