© The Author 2008. Published by Oxford University Press.
The Utility of t(14;18) in Understanding Risk Factors for Non-Hodgkin Lymphoma
Affiliations of authors: Department of Preventive Medicine, Feinberg School of Medicine (BCHC) and The Robert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, IL (BCHC); Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, DHHS, Bethesda, MD (QL, AB, SHZ); Munroe Meyer Institute for Genetics and Rehabilitation (BJD) and Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE (BJD, DDW)
Correspondence to: Brian C.-H. Chiu, PhD, Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, 680 North Lake Shore Drive, Suite 1102, Chicago, IL 60611 (e-mail: bchiu{at}northwestern.edu).
Characteristic chromosomal abnormalities are associated with specific histological subtypes of non-Hodgkin lymphoma (NHL). The chromosomal translocation t(14;18)(q32;q21) is one of the most common chromosomal abnormalities in NHL, occurring in 70%–90% of cases of follicular lymphoma, 20%–30% of diffuse large B-cell lymphoma, and 5%–10% of other less common subtypes. The t(14;18)-positive NHL may represent a homogenous group and, consequently, increase etiologic specificity in epidemiological studies. Although the t(14;18) has important clinical ramifications, its etiologic significance remains to be determined. Two population-based, case–control studies addressed this issue by evaluating potential risk factors for t(14;18)-positive and t(14;18)-negative subgroups of NHL. Both studies found that the association between pesticide exposures and risk of NHL was largely limited to t(14;18)-positive NHL cases. However, the findings regarding cigarette smoking, family history of hematopoietic cancer, and hair dye use were not entirely consistent. These results indicate that defining subgroups of NHL according to t(14;18) status may be useful for etiologic research, particularly for exposures that are genotoxic or may contribute to the development of NHL through pathways involving the t(14;18). Studies to further evaluate these associations and delineate the effects of various exposures in other genetically defined subgroups of NHL are warranted.
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