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Biallelic inactivation of TRAF3 in a subset of B-cell lymphomas with interstitial del(14)(q24.1q32.33)

Leukemia volume 23, pages 2153–2155 (2009)Cite this article

The interstitial deletion del(14)(q24.1q32.33) is a recurrent chromosomal change in B-cell chronic lymphocytic leukemia (CLL) and other B-cell lymphomas.1, 2 The break points of this deletion are located in the immunoglobulin heavy chain (IGH)-locus in 14q32.33 and in a region in 14q24.1 containing the ZFP36L1 gene (1and our own unpublished observations). Activation of a candidate oncogene centromeric of the deletion break point in 14q24.1 through juxtaposition to the IGH locus, yet could not be unambiguously shown.1 An alternative hypothesis is that the deletion might inactivate a tumor suppressor gene.

Among many other genes, the TNF receptor-associated factor 3 (TRAF3)-gene in 14q32.32 is located within the deleted region. The TRAF3 protein negatively regulates the NF-κB pathway and has been shown to be recurrently affected by biallelic TRAF3 deletion and inactivating mutation in multiple myeloma and Waldenström's macroglobulinemia.3, 4, 5 Furthermore, B-cell-specific TRAF3−/− mice show remarkably prolonged B-cell survival and highly expanded B-cell compartments in secondary lymphoid organs.6 These facts qualify TRAF3 as a candidate tumor suppressor gene involved in lymphomagenesis.

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Acknowledgements

We gratefully thank Kerstin Runde, Reina Zühlke-Jenisch, Magret Ratjen, Dorit Schuster, Claudia Becher and Ursula Schnaidt for their technical assistance. Supported by the Network Project of the Deutsche Krebshilfe ‘Molecular Mechanisms in Malignant Lymphomas’ 70-3173-TR3, the Wilhelm Sander-Stiftung 2005.168.2 and RETICS. Instituto de Salud Carlos III, RETICS. Convocatoria 2008. RD07/0020/2004.

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Authors and Affiliations

  1. Institute of Human Genetics, Christian-Albrechts University Kiel and University Hospital Schleswig-Holstein, Kiel, Germany

    I Nagel, S Bug, H Tönnies, O Ammerpohl, J Richter, I Vater, J I Martin-Subero, S Gesk, L Harder & R Siebert

  2. Laboratoire d’Hematologie et de cytogénétique, Centre Hospitalier Lyon Sud, Lyon, France

    E Callet-Bauchu

  3. Department of Genetics, University of Navarra, Pamplona, Spain

    M J Calasanz

  4. Division of Oncology, Center for Applied Medical Research, University of Navarra, Pamplona, Spain

    J A Martinez-Climent

  5. Groupe d’Etude des Proliférations Lymphoides (GPL), European Institute for Peptides Research (IFRMP23), Centre Henri Becquerel, Rouen, France

    C Bastard

  6. Servei de Patologia, Laboratori de Citogenètica Molecular, Hospital del Mar, GRETNHE, IMIM, Barcelona, Spain

    M Salido

  7. MVZ Dr Eberhard and Partner, Dortmund, Germany

    E Schroers

  8. Medical Research Council (MRC) Toxicology Unit, University of Leicester, Leicester, UK

    A Majid & M J S Dyer

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Correspondence to I Nagel.

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Supplementary Information accompanies the paper on the Leukemia website (http://www.nature.com/leu)

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Nagel, I., Bug, S., Tönnies, H. et al. Biallelic inactivation of TRAF3 in a subset of B-cell lymphomas with interstitial del(14)(q24.1q32.33). Leukemia 23, 2153–2155 (2009). https://doi.org/10.1038/leu.2009.149

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