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Molecular Medicine

, Volume 9, Issue 3–4, pp 85–95 | Cite as

Profiling of Hodgkin’s Lymphoma Cell Line L1236 and Germinal Center B Cells: Identification of Hodgkin’s Lymphoma-specific Genes

  • Ines Schwering
  • Andreas Bräuninger
  • Verena Distler
  • Julia Jesdinsky
  • Volker Diehl
  • Martin-Leo Hansmann
  • Klaus Rajewsky
  • Ralf Küppers
Articles
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Abstract

The malignant cells of classical Hodgkin’s lymphoma (cHL), Hodgkin and Reed-Sternberg (HRS) cells, appear to be derived from germinal center (GC) B cells in most cases of the disease. Apart from recent findings of constitutive activation of some transcription factors and autocrine stimulation by cytokine receptors, the mechanisms of malignant transformation in cHL still remain poorly understood. We performed a large scale gene expression study using serial analysis of gene expression (SAGE), comparing the cHL cell line L1236 and human GC B cells. Semiquantitative RT-PCR was used to confirm results from the SAGE and to analyze gene expression in 3 additional cHL cell lines. To investigate expression of some genes in cHL cases, we applied RT-PCR on microdissected HRS cells. In total, 464 genes showed a change in expression level of 5-fold or higher. For 12 genes (out of 177) identified as upregulated in L1236 cells, RT-PCR confirmed the SAGE results and also showed elevated expression in 3 other cHL cell lines. For 3 of the upregulated genes, expression by HRS cells in the tissue also was confirmed. Several of the differentially expressed genes may play a role in the pathogenesis of cHL because they represent potential oncogenes, such as rhoC, L-myc, and PTP4A, or transcription factors, such as ATF-5, ATBF1, and p21SNFT. The genes that showed significantly deregulated expression in HRS cells should be helpful not only for the identification of genes involved in the pathogenesis of cHL but also for discovering potential prognostic markers or therapeutic targets.

Notes

Acknowledgments

This work was supported through the Deutsche Forschungsgemeinschaft by SFB502 and a Heisenberg award to RK. We are grateful to Yvonne Blum, Michaela Fahrig, Christine Gerhardt, and Tanja Schaffer for excellent technical assistance, to Berit Jungnickel for stimulating discussions, and to Carel van Noesel for critically reading this manuscript.

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Copyright information

© Feinstein Institute for Medical Research 2003

Authors and Affiliations

  • Ines Schwering
    • 1
    • 2
  • Andreas Bräuninger
    • 3
  • Verena Distler
    • 3
  • Julia Jesdinsky
    • 2
  • Volker Diehl
    • 2
  • Martin-Leo Hansmann
    • 3
  • Klaus Rajewsky
    • 1
  • Ralf Küppers
    • 1
    • 2
  1. 1.Institute for GeneticsUniversity of CologneCologneGermany
  2. 2.Department of Internal Medicine I, LFI, E4, R706University of CologneCologneGermany
  3. 3.Department of PathologyUniversity of FrankfurtFrankfurt/MainGermany

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