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Blood, 1 November 2006, Vol. 108, No. 9, pp. 3161-3167.
Prepublished online as a Blood First Edition Paper on July 20, 2006; DOI 10.1182/blood-2005-01-026690.
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NEOPLASIA
Risk of non-Hodgkin lymphoma (NHL) in relation to germline variation in DNA repair and related genes
Deirdre A. Hill,
Sophia S. Wang,
James R. Cerhan,
Scott Davis,
Wendy Cozen,
Richard K. Severson,
Patricia Hartge,
Sholom Wacholder,
Meredith Yeager,
Stephen J. Chanock, and
Nathaniel Rothman
From the Cancer Center and Department of Internal Medicine, University of New Mexico, Albuquerque, NM; Division of Cancer Epidemiology and Genetics, National Cancer Institute (NCI), National Institutes of Health (NIH), Department of Health and Human Services (DHHS), Bethesda, MD; Department of Health Sciences Research, Mayo Clinic College of Medicine, Rochester, MN; University of Iowa, Iowa City; Fred Hutchinson Cancer Research Center and the University of Washington, Seattle; Department of Preventive Medicine, University of Southern California Keck School of Medicine, Los Angeles; Karmanos Cancer Institute and Department of Family Medicine, Wayne State University, Detroit, MI; and Core Genotyping Facility, Advanced Technology Corporation, NCI, NIH, DHHS, Gaithersburg, MD.
Chromosomal translocations, insertions, and deletions are common early events in non-Hodgkin lymphoma (NHL) carcinogenesis, and implicated in their formation are endogenous processes involved in antigen-receptor diversification, such as V(D)J recombination. DNA repair genes respond to the double- and single-strand breaks induced by these processes and may influence NHL etiology. We examined 34 genetic variants in 19 genes within or related to 5 DNA repair pathways among 1172 cases and 982 matched controls who participated in a population-based NHL study in Los Angeles, Seattle, Detroit, and Iowa from 1998 to 2000. Cases were more likely than controls to have the RAG1 820 R/R (odds ratio [OR] = 2.7; 95% confidence interval [CI] = 1.4 to 5.0) than Lys/Lys genotypes, with evidence of a gene dosage effect (P trend < .001), and less likely to have the LIG4 (DNA ligase IV) 9 Ile/Ile (OR = 0.5; 95% CI = 0.3 to 0.9) than T/T genotype (P trend = .03) in the nonhomologous end joining (NHEJ)/V(D)J pathway. These NHEJ/V(D)J-related gene variants represent promising candidates for further studies of NHL etiology and require replication in other studies.
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