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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. This Article Full Text Full Text (PDF) Supplemental Table and Figures All Versions of this Article: blood-2006-11-058446v1 110/2/743    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Zhang, B. Articles by Ding, H.-F. Search for Related Content PubMed PubMed Citation Articles by Zhang, B. Articles by Ding, H.-F. Related Collections Neoplasia Oncogenes and Tumor Suppressors Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  NEOPLASIA NF-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-B2 gene is recurrently mutated in human lymphoid malignancies. However, a causal relationship between NF-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-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-B2 mutation as an oncogenic event in vivo and suggest a molecular pathway for TRAF1 activation in the pathogenesis of lymphomas. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. M. Dagle, N. T. Lepp, M. E. Cooper, K. L. Schaa, K. J.P. Kelsey, K. L. Orr, D. Caprau, C. R. Zimmerman, K. M. Steffen, K. J. Johnson, et al. Determination of Genetic Predisposition to Patent Ductus Arteriosus in Preterm Infants Pediatrics, April 1, 2009; 123(4): 1116 - 1123. [Abstract] [Full Text] [PDF] 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. [Abstract] [Full Text] [PDF]

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