Shi Y F, Gao Z F, Liu C L, Li M, Lin D M, Zhou L X, Lai Y M, Liu X L, Huang X
Department of Pathology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
Zhonghua Xue Ye Xue Za Zhi. 2016 Dec 14;37(12):1060-1064. doi: 10.3760/cma.j.issn.0253-2727.2016.12.010.
To investigate the TNFAIP3/A20 abnormalities and its association with Epstein-Barr virus (EBV) in classical Hodgkin lymphoma (CHL). Formalin-fixed, paraffinembedded tissue blocks of 54 CHL patients were collected and subjected to the construction of tissue microarray (TMA) for further analyses. EBV status was evaluated by in situ hybridization (ISH) for EBER1/2 and immunohistochemistry (IHC) with anti-LMP-1 antibody. Fluorescence in situ hybridization (FISH) and IHC were performed to determine the copy number alterations of TNFAIP3 and A20 protein expression respectively. The concordance rate of IHC for LMP-1 and ISH for EBER1/2 was100%, and 25.9% (14/54) cases were identified with EBV infection. Immunohistochemistry analysis demonstrated 27.8% (15/54) cases with A20 expression deficiency. Of the 54 cases tested for A20 expression, 49 cases were simultaneously analyzed by FISH, which showed 10 (20.4% ) cases harboring TNFAIP3 deletion. However, discrepancy was observed between the results of A20 by IHC and TNFAIP3 deletion by FISH. Only 1 case with TNFAIP3 deletion demonstrated complete loss of A20 immunoreactivity. In addition, comparison of the frequency of either A20 expression loss or TNFAIP3 deletion between EBV-positive and-negative cases did not reveal any significance (>0.05). TNFAIP3 deletion could be observed in both EBV-positive and - negative CHL cases. A20 expression by IHC could not confirm TNFAIP3 deletion by FISH, which might be related to the technical issues.
研究经典型霍奇金淋巴瘤（CHL）中TNFAIP3/A20异常及其与爱泼斯坦-巴尔病毒（EBV）的关联。收集54例CHL患者的福尔马林固定、石蜡包埋组织块，构建组织芯片（TMA）用于进一步分析。通过EBER1/2原位杂交（ISH）和抗LMP-1抗体免疫组化（IHC）评估EBV状态。分别采用荧光原位杂交（FISH）和IHC检测TNFAIP3的拷贝数改变和A20蛋白表达。LMP-1的IHC与EBER1/2的ISH一致性率为100%，25.9%（14/54）的病例被鉴定为EBV感染。免疫组化分析显示27.8%（15/54）的病例存在A20表达缺失。在检测A20表达的54例病例中，49例同时进行FISH分析，结果显示10例（20.4%）存在TNFAIP3缺失。然而，IHC检测A20的结果与FISH检测TNFAIP3缺失的结果存在差异。只有1例TNFAIP3缺失的病例显示A20免疫反应性完全丧失。此外，比较EBV阳性和阴性病例中A20表达缺失或TNFAIP3缺失的频率，未发现任何显著差异（>0.05）。EBV阳性和阴性CHL病例中均可见TNFAIP3缺失。IHC检测的A20表达不能证实FISH检测的TNFAIP3缺失，这可能与技术问题有关。
