A20 (TNFAIP3) genetic alterations in EBV-associated AIDS-related lymphoma
A20 (TNFAIP3) genetic alterations in EBV-associated AIDS-related lymphoma
复制标题
DOI：
10.1182/blood-2010-10-310995
复制
发表时间：
2011-05-05
期刊：
影响因子：
20.3
通讯作者：
Cesarman, Ethel
中科院分区：
文献类型：
--
作者：
Giulino, Lisa;Mathew, Susan;Cesarman, Ethel
A20是NF-κ B B的负调节因子，在多种类型的B细胞淋巴瘤中被认为是肿瘤抑制基因。艾滋病相关淋巴瘤（ARL）是高度B细胞淋巴瘤，通常与EBV感染有关。我们检查了一组ARL的A20改变。FISH检测A20基因缺失6例（18%）。A20基因突变3例（16%），其中2例为互补等位基因缺失。免疫组化结果显示A20蛋白在55例中7例（13%）缺失。与霍奇金淋巴瘤中EBV感染和A20改变相互排斥的报道相反，在EBV+和EBV-病例中均观察到A20失活。激活NF-κ B的EBV潜伏膜蛋白1在13例A20缺失的病例中有12例不表达。在ARLs中，A20的缺失可能是在不存在潜在膜蛋白1表达的情况下NF-κ B活化的另一种机制。（血。2011;117（18）：852-4854）
A20, a negative regulator of NF-kappa B, has been implicated as a tumor suppressor gene in multiple types of B-cell lymphoma. AIDS-related lymphomas (ARLs) are high-grade B-cell lymphomas that are frequently associated with EBV infection. We examined a panel of ARLs for A20 alterations. FISH showed A20 deletion in 6 of 33 cases (18%). A20 mutations were found in 3 of 19 cases (16%), including 2 cases with deletions of the complementary allele. Immunohistochemistry showed the absence of A20 protein in 7 of 55 samples (13%). In contrast to reports in Hodgkin lymphoma in which EBV infection and A20 alteration are mutually exclusive, A20 inactivation was observed in both EBV+ and EBV- cases. The EBV latent membrane protein 1, which activates NF-kappa B, was not expressed in 12 of 13 cases with A20 loss. In ARLs loss of A20 may be an alternative mechanism of NF-kappa B activation in the absence of latent membrane protein 1 expression. (Blood. 2011;117(18):852-4854)