Abstract
Chromosomal translocations involving the immunoglobulin (IG) loci play a pivotal role in the pathogenesis of many subtypes of mature B-cell malignancy. Although all the commonIG translocations have been cloned, cloning of rare but nonetheless recurrent translocations continues to allow identification of genes of importance to the development of both normal and malignant B-cells. Clustering of breakpoints within theIG gene segments has allowed development of polymerase chain reaction methods that facilitate cloning.IG translocations result in overexpression of a wide variety of genes ranging from cell surface receptors to transcriptional repressors. Genes recently shown to be involved in such translocations includeBCL11A andMALT1. As with the acute leukemias, different translocations in B-cell lymphomas may target different proteins that interact directly. A common endpoint for several translocations is activation of the nuclear factor κB pathway. Analysis of the mechanisms of transformation may define new therapeutic strategies.
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Dyer, M.J.S. The Pathogenetic Role of Oncogenes Deregulated by Chromosomal Translocation in B-Cell Malignancies. Int J Hematol 77, 315–320 (2003). https://doi.org/10.1007/BF02982637
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DOI: https://doi.org/10.1007/BF02982637