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 Blood, 1 May 2008, Vol. 111, No. 9, pp. 4706-4715.
Prepublished online as a Blood First Edition Paper on February 22, 2008; DOI 10.1182/blood-2007-08-105643.

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NEOPLASIA

IL-21 is expressed in Hodgkin lymphoma and activates STAT5: evidence that activated STAT5 is required for Hodgkin lymphomagenesis

Ferenc A. Scheeren1, Sean A. Diehl*,1, Laura A. Smit*,2, Tim Beaumont3, Marianne Naspetti1, Richard J. Bende2, Bianca Blom1, Kennosuke Karube4, Koichi Ohshima4, Carel J. M. van Noesel2, and Hergen Spits1

1 Department of Cell Biology and Histology and 2 Department of Pathology of the Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; 3 AIMM Therapeutics, Amsterdam, The Netherlands; and 4 Department of Pathology, Kurume University School of Medicine, Kurume, Japan

Classical Hodgkin lymphoma (HL) is a malignant disorder characterized by the presence of neoplastic mononucleated Hodgkin and multinucleated Reed-Sternberg cells. Here, we show that both the interleukin (IL)–21 receptor as well as IL-21 are expressed by HL cells. IL-21 activates signal transducer of activation and transcription 3 (STAT3) and STAT5 in HL cell lines and activated human B cells. Ectopic expression of constitutively active STAT5 in primary human B cells resulted in immortalized B cells that have lost the B-cell phenotype and strongly resembled HL cells, which could partially be rescued by ectopic expression of the B cell–determining transcription factor E47. Data from experiments using reporter assays and overexpression of constitutively active IKK2 support the hypothesis that the STAT5 and nuclear factor-{kappa}B (NF-{kappa}B) pathways colaborate in HL genesis.


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