Volume 7 Supplement 1

12th Joint Meeting of the Signal Transduction Society (STS). Signal Transduction: Receptors, Mediators and Genes

Open Access

Dissecting the molecular pathogenisis of Burkitt lymphoma

  • D Kube1,
  • K Matulewicz1,
  • A Schrader1,
  • S Bentink3,
  • R Spang3,
  • P Murray4,
  • L Trümper1 and
  • M Vockerodt2
Cell Communication and Signaling20097(Suppl 1):A33

DOI: 10.1186/1478-811X-7-S1-A33

Published: 26 February 2009

Burkitt lymphoma (BL) is a high grade B cell malignancy (Non-Hodgkin Lymphoma (NHL)) derived from germinal center B cells (GCB) that harbours a chromosomal translocation juxtaposing the protooncogene MYC next to the regulatory elements of one of the immunoglobulin loci. However, the precise contribution of Myc to the pathogenesis of this tumour is poorly understood. Based on the definition of a distinguishing gene expression signature for the molecular BL (mBL) with Myc as one hallmarking signature gene we are interested in getting answers to the questions (i) what are the target genes of Myc in primary human GCB cells and (ii) what is the functional significance of signature genes identified?

We describe a non-viral vector based approach (Vockerodt et al. 2008) to express Myc in primary human GCB cells. Comparative gene expression profiling was performed accompanied by qRT-PCR. In addition elucidation of the function of selected signature genes in BL is accomplished. In a representative cell line with a mBL signature RNAi directed inhibition of elements of the CD40 signaling cascade was conducted. After activating this particular signaling cascade in a BL cell line we analysed respective gene expression profiles of IKKa, IKKb, TRAF2, TRAF6, Jak3, BCL-3 and p38 deficient cells. Based on these different RNAi-mediated GE-profiles we reconstruct the topology of the respective signaling pathway by using the nested effects bioinformatic model, which has been described recently (Markowetz et al. 2005).

Declarations

Acknowledgements

This work is supported by the DFG GRK1034, the Deutsche Krebshilfe Network MMML and the UICC

Authors’ Affiliations

(1)
Georg-August Universität Göttingen, Universitätsmedizin, Abteilung für Hämatologie und Onkologie
(2)
Georg-August Universität Göttingen, Universitätsmedizin
(3)
Institut für Funktionsgenomik, University of Regensburg
(4)
CRC for Cancer studies University

Copyright

© Kube et al; licensee BioMed Central Ltd. 2009

This article is published under license to BioMed Central Ltd.

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