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Carcinogenesis Advance Access originally published online on March 16, 2006
Carcinogenesis 2006 27(9):1828-1834; doi:10.1093/carcin/bgl013
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Published by Oxford University Press 2006
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Polymorphisms in oxidative stress genes and risk for non-Hodgkin lymphoma

Sophia S. Wang*, Scott Davis1, James R. Cerhan2, Patricia Hartge, Richard K. Severson3, Wendy Cozen4, Qing Lan, Robert Welch5, Stephen J. Chanock5 and Nathaniel Rothman

Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health Rockville, MD, USA
1 Fred Hutchinson Cancer Research Center and the University of Washington Seattle, WA, USA
2 Department of Health Sciences Research, Mayo Clinic College of Medicine Rochester, MN, USA University of Iowa, Iowa City IA, USA
3 Karmanos Cancer Institute and Department of Family Medicine, Wayne State University Detroit, MI, USA
4 University of Southern California Los Angeles, CA, USA
5 Core Genotyping Facility, Advanced Technology Corporation, National Cancer Institute Gaithersburg, MD, USA

*To whom correspondence should be addressed at: Division of Cancer Epidemiology and Genetics, National Cancer Institute, 6120 Executive Boulevard, EPS MSC No. 7234, Bethesda, MD 20892-7234, USA. Tel: +1 301 402 5374; Fax: +1 301 402 0916; Email: wangso{at}mail.nih.gov

Evidence supporting the contribution of oxidative stress to key pathways in cancer, such as inflammation and DNA damage, continues to mount. We investigated variations within genes mediating oxidative stress to determine whether they alter risk for non-Hodgkin lymphoma (NHL). Thirteen single nucleotide polymorphisms (SNPs) from 10 oxidative stress genes (AKR1A1, AKR1C1, CYBA, GPX, MPO, NOS2A, NOS3, OGG1, PPARG and SOD2) were genotyped in 1172 NHL cases and 982 population-based controls from a USA multicenter case–control study. For NHL and five subtypes (diffuse large B-cell, follicular, marginal zone, small lymphocytic and T-cell), SNP associations were calculated. Odds ratios (OR) and 95% confidence intervals (CI) were adjusted for sex, age (<45, 45–64, 65+ years), race (white, black, other) and study site. Overall, the oxidative stress pathway was associated significantly with the B-cell NHL subtype, diffuse large B-cell lymphoma (DLBCL) (global P-value = 0.003). Specifically, for nitric oxide synthase (NOS2A Ser608Leu, rs2297518) Leu/Leu homozygotes, there was a 2-fold risk increase for NHL (OR = 2.2, 95% CI = 1.1–4.4) (referent = Ser/Ser and Ser/Leu). This risk increase was consistent by cell lineage (B- and T-cell NHL) and pronounced for the two most common subtypes, diffuse large B-cell (OR = 3.4, 95% CI = 1.5–7.8) and follicular lymphoma (OR = 2.6, 95% CI = 1.0–6.8). In an analysis of manganese superoxide dismutase (SOD2 Val16Ala, rs1799725) Ala/Ala homozygotes, we observed moderately increased risks for B-cell lymphomas (OR = 1.3, 95% CI = 1.0–1.6; referent = Val/Val and Val/Ala) that was consistent across the B-cell subtypes. Genetic variations that result in an increased generation of reactive oxygen species appear to increase risk for NHL and its major subtypes, particularly DLBCL. Independent replication of our findings are warranted and further evaluation of oxidative stress in the context of inflammation, DNA repair and the induction of the NF-{kappa}B pathway may further reveal important clues for lymphomagenesis.


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