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 Blood, 15 July 2007, Vol. 110, No. 2, pp. 743-751.
Prepublished online as a Blood First Edition Paper on April 3, 2007; DOI 10.1182/blood-2006-11-058446.

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NEOPLASIA

NF-{kappa}B2 mutation targets TRAF1 to induce lymphomagenesis

Baochun Zhang1, Zhe Wang1, Tai Li1, Erdyni N. Tsitsikov2, and Han-Fei Ding1

1 Department of Biochemistry and Cancer Biology, University of Toledo Health Science Campus, Toledo, OH; and 2 Department of Pediatrics, Harvard Medical School, Boston, MA

The NF-{kappa}B2 gene is recurrently mutated in human lymphoid malignancies. However, a causal relationship between NF-{kappa}B2 mutation and lymphomagenesis has not been established. It is also unclear how the mutation may lead to lymphoid malignancies. We report the generation of transgenic mice with targeted expression of p80HT, a lymphoma-associated NF-{kappa}B2 mutant, in lymphocytes. The transgenic mice display a marked expansion of peripheral B cell populations and develop predominantly small B cell lymphomas. p80HT expression has no apparent effect on the proliferation of B cells, but renders them specifically resistant to apoptosis induced by cytokine deprivation and mitogenic stimulation. Lymphocytes and lymphoma cells from p80HT mice express high levels of TRAF1, an antiapoptotic protein also implicated in lymphoid malignancies. p80HT binds the TRAF1 promoter in vivo and activates TRAF1 transcription. Moreover, TRAF1 knockdown abrogates the antiapoptotic activity of p80HT and TRAF1 deficiency reestablishes B cell homeostasis in p80HT mice. These findings demonstrate NF-{kappa}B2 mutation as an oncogenic event in vivo and suggest a molecular pathway for TRAF1 activation in the pathogenesis of lymphomas.


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This article has been cited by other articles:


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Z. Wang, B. Zhang, L. Yang, J. Ding, and H.-F. Ding
Constitutive Production of NF-{kappa}B2 p52 Is Not Tumorigenic but Predisposes Mice to Inflammatory Autoimmune Disease by Repressing Bim Expression
J. Biol. Chem., April 18, 2008; 283(16): 10698 - 10706.
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