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Mutation analysis of the TNFAIP3 (A20) tumor suppressor gene in CLL

✍ Scribed by Claudia Philipp; Jennifer Edelmann; Andreas Bühler; Dirk Winkler; Stephan Stilgenbauer; Ralf Küppers

Publisher
John Wiley and Sons
Year
2010
Tongue
French
Weight
115 KB
Volume
128
Category
Article
ISSN
0020-7136

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✦ Synopsis

Abstract

Chronic lymphocytic leukemia (CLL) cells show constitutive nuclear factor kappa B (NF‐κB) activation, which may have a pathogenetic role. The mechanisms causing this NF‐κB activity are poorly understood. A20, encoded by the TNFAIP3 gene, is a repressor of the NF‐κB pathway and was recently shown to be frequently inactivated by deletions and/or point mutations in several types of B‐cell lymphomas. Here, we studied 48 CLL, including at least 12 cases with a deletion of one allele of TNFAIP3, for mutations. However, only one case harboured a silent mutation, all other cases were unmutated. Therefore, A20 inactivation plays no significant role in the pathogenesis of CLL, and the recurrent deletion in CLL on 6q21‐23, where TNFAIP3 is located, likely affects other gene(s).

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