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Updated: Jun 2, 2026

Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
Published on: November 1, 2011
Collateral damage from antigen receptor gene diversification
Grace K Mahowald1, Jason M Baron, Barry P Sleckman
1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Abstract:
Chromosomal translocations that juxtapose antigen receptor genes and oncogenes are frequently associated with lymphoid malignancies. In this issue, Robbiani et al. (2008) show that activation-induced deaminase (AID), an enzyme involved in antigen receptor gene diversification, generates DNA double-strand breaks (DSBs) in oncogenes, and Tsai et al. (2008) propose that AID and the recombinase-activating gene (RAG) endonuclease may collaborate to generate off-target DSBs.
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