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Frequent Joining of Bcl-2 to a J_H6 Gene in Hepatitis C Virus-Associated t(14;18)¹

Eric H. Sasso^2,*, Marina Martinez^*, Stuart L. Yarfitz, Pascale Ghillani, Lucile Musset, Jean-Charles Piette and Patrice Cacoub

^* Department of Medicine and Division of Bioinformatics, University of Washington, Seattle, WA 98105; and Department of Internal Medicine, Centre Hospitalier Universitaire La Pitié-Salpêtrière, Paris, France

The t(14;18) chromosomal translocation, which joins the Bcl-2 proto-oncogene to an Ig J_H gene, has increased prevalence in patients chronically infected with hepatitis C virus (HCV). We now establish a link between the molecular structure and clinical occurrence of HCV-associated t(14;18). A t(14;18) was detected by PCR in leukocytes from 22 of 46 HCV-infected patients (48%) and 11 of 54 healthy controls (20%) (p = 0.0053). Nucleotide sequence analysis of the Bcl-2/J_H joins found a J_H6 gene in 18 of 22 (82%) t(14;18) from HCV⁺ patients, and 3 of 8 (38%) from controls (p = 0.031). The t(14;18) rarely contained J_H gene mutations, or an intervening region sequence suggestive of D gene rearrangement or templated nucleotide insertion. Analysis of published t(14;18) nucleotide sequences established that the J_H6 prevalence in t(14;18) from normal/nonneoplastic controls (48%) was significantly lower than in t(14;18) from our HCV⁺ patients (p = 0.004) or from non-Hodgkin’s lymphomas (66%, p = 0.003). We conclude that the increased prevalence of t(14;18) in HCV⁺ patients occurs with a strong bias for Bcl-2/J_H6 joins. In this regard, HCV-associated t(14;18) more closely resemble t(14;18) in lymphomas than t(14;18) from normal subjects.

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