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Gains of the proto-oncogene BCL11A and nuclear accumulation of BCL11AXL protein are frequent in primary mediastinal B-cell lymphoma

Leukemia volume 20, pages 1880–1882 (2006)Cite this article

Primary mediastinal B-cell lymphoma (PMBL) is a well-defined subtype of diffuse large B-cell lymphoma (DLBCL), distinct from germinal center B-cell (GCB) and activated B-cell (ABC) subtypes.1 PMBL is cytogenetically characterized by frequent gains/amplifications of 2p14–p16 found in up to 47% of cases by comparative genomic hybridization (CGH).1 The proto-oncogene BCL11A (B-cell lymphoma/leukemia 11A) at 2p16 is regarded as candidate target gene of these imbalances, as it was often co-amplified with the REL proto-oncogene in non-Hodgkin's lymphoma (NHL) as well as in classical Hodgkin's lymphoma.2, 3

Initially, the BCL11A gene was identified as recurrent translocation partner with the immunoglobulin heavy chain locus in B-cell NHLs.3 Furthermore, retroviral integration to the BCL11A locus has been shown to activate its expression, transform NIH 3T3 cells and induce myeloid leukemias in mice.4 In the Burkitt's lymphoma cell line NAB-2, the Epstein–Barr virus (EBV) is integrated in the BCL11A locus leading to slightly higher BCL11A expression compared to other EBV-positive as well as EBV-negative Burkitt's lymphoma-derived cell lines.5 Thus, deregulated expression of BCL11A through either genomic amplification, chromosomal translocation or abnormal activation (e.g., upon viral integration) is suggested to play a role in lymphomagenesis.

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Acknowledgements

We thank Iwona Nerbas, Claudia Becher and Dorit Schuster for excellent technical assistance and Reina Zühlke-Jenisch for support with FICTION analysis. Further, we thank Dr Frank Leithäuser for technical support. This work was financed by the Deutsche Krebshilfe (106367) and the Deutsche Krebshilfe Verbundprojekt für ‘Molekulare Mechanismen bei malignen Lymphomen’ (70-3173-Tr3). KP, AHB and LL are supported by the Leukaemia Research Fund. MJSD is supported by the Medical Research Council.

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Author notes

  1. M A Weniger, K Pulford and S Gesk: These authors contributed equally to this work.

Authors and Affiliations

  1. Department of Pathology, University of Ulm, Ulm, Germany

    M A Weniger, S Ehrlich, P Möller & T F E Barth

  2. Nuffield Department of Clinical Laboratory Sciences, University of Oxford, Oxford, UK

    K Pulford, A H Banham & L Lyne

  3. Institute of Human Genetics, University Hospital Schleswig-Holstein, Campus Kiel, Kiel, Germany

    S Gesk, J I Martin-Subero & R Siebert

  4. MRC Toxicology Unit/Leicester University, Leicester, UK

    M J S Dyer

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  1. M A Weniger
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Correspondence to P Möller.

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

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Weniger, M., Pulford, K., Gesk, S. et al. Gains of the proto-oncogene BCL11A and nuclear accumulation of BCL11AXL protein are frequent in primary mediastinal B-cell lymphoma. Leukemia 20, 1880–1882 (2006). https://doi.org/10.1038/sj.leu.2404324

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