| Autor: |
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 |
| Zdroj: |
International Journal of Cancer; Jan2016, Vol. 138 Issue 1, p121-124, 4p |
| Abstrakt: |
The pathogenesis of T-cell large granular lymphocytic leukemia (T-LGL) is poorly understood, as STAT3 mutations are the only known frequent genetic lesions. Here, we identified non-synonymous alterations in the TNFAIP3 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, TNFAIP3 mutations represent recurrent genetic lesions in T-LGL that affect about 8% of cases, likely contributing to deregulated NF-κB activity in this leukemia. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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