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首页> 外文期刊>Neuropathology: official journal of the Japanese Society of Neuropathology >EZH2 expression in gliomas: Correlation with CDKN2A gene deletion/ p16 loss and MIB-1 proliferation index
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EZH2 expression in gliomas: Correlation with CDKN2A gene deletion/ p16 loss and MIB-1 proliferation index

机译：脑胶质瘤中EZH2表达：与CDKN2A基因缺失/ p16丢失和MIB-1增殖指数的关系

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摘要

Enhancer of zeste homolog 2 (EZH2) mediated down-regulation of CDKN2A/p16 has been observed in cell lines as well as in a few carcinomas. However, there is no study correlating EZH2 expression with CDKN2A/p16 status in gliomas. Hence, the present study was conducted to evaluate EZH2 expression in astrocytic and oligodendroglial tumors and correlate with CDKN2A/p16 status as well as MIB-1 labeling index (LI). Gliomas of all grades (n=118) were studied using immunohistochemistry to assess EZH2, p16 and MIB-1 LI and fluorescence in situ hybrization to evaluate CDKN2A gene status. EZH2 expression and CDKN2A homozygous deletion (HD) were both significantly more frequent in high-grade gliomas (HGG). Further, strong EZH2 expression (LI25%) was significantly more common in HGGs without CDKN2A HD (48.7%; 19/39) as compared to cases with deletion (15.8%; 3/19). Loss of p16 expression was noted in 100% and 51.3% of CDKN2A deleted and non-deleted tumors, respectively. Notably, 80% (16/20) of the CDKN2A non-deleted HGGs with p16 loss had strong EZH2 expression, in contrast to only 15.8% (3/19) in the deleted group. Loss of p16 expression significantly correlated with MIB-1 LI, irrespective of EZH2 status. Thus, this study shows that EZH2 expression correlates with tumor grade in both astrocytic and oligodendroglial tumors and hence can be used as a diagnostic marker to differentiate between low and HGGs. Further, this is the first report demonstrating an inverse correlation of strong EZH2 expression with CDKN2A HD in HGGs. Loss of p16 protein expression is mostly attributable to CDKN2A HD and correlates significantly with MIB-1 LI. Notably, our study for the first time suggests a possible epigenetic mechanism of p16 loss in CDKN2A non-deleted HGGs mediated by strong EZH2 expression. A hypothetical model for control of proliferative activity in low versus HGGs is therefore proposed.
机译：在细胞系以及一些癌中已经观察到zeste同源物2（EZH2）的增强子介导的CDKN2A / p16的下调。然而，尚无研究将脑胶质瘤中EZH2表达与CDKN2A / p16状态相关联。因此，本研究旨在评估星形细胞和少突胶质细胞肿瘤中EZH2的表达，并与CDKN2A / p16状态以及MIB-1标记指数（LI）相关。使用免疫组织化学评估EZH2，p16和MIB-1 LI以及荧光原位杂交以评估CDKN2A基因状态，研究了所有等级（n = 118）的胶质瘤。 EZH2表达和CDKN2A纯合缺失（HD）在高级神经胶质瘤（HGG）中均显着更频繁。此外，与没有缺失的病例（15.8％; 3/19）相比，在没有CDKN2A HD的HGG中，强EZH2表达（LI25％）更为常见（48.7％; 19/39）。在分别缺失和未缺失的CDKN2A肿瘤中分别发现100％和51.3％的p16表达缺失。值得注意的是，缺失p16的CDKN2A未删除的HGG中80％（16/20）具有较强的EZH2表达，而删除组中只有15.8％（3/19）。无论EZH2状态如何，p16表达的丧失均与MIB-1 LI显着相关。因此，这项研究表明，在星形细胞和少突胶质细胞肿瘤中，EZH2表达与肿瘤等级相关，因此可以用作区分低水平和高血糖的诊断标志。此外，这是第一个证明强EZH2表达与HGG中CDKN2A HD呈负相关的报道。 p16蛋白表达的丧失主要归因于CDKN2A HD，并与MIB-1 LI显着相关。值得注意的是，我们的研究首次提出了由强EZH2表达介导的CDKN2A未缺失HGG中p16缺失的可能表观遗传机制。因此，提出了一种假设模型，用于控制低水平与HGGs的增殖活性。

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