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Blood, 1 November 2007, Vol. 110, No. 9, pp. 3387-3390. Prepublished online as a Blood First Edition Paper on July 25, 2007; DOI 10.1182/blood-2007-03-082511. This Article Full Text (PDF) Supplemental Tables and Figures All Versions of this Article: blood-2007-03-082511v1 110/9/3387    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Mottok, A. Articles by Brauninger, A. Search for Related Content PubMed PubMed Citation Articles by Mottok, A. Articles by Brauninger, A. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted March 27, 2007 Accepted July 23, 2007 Somatic hypermutation of SOCS1 in lymphocyte-predominant Hodgkin lymphoma is accompanied by high JAK2 expression and activation of STAT6 Anja Mottok, Christoph Renne, Klaus Willenbrock, Martin-Leo Hansmann, and Andreas Brauninger* Senckenberg Institute of Pathology, University of Frankfurt, Frankfurt, Germany * Corresponding author; email: braeuninger{at}em.uni-frankfurt.de. Aberrant activities of JAK/STAT signalling pathways have been observed in several hematological malignancies. Here we show high expression of JAK2 in the tumor cells of lymphocyte-predominant Hodgkin lymphoma in 85% of cases and activation of JAK2 in 39% of cases. STAT6, which is a target of JAK2, was activated in 50% of the cases. SOCS1 controls JAK2 activity and degradation. Mutations in SOCS1 of either somatic or germline origin were observed in micromanipulated tumor cells of 50% of cases. Most mutations truncated SOCS1 or caused replacement of amino acids in functional important regions. Activating mutations in exon 12 of JAK2, which are frequent in myeloproliferative diseases, were not observed. In lymphocyte-predominant Hodgkin lymphoma SOCS1 function may thus be frequently impaired by mutations and this may contribute to high JAK2 expression and activation of the JAK2/STAT6 pathway. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Mottok, C. Renne, M. Seifert, E. Oppermann, W. Bechstein, M.-L. Hansmann, R. Kuppers, and A. Brauninger Inactivating SOCS1 mutations are caused by aberrant somatic hypermutation and restricted to a subset of B-cell lymphoma entities Blood, November 12, 2009; 114(20): 4503 - 4506. [Abstract] [Full Text] [PDF] O. Ritz, C. Guiter, F. Castellano, K. Dorsch, J. Melzner, J.-P. Jais, G. Dubois, P. Gaulard, P. Moller, and K. Leroy Recurrent mutations of the STAT6 DNA binding domain in primary mediastinal B-cell lymphoma Blood, August 6, 2009; 114(6): 1236 - 1242. [Abstract] [Full Text] [PDF] K. R. Calvo, B. Dabir, A. Kovach, C. Devor, R. Bandle, A. Bond, J. H. Shih, and E. S. Jaffe IL-4 protein expression and basal activation of Erk in vivo in follicular lymphoma Blood, November 1, 2008; 112(9): 3818 - 3826. [Abstract] [Full Text] [PDF]

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