Institute of Cell Biology, University of Duisburg-Essen, Medical School, Essen, Germany.
Int J Cancer. 2011 Apr 1;128(7):1747-50. doi: 10.1002/ijc.25497. Epub 2010 Jun 7.
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).
慢性淋巴细胞白血病 (CLL) 细胞表现出组成性核因子 kappa B (NF-κB) 激活,这可能具有发病作用。导致这种 NF-κB 活性的机制知之甚少。A20 由 TNFAIP3 基因编码,是 NF-κB 途径的抑制剂,最近在几种 B 细胞淋巴瘤中发现其经常因缺失和/或点突变而失活。在这里,我们研究了 48 例 CLL,包括至少 12 例 TNFAIP3 等位基因缺失的病例,以研究突变情况。然而,只有一个病例存在沉默突变,其他所有病例均未突变。因此,A20 失活在 CLL 的发病机制中不起重要作用,而 CLL 中经常发生的 6q21-23 缺失(TNFAIP3 所在位置)可能影响其他基因。