Publication: Pathogenetic role of BCL6
translocation in B-cell non-Hodgkin’s lymphoma
Authors
Ohno, H.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
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 BNHL
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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