Chromosome translocation, B cell lymphoma, and activation-induced cytidine deaminase

Annu Rev Pathol. 2013 Jan 24;8:79-103. doi: 10.1146/annurev-pathol-020712-164004. Epub 2012 Sep 4.

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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Base Sequence
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism
  • Cell Transformation, Neoplastic / pathology
  • Chromosome Breakpoints
  • Cytidine Deaminase / metabolism*
  • Humans
  • Lymphoma, B-Cell / enzymology*
  • Lymphoma, B-Cell / genetics*
  • Lymphoma, B-Cell / pathology
  • Molecular Sequence Data
  • Translocation, Genetic*

Substances

  • AICDA (activation-induced cytidine deaminase)
  • Cytidine Deaminase