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Infarction with associated pseudosarcomatous changes mimics anaplasia in otherwise grade I meningiomas.
Modern Pathology ( IF 7.1 ) Pub Date : 2020-02-11 , DOI: 10.1038/s41379-020-0491-6
Tejus A Bale 1 , Jamal Benhamida 1 , Sudarshana Roychoudury 1 , Liliana Villafania 1 , Monika A Wrzolek 2 , John-Paul Bouffard 3 , Kalyani Bapat 4 , Marc Ladanyi 1 , Marc K Rosenblum 1
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We describe a morphologically distinct pattern of tumor infarction and associated sarcoma-like changes, mimicking focal anaplasia, in otherwise WHO grade I meningiomas. The described cases (n = 9) all demonstrated a discrete spindle-cell (pseudosarcomatous) component with brisk mitotic activity (12-14 mitoses/10 HPF), elevated Ki-67 (mean 75.5 ± 25.0%, quantified), absence of PR, SSTR2A, or EMA expression, and potential SMA expression (50%). Despite these high-grade features, all nine patients remained free of progression or recurrence post resection (follow-up mean: 49.8 months). In contrast, among a comparison (control) cohort of consecutive WHO grade II and III meningiomas (n = 16), as expected, progression rate was high (68.8%, P = 0.002, Fisher's exact, average time to progression = 25 months, follow-up mean: 39.8 months). While necrosis was a frequent feature among atypical/anaplastic meningiomas (12/16, 75%), and elevated mitoses and proliferative index were present consistent with histologic grade, a well-defined zonal pattern with pseudosarcomatous component was not present among these tumors. DNA methylation-based analysis readily distinguished meningiomas by copy number profiles and DNA-based methylation meningioma random forest classification analysis (meningioma v2.4 classifier developed at University of Heidelberg); all pseudosarcomatous cases analyzed (4/9) matched with high level calibrated classifier score to "MC benign-1", with isolated loss of chromosome 22q identified as the sole copy number alteration. In contrast, multiple chromosomal losses were detected among the comparison cohort and classifier results demonstrated good concordance with histologic grade. Our findings suggest that pseudosarcomatous alterations represent reactive changes to central meningioma infarction, rather than focal anaplasia, and further support the use of DNA methylation-based analysis as a useful adjunct for predicting meningioma behavior. These indolent tumors should be distinguished from their atypical and anaplastic counterparts.

中文翻译:


伴有相关假肉瘤变化的梗死与 I 级脑膜瘤中的退变相似。



我们描述了一种形态学上不同的肿瘤梗塞模式和相关的肉瘤样变化,类似于世界卫生组织 I 级脑膜瘤中的局灶性退行性变。所描述的病例 (n = 9) 均表现出离散的梭形细胞(假肉瘤)成分,具有活跃的有丝分裂活性(12-14 个有丝分裂/10 HPF)、Ki-67 升高(平均 75.5 ± 25.0%,量化)、缺乏 PR 、SSTR2A 或 EMA 表达,以及潜在的 SMA 表达 (50%)。尽管具有这些高级特征,所有 9 名患者在切除后均未出现进展或复发(平均随访时间:49.8 个月)。相比之下,在连续 WHO II 级和 III 级脑膜瘤的比较(对照)队列中(n = 16),正如预期的那样,进展率很高(68.8%,P = 0.002,Fisher 精确平均进展时间 = 25 个月,随访平均时间:39.8 个月)。虽然坏死是非典型/间变性脑膜瘤的常见特征(12/16,75%),并且存在与组织学分级一致的有丝分裂和增殖指数升高,但这些肿瘤中不存在具有假肉瘤成分的明确的带状模式。基于 DNA 甲基化的分析通过拷贝数谱和基于 DNA 的甲基化脑膜瘤随机森林分类分析(海德堡大学开发的脑膜瘤 v2.4 分类器)轻松区分脑膜瘤;所有分析的假肉瘤病例 (4/9) 均与“MC良性-1”的高水平校准分类器评分相匹配,染色体 22q 的孤立丢失被确定为唯一的拷贝数改变。相比之下,在比较队列中检测到多条染色体丢失,并且分类器结果证明与组织学分级具有良好的一致性。 我们的研究结果表明,假肉瘤性改变代表了中央脑膜瘤梗死的反应性变化,而不是局灶性退变,并进一步支持使用基于 DNA 甲基化的分析作为预测脑膜瘤行为的有用辅助手段。这些惰性肿瘤应与其非典型和间变性肿瘤区分开来。
更新日期:2020-02-11
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