Wednesday 28 November 2012
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.
One-fourth of diffuse large B-cell lymphoma and follicular lymphomas carry SOCS1 mutations, which are preferentially targeted to SHM hotspot motifs and frequently obviously inactivating.
Rare mutations are 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 are 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.
BOB.1, CD79a and cyclin E are the most appropriate markers to discriminate classical Hodgkin’s lymphoma from primary mediastinal large B-cell lymphoma. Hoeller S, Zihler D, Zlobec I, Obermann EC, Pileri SA, Dirnhofer S, Tzankov A. Histopathology. 2010 Jan;56(2):217-28. PMID: 20102401