Recurrent alterations of TNFAIP3 (A20) in T‐cell large granular lymphocytic leukemia. Issue 1 (30th July 2015)

• Record Type: Journal Article
• Authors: Johansson, Patricia; Bergmann, Anke; Rahmann, Sven; Wohlers, Inken; Scholtysik, René; Przekopowitz, Martina; Seifert, Marc; Tschurtschenthaler, Gertraud; Webersinke, Gerald; Jäger, Ulrich; Siebert, Reiner; Klein‐Hitpass, Ludger; Dührsen, Ulrich; Dürig, Jan; Küppers, Ralf
• Is Part Of: International journal of cancer. Volume 138:Issue 1(2016:Jan. 01)
• Page Start: 121
• Page End: 124
• Publication Date: 2015-07-30
• Subjects: Cancer -- Periodicals; Cancer -- Prevention -- Periodicals; 616.994
• DOI: 10.1002/ijc.29697
• Languages: English
• ISSNs: 0020-7136

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>The pathogenesis of T‐cell large granular lymphocytic leukemia (T‐LGL) is poorly understood, as <italic>STAT3</italic> mutations are the only known frequent genetic lesions. Here, we identified non‐synonymous alterations in the <italic>TNFAIP3</italic> tumor suppressor gene in 3 of 39 T‐LGL. In two cases these were somatic mutations, in one case the somatic origin was likely. A further case harbored a SNP that is a known risk allele for autoimmune diseases and B cell lymphomas. Thus, <italic>TNFAIP3</italic> mutations represent recurrent genetic lesions in T‐LGL that affect about 8% of cases, likely contributing to deregulated NF‐κB activity in this leukemia.</p> </abstract>