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Blood, 15 December 2007, Vol. 110, No. 13, pp. 4455-4463. Prepublished online as a Blood First Edition Paper on September 7, 2007; DOI 10.1182/blood-2007-05-088682. This Article Full Text Full Text (PDF) Supplemental Tables and Figure All Versions of this Article: blood-2007-05-088682v1 110/13/4455    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Cerhan, J. R. Articles by Slager, S. L. Search for Related Content PubMed PubMed Citation Articles by Cerhan, J. R. Articles by Slager, S. L. Related Collections Gene Expression Genomics Neoplasia Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA Genetic variation in 1253 immune and inflammation genes and risk of non-Hodgkin lymphoma James R. Cerhan1, Stephen M. Ansell2, Zachary S. Fredericksen3, Neil E. Kay2, Mark Liebow4, Timothy G. Call2, Ahmet Dogan5, Julie M. Cunningham6, Alice H. Wang3, Wen Liu-Mares1, William R. Macon5, Diane Jelinek7, Thomas E. Witzig2, Thomas M. Habermann2, and Susan L. Slager3 1 Division of Epidemiology, Department of Health Sciences Research; 2 Division of Hematology, Department of Medicine; 3 Division of Biostatistics, Department of Health Sciences Research; 4 Division of General Internal Medicine, Department of Medicine; 5 Division of Hematopathology, Department of Laboratory Medicine and Pathology; 6 Division of Experimental Pathology, Department of Laboratory Medicine and Pathology; and 7 Department of Immunology; all at the Mayo Clinic College of Medicine; Rochester, MN Smaller-scale evaluations suggest that common genetic variation in candidate genes related to immune function may predispose to the development of non-Hodgkin lymphoma (NHL). We report an analysis of variants within genes associated with immunity and inflammation and risk of NHL using a panel of 9412 single-nucleotide polymorphisms (SNPs) from 1253 genes in a study of 458 patients with NHL and 484 frequency-matched controls. We modeled haplotypes and risk of NHL, as well as the main effects for all independent SNPs from a gene in multivariate logistic regression models; we separately report results for nonsynonymous (ns) SNPs. In gene-level analyses, the strongest findings (P .001) were for CREB1, FGG, MAP3K5, RIPK3, LSP1, TRAF1, DUSP2, and ITGB3. In nsSNP analyses, the strongest findings (P .01) were for ITGB3 L59P (odds ratio [OR] = 0.66; 95% confidence interval [CI] 0.52-0.85), TLR6 V427A (OR = 5.20; CI 1.77-15.3), SELPLG M264V (OR = 3.20; CI 1.48-6.91), UNC84B G671S (OR = 1.50; CI 1.12-2.00), B3GNT3 H328R (OR = 0.74; CI 0.59-0.93), and BAT2 V1883L (OR = 0.64; CI 0.45-0.90). Our results suggest that genetic variation in genes associated with immune response (TRAF1, RIPK3, BAT2, and TLR6), mitogen-activated protein kinase (MAPK) signaling (MAP3K5, DUSP2, and CREB1), lymphocyte trafficking and migration (B3GNT3, SELPLG, and LSP1), and coagulation pathways (FGG and ITGB3) may be important in the etiology of NHL, and should be prioritized in replication studies. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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