| Literature DB >> 20533286 |
Claudia Philipp1, Jennifer Edelmann, Andreas Bühler, Dirk Winkler, Stephan Stilgenbauer, Ralf Küppers.
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).Entities:
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Year: 2010 PMID: 20533286 DOI: 10.1002/ijc.25497
Source DB: PubMed Journal: Int J Cancer ISSN: 0020-7136 Impact factor: 7.396