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JNCI Journal of the National Cancer Institute 2005 97(21):1616-1618; doi:10.1093/jnci/dji344
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© 2005 Oxford University Press

BRIEF COMMUNICATION

A Putative Exonic Splicing Polymorphism in the BCL6 Gene and the Risk of Non-Hodgkin Lymphoma

Yawei Zhang, Qing Lan, Nathaniel Rothman, Yong Zhu, Shelia Hoar Zahm, Sophia S. Wang, Theodore R. Holford, Brian Leaderer, Peter Boyle, Bing Zhang, Kaiyong Zou, Stephen Chanock, Tongzhang Zheng

Affiliations of authors: Department of Epidemiology and Public Health, Yale School of Medicine, New Haven, CT (Y. Zhang, Y. Zhu, TRH, BL, TZ); Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, MD (Y. Zhang, QL, NR, SHZ, SSW, SC); International Agency for Research on Cancer, Lyon, France (PB); Department of Epidemiology and Biostatistics, McGill University, Montreal, Quebec, Canada (BZ); Department of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, CT (KZ); Center for Cancer Research, National Cancer Institute, NIH, Bethesda, MD (SC)

Correspondence to: Tongzhang Zheng, ScD, Department of Epidemiology and Public Health, Yale University School of Medicine, 60 College Street, Room 442, P.O. Box 208034, New Haven, CT 06520-8034 (e-mail: tongzhang.zheng{at}yale.edu), or Yawei Zhang, PhD, Department of Epidemiology and Public Health, Yale University School of Medicine, 60 College Street, LEPH 440, P.O. Box 208034, New Haven, CT 06520-8034 (e-mail: yawei.zhang{at}yale.edu).

Recent studies have shown that the B-cell lymphoma 6 gene (BCL6) is an oncogene that contributes to lymphomagenesis. Exon 6 of BCL6 contains a common single nucleotide polymorphism (SNP) (–195 C>T; dbSNP ID: rs1056932) that alters a potential binding site for an exonic splicing enhancer. We used unconditional logistic regression models to examine the association between this SNP and the risk of non-Hodgkin lymphoma (NHL) in a population-based case–control study of women residing in Connecticut (461 case patients and 535 control subjects). The risk of NHL among women with the CC genotype was more than double that of women with the TT genotype (odds ratio [OR] = 2.2, 95% confidence interval [CI] = 1.5 to 3.3). Higher risks were observed for two NHL subtypes, namely B-cell chronic lymphatic leukemia/prolymphocytic leukemia/small lymphocytic lymphoma (OR = 3.5, 95% CI = 1.6 to 7.8) and T-cell lymphoma (OR = 5.2, 95% CI = 2.0 to 13.3). Our results support the hypothesis that a genetic variant that could alter mRNA transcripts of BCL6 may contribute to the etiology of NHL and suggest that this variant warrants further investigation.


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