TY - JOUR
T1 - Polymorphisms in immune function genes and risk of non-Hodgkin lymphoma
T2 - Findings from the New South Wales non-Hodgkin Lymphoma Study
AU - Purdue, Mark P.
AU - Lan, Qing
AU - Kricker, Anne
AU - Grulich, Andrew E.
AU - Vajdic, Claire M.
AU - Turner, Jennifer
AU - Whitby, Denise
AU - Chanock, Stephen
AU - Rothman, Nathaniel
AU - Armstrong, Bruce K.
N1 - Funding Information:
at the NSW Central Cancer Registry and the Hunter Valley Research Foundation. Special thanks to Melisa Litchfield, Maria Agaliotis and Chris Goumas for data collection and data entry and to Jackie Turner for telephone follow-up. We thank Wendell Miley for co-ordinating DNA extraction and sample aliquoting and the members of the VES who performed DNA extractions. We also thank Robert Welch and Sunita Yadavalli at the NCI Core Genotyping Facility for their work in the specimen handling and laboratory analysis of genotyping data, and Sonja Berndt at the NCI Division of Cancer Epidemiology and Genetics for conducting the meta-analysis. The NSWNHL study was funded by the National Health and Medical Research Council of Australia, The Cancer Council NSW, and The University of Sydney Medical Foundation. The genotyping project was funded by the Intramural Research Program at the NIH (National Cancer Institute).
PY - 2007/3
Y1 - 2007/3
N2 - Recent findings suggest that genetic polymorphisms in TNF and IL10 are associated with an increased risk of non-Hodgkin lymphoma (NHL), particularly for diffuse large B-cell lymphoma (DLBCL). To further investigate the contribution of common genetic variation in key cytokine and innate immunity genes to the etiology of NHL, we genotyped participants in a case-control study of NHL conducted in Australia (545 cases, 498 controls). We investigated 36 single nucleotide polymorphisms in IL10, TNF and 21 other immune function genes. We observed an elevated risk of DLBCL with the IL10 - 3575T>A polymorphism [TA genotype: odds ratio (OR) = 1.32, 95% confidence interval (CI) = 0.86-2.02; AA, OR = 1.84, 95% CI = 1.10-3.08; trend test, P = 0.02]. Our most noteworthy TNF finding was an association between -857C>T and a decreased risk of NHL (CT or TT, OR = 0.59, 95% CI = 0.42-0.84, P = 0.003) and particularly follicular lymphoma (OR = 0.40, 95% CI = 0.23-0.68, P = 0.0009). Additionally, TNF -863C>A was associated with an elevated risk of DLBCL (CA, OR = 1.45, 95% CI = 0.95-2.21; AA, OR = 2.06, 95% CI = 0.88-4.83; trend test, P = 0.02). Our findings offer further evidence that variation in the IL10 and TNF loci influences NHL risk. Additional studies are needed to clarify the genetic and biologic basis for these relationships.
AB - Recent findings suggest that genetic polymorphisms in TNF and IL10 are associated with an increased risk of non-Hodgkin lymphoma (NHL), particularly for diffuse large B-cell lymphoma (DLBCL). To further investigate the contribution of common genetic variation in key cytokine and innate immunity genes to the etiology of NHL, we genotyped participants in a case-control study of NHL conducted in Australia (545 cases, 498 controls). We investigated 36 single nucleotide polymorphisms in IL10, TNF and 21 other immune function genes. We observed an elevated risk of DLBCL with the IL10 - 3575T>A polymorphism [TA genotype: odds ratio (OR) = 1.32, 95% confidence interval (CI) = 0.86-2.02; AA, OR = 1.84, 95% CI = 1.10-3.08; trend test, P = 0.02]. Our most noteworthy TNF finding was an association between -857C>T and a decreased risk of NHL (CT or TT, OR = 0.59, 95% CI = 0.42-0.84, P = 0.003) and particularly follicular lymphoma (OR = 0.40, 95% CI = 0.23-0.68, P = 0.0009). Additionally, TNF -863C>A was associated with an elevated risk of DLBCL (CA, OR = 1.45, 95% CI = 0.95-2.21; AA, OR = 2.06, 95% CI = 0.88-4.83; trend test, P = 0.02). Our findings offer further evidence that variation in the IL10 and TNF loci influences NHL risk. Additional studies are needed to clarify the genetic and biologic basis for these relationships.
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U2 - 10.1093/carcin/bgl200
DO - 10.1093/carcin/bgl200
M3 - Article
C2 - 17056605
AN - SCOPUS:34047119220
VL - 28
SP - 704
EP - 712
JO - Carcinogenesis
JF - Carcinogenesis
SN - 0143-3334
IS - 3
ER -