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首页> 外文期刊>Neurosurgery >Loss of Heterozygosity Analysis of Benign, Atypical, and Anaplastic Meningiomas.
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Loss of Heterozygosity Analysis of Benign, Atypical, and Anaplastic Meningiomas.

机译：良性，非典型性和间变性脑膜瘤的杂合度分析损失。

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OBJECTIVE: Up to 70% of typical meningiomas demonstrate allelic loss at chromosome 22q. Allelic loss at additional chromosomal loci is associated with atypia and anaplasia in meningiomas. The pattern of allelic loss or loss of heterozygosity (LOH) follows a nonrandom, multistep pattern. METHODS: All surgical meningioma samples obtained from 1991 to 1992 at the University of Pittsburgh Medical Center were analyzed according to current World Health Organization criteria. Samples without constitutional deoxyribonucleic acid (DNA) were excluded from this analysis. Individual hematoxylin and eosin slides from 43 patients were microdissected, and the DNA was harvested and amplified in the presence of 24 pairs of polymerase chain reaction primers, representing 24 microsatellite loci. The polymerase chain reaction products were subjected to capillary gel electrophoresis and a fluorescence-based DNA analysis system. LOH was defined as ratios of allelic peak heights falling within a conservative threshold of less than 0.5 or more than 2.0. Fisher's exact test and receiver operator characteristic curves were used to test the relationship between benign versus atypical and malignant pathological features and LOH at specific loci or combinations of loci. RESULTS: On review by two independent pathologists, 34 benign meningiomas, 6 atypical meningiomas, and 3 anaplastic meningiomas were identified. The mean number of alleles with LOH was 1.5 +/- 1.2 for benign meningiomas, 6.7 +/- 2.7 for atypical meningiomas, and 8.3 +/- 2.3 for anaplastic meningiomas (P < 0.001). The most important individual loci to predict malignancy were D1S407 (P = 0.006), L-myc (P < 0.001), D10S520 (P = 0.003), D10S1173 (P = 0.042), D11S1920 (P < 0.001), D14S555 (P = 0.041), D17S1289 (P < 0.001), D22S417 (P = 0.001), D22S431 (P = 0.019), and D22S532 (P = 0.028). Combining the LOH data across loci, the area under the receiver operator characteristic curve was 0.993, corresponding to virtually perfect prediction of pathological characteristics. CONCLUSION: Microsatellite marker analysis of allelic loss is a useful method of predicting atypia and anaplasia in meningiomas. More regions of allelic loss are seen in anaplastic and atypical meningiomas as compared with benign meningiomas. This study confirms previously reported chromosomal regions of allelic loss in atypical and anaplastic meningiomas and suggests additional chromosomal regions that may represent heretofore uncharacterized deletions within meningiomas. This type of genetic fingerprint ultimately may serve both a diagnostic and therapeutic role.
机译：目的：高达70％的典型脑膜瘤在22q染色体上表现出等位基因缺失。在其他染色体基因座处的等位基因缺失与脑膜瘤的非典型性和发育不良有关。等位基因缺失或杂合性缺失（LOH）的模式遵循非随机多步模式。方法：根据世界卫生组织现行标准，分析了从1991年至1992年在匹兹堡大学医学中心获得的所有外科脑膜瘤样本。没有构成脱氧核糖核酸（DNA）的样品从该分析中排除。显微解剖了来自43例患者的单个苏木和曙红玻片，并在代表24个微卫星基因座的24对聚合酶链反应引物的存在下收集和扩增了DNA。对该聚合酶链反应产物进行毛细管凝胶电泳和基于荧光的DNA分析系统。 LOH被定义为等位基因峰高之比落入小于0.5或大于2.0的保守阈值内。 Fisher的精确测试和接收者操作员特征曲线用于测试在特定位点或位点组合下良性，非典型和恶性病理特征与LOH之间的关系。结果：经两名独立病理学家的审查，确定了34例良性脑膜瘤，6例非典型性脑膜瘤和3例间变性脑膜瘤。良性脑膜瘤的LOH等位基因平均数为1.5 +/- 1.2，非典型脑膜瘤为6.7 +/- 2.7，间变性脑膜瘤为8.3 +/- 2.3（P <0.001）。预测恶性肿瘤最重要的个体位点是D1S407（P = 0.006），L-myc（P <0.001），D10S520（P = 0.003），D10S1173（P = 0.042），D11S1920（P <0.001），D14S555（P = 0.041），D17S1289（P <0.001），D22S417（P = 0.001），D22S431（P = 0.019）和D22S532（P = 0.028）。结合整个基因座的LOH数据，接收者操作员特征曲线下的面积为0.993，对应于病理特征的几乎完美的预测。结论：等位基因缺失的微卫星标记分析是预测脑膜瘤非典型和发育不良的有用方法。与良性脑膜瘤相比，间变性和非典型脑膜瘤中见到更多的等位基因缺失区域。这项研究证实了先前报道的非典型和间变性脑膜瘤等位基因缺失的染色体区域，并提出了可能代表迄今为止脑膜瘤内未表征缺失的其他染色体区域。这种类型的遗传指纹最终可以起到诊断和治疗的作用。

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