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Common Variation in Genes Related to Innate Immunity and Risk of Adult Glioma

Current evidence suggests that immune system alterations contribute to the etiology of adult glioma, the most common adult brain tumor. Although previous studies have focused on variation in candidate genes in the adaptive immune system, the innate immune system has emerged as a critical avenue for...

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Published in:Cancer epidemiology, biomarkers & prevention biomarkers & prevention, 2009-05, Vol.18 (5), p.1651-1658
Main Authors: RAJARAMAN, Preetha, BRENNER, Alina V, FINE, Howard A, KWON, Deukwoo, THOMAS, Gilles, ROTHMAN, Nathaniel, INSKIP, Peter D, CHANOCK, Stephen J, BUTLER, Mary Ann, WANG, Sophia S, PFEIFFER, Ruth M, RUDER, Avima M, LINET, Martha S, YEAGER, Meredith, ZHAOMING WANG, ORR, Nick
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Language:English
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Summary:Current evidence suggests that immune system alterations contribute to the etiology of adult glioma, the most common adult brain tumor. Although previous studies have focused on variation in candidate genes in the adaptive immune system, the innate immune system has emerged as a critical avenue for research given its known link with carcinogenesis. To identify genetic markers in pathways critical to innate immunity, we conducted an association study of 551 glioma cases and 865 matched controls of European ancestry to investigate “tag” single nucleotide polymorphisms (SNP) in 148 genetic regions. Two independent U.S. case-control studies included were as follows: a hospital-based study conducted by the National Cancer Institute (263 cases, 330 controls) and a community-based study conducted by the National Institute for Occupational Safety and Health (288 cases, 535 controls). Tag SNPs (1,397) chosen on the basis of an r 2 of >0.8 and minor allele frequency of >5% in Caucasians in HapMap1 were genotyped. Glioma risk was estimated by odds ratios. Nine SNPs distributed across eight genetic regions ( ALOX5, IRAK3, ITGB2, NCF2, NFKB1, SELP, SOD1 , and STAT1 ) were associated with risk of glioma with P value of
ISSN:1055-9965
1538-7755
DOI:10.1158/1055-9965.EPI-08-1041