International journal of cancer · 2010
Mutation analysis of the TNFAIP3 (A20) tumor suppressor gene in CLL.
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Philipp Claudia, Edelmann Jennifer, Bühler Andreas, Winkler Dirk, Stilgenbauer Stephan, Küppers Ralf
Аннотация
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).
Предметные рубрики MeSH
AgedChromosomes, Human, Pair 6DNA Mutational AnalysisDNA-Binding ProteinsExonsGene DeletionGenes, Tumor SuppressorHumansIntracellular Signaling Peptides and ProteinsLeukemia, Lymphocytic, Chronic, B-CellMiddle AgedMutationNF-kappa BNuclear ProteinsPolymerase Chain ReactionTumor Necrosis Factor alpha-Induced Protein 3