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Recombination Activating Genes (RAG) in Lymphoma Development
Brian B. Haines, Chun Jeih Ryu and Jianzhu Chen
volume 5 | issue 9
1 may 2006Pages: 913 - 916
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The recombination activating genes (RAG) play a central role in the generation of a diverse immune repertoire by mediating DNA recombination events at antigen receptor loci in developing B and T lymphocytes. However, inappropriate RAG activity throughout the genome has been implicated in a large variety of human and mouse lymphomas. Mechanisms by which RAG can provoke or perpetuate lymphoma include deregulation of certain genes by translocation to antigen receptor regulatory regions, the formation of chimeric oncogenes, inactivation of tumor suppressor or micro-RNA loci, or activation of oncogenes. Here we present the T cell receptor enhancer (Eb) deficient mouse as a tractable in vivo model system to study the role of RAG activity in the context of lymphoma development, and contrast our system with those of others. We posit a general hypothesis that virtually any mutation that impairs early lymphocyte development at stages when RAG is expressed can constitute a pro-carcinogenic event. Our model system provides a means to assess the roles of RAG activity in human lymphoid malignancies.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.