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Blood, 15 December 2008, Vol. 112, No. 13, pp. 5150-5160. Prepublished online as a Blood First Edition Paper on September 16, 2008; DOI 10.1182/blood-2008-01-133587.
NEOPLASIA Etiologic heterogeneity among non-Hodgkin lymphoma subtypes1 Division of Cancer Epidemiology and Genetics, National Cancer Institute (NCI), National Institutes of Health (NIH), Rockville, MD; 2 Norris Comprehensive Cancer Center, University of Southern California, Los Angeles; 3 Fred Hutchinson Cancer Research Center and University of Washington, Seattle; 4 Department of Family Medicine and Karmanos Cancer Institute, Wayne State University, Detroit, MI; 5 Department of Pathology, University of New Mexico, Albuquerque; 6 City of Hope Comprehensive Cancer Center and Beckman Research Institute, Duarte, CA; 7 Department of Pharmacology and Toxicology and James Graham Brown Cancer Center, University of Louisville School of Medicine, KY; 8 Cancer Center and Department of Internal Medicine, University of New Mexico, Albuquerque; 9 Mayo Clinic College of Medicine, Rochester, MN; 10 Department of Epidemiology, University of Iowa, Iowa City; and 11 Core Genotyping Facility, Advanced Technology Center, NCI, NIH, Gaithersburg, MD
Understanding patterns of etiologic commonality and heterogeneity for non-Hodgkin lymphomas may illuminate lymphomagenesis. We present the first systematic comparison of risks by lymphoma subtype for a broad range of putative risk factors in a population-based case-control study, including diffuse large B-cell (DLBCL; N = 416), follicular (N = 318), and marginal zone lymphomas (N = 106), and chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL; N = 133). We required at least 2 of 3 analyses to support differences in risk: (1) polytomous logistic regression, (2) homogeneity tests, or (3) dichotomous logistic regression, analyzing all 7 possible pairwise comparisons among the subtypes, corresponding to various groupings by clinical behavior, genetic features, and differentiation. Late birth order and high body mass index (
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| Copyright © 2008 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
35) kg/m2) increased risk for DLBCL alone. Autoimmune conditions increased risk for marginal zone lymphoma alone. The tumor necrosis factor G-308A polymorphism (rs1800629) increased risks for both DLBCL and marginal zone lymphoma. Exposure to certain dietary heterocyclic amines from meat consumption increased risk for CLL/SLL alone. We observed no significant risk factors for follicular lymphoma alone. These data clearly support both etiologic commonality and heterogeneity for lymphoma subtypes, suggesting that immune dysfunction is of greater etiologic importance for DLBCL and marginal zone lymphoma than for CLL/SLL and follicular lymphoma. 
