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Histol Histopathol. 2004 Apr;19(2):637-50. doi: 10.14670/HH-19.637.

Pathogenetic role of BCL6 translocation in B-cell non-Hodgkin's lymphoma.

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Department of Hematology and Oncology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.


Chromosomal translocation affecting the 3q27 band, where the BCL6 gene is localized, is one of the most common genetic abnormalities in non-Hodgkin's lymphoma of B-cell type (B-NHL). The translocation occurs within the major translocation cluster (MTC) of BCL6, and as the result of translocation either one of the three immunoglobulin (Ig) genes or a heterogeneous non-Ig gene is juxtaposed to the coding regions of BCL6. On the other hand, somatic hypermutation involves the BCL6 gene of not only B-NHL but also B-cells from normal individuals. The mutations are clustered within a region of the MTC, suggesting that a common molecular mechanism is operating for the two genetic lesions of BCL6. The Bcl-6 protein is a transcriptional repressor that is an important regulator of lymphoid development and function. The protein is preferentially expressed in germinal center (GC) B-cells of normal lymphoid tissues as well as in a variety of B-NHL subtypes derived from GC B-cells irrespective of whether the BCL6 is rearranged. Although there is no consensus on the effect of BCL6 translocation on the clinical outcome of B-NHL, many studies coincide in showing that a high-level of BCL6 expression at either or both the mRNA and protein levels is a favorable prognostic marker of diffuse large B-cell lymphoma. In vitro evidence suggests that non-Ig/BCL6 translocation transiently enhances the level of Bcl-6 expression, which may perturb a molecular network that controls the differentiation of GC B-cells to Ig-secreting plasma cells, thereby predisposing the B-cells to neoplastic transformation.

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