Abstract
Studies of B cell lymphomas in the early 1980s led to the cloning of genes (c-MYC and IGH) at a chromosome translocation breakpoint. A rush followed to identify recurrently translocated genes in all types of cancer, which led to remarkable advances in our understanding of cancer genetics. B lymphocyte tumors commonly bear chromosome translocations to immunoglobulin genes, which points to a role for antibody gene diversification processes in tumorigenesis. The discovery of activation-induced cytidine deaminase (AID) and the use of murine models to study translocation have led to a new understanding of how these events contribute to the genesis of lymphomas. Here, we review these advances with a focus on AID and insights gained from the study of translocations in primary cells.
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