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 Blood, 12 November 2009, Vol. 114, No. 20, pp. 4503-4506.
Prepublished online as a Blood First Edition Paper on September 4, 2009; DOI 10.1182/blood-2009-06-225839.

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LYMPHOID NEOPLASIA

Brief report

Inactivating SOCS1 mutations are caused by aberrant somatic hypermutation and restricted to a subset of B-cell lymphoma entities

Anja Mottok1,2,*, Christoph Renné1,*, Marc Seifert3, Elsie Oppermann4, Wolf Bechstein4, Martin-Leo Hansmann1, Ralf Küppers3, and Andreas Bräuninger1,5

1 Senckenberg Institute for Pathology, University of Frankfurt, Frankfurt; 2 Department of Pathology, University of Würzburg, Würzburg; 3 Institute of Cell Biology (Cancer Research), University of Duisburg-Essen, Essen; 4 Department of Surgery, University of Frankfurt, Frankfurt; and 5 Gerhard-Domagk-Institute for Pathology, University of Münster, Münster, Germany

STATs are constitutively activated in several malignancies. In primary mediastinal large B-cell lymphoma and Hodgkin lymphoma (HL), inactivating mutations in SOCS1, an inhibitor of JAK/STAT signaling, contribute to deregulated STAT activity. Based on indications that the SOCS1 mutations are caused by the B cell–specific somatic hypermutation (SHM) process, we analyzed B-cell non-HL and normal B cells for mutations in SOCS1. One-fourth of diffuse large B-cell lymphoma and follicular lymphomas carried SOCS1 mutations, which were preferentially targeted to SHM hotspot motifs and frequently obviously inactivating. Rare mutations were observed in Burkitt lymphoma, plasmacytoma, and mantle cell lymphoma but not in tumors of a non–B-cell origin. Mutations in single-sorted germinal center B cells were infrequent relative to other genes mutated as byproducts of normal SHM, indicating that SOCS1 inactivation in primary mediastinal large B-cell lymphoma, HL, diffuse large B-cell lymphoma, and follicular lymphoma is frequently the result of aberrant SHM.


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