Allelic losses at 1p, 9q, 10q, 14q, and 22q in the progression of aggressive meningiomas and undifferentiated meningeal sarcomas
Allelic losses at 1p, 9q, 10q, 14q, and 22q in the progression of aggressive meningiomas and undifferentiated meningeal sarcomas
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DOI：
10.1016/s0165-4608(98)00209-x
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发表时间：
1999-04-15
影响因子：
--
通讯作者：
Westphal, M
中科院分区：
文献类型：
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作者：
Lamszus, K;Kluwe, L;Westphal, M
脑膜瘤通常是良性肿瘤;然而，它们在手术切除后可能会复发，有时组织学进展为更高的恶性程度。在我科17年内手术治疗的923例原发性脑膜瘤中，有5例罕见的侵袭性复发脑膜瘤。本研究还纳入了其他4例临床和组织形态学表现非常相似的侵袭性复发脑膜肿瘤（3例未分化脑膜肉瘤，1例血管外皮细胞瘤）。我们研究了疾病进展是否可以通过遗传改变来追踪，以及遗传改变的模式是否对脑膜瘤特异。共40例原发性肿瘤和9例多发性复发患者的标本进行了分析与26个多态性等位基因标记的缺失1 p，Iq，9 q，10 q，14 q和22 q。所有脑膜瘤病例在分析的最早时间点均观察到22 q杂合性丢失（洛）。两例原发肿瘤和另外两例脑膜瘤复发时，1 p等位基因丢失。10 q缺失发生在2例肿瘤进展期间，1例发生在9 q和14 q。虽然22 q的等位基因丢失似乎是侵袭性脑膜瘤疾病的早期事件，但染色体臂Ip，Sq，10 q和14 q的进一步缺失与组织病理学和临床进展有明显的相关性，如这些个体内追踪所示。这些遗传学发现在非脑膜瘤性脑膜肿瘤中均不存在，表明脑膜瘤细胞具有其自身的谱系特异性遗传通路，可导致临床恶性肿瘤。(C)Elsevier Science Inc.，1999. All rights reserved.
Meningiomas are usually benign tumors; however, they can recur after surgical resection and occasionally shaw histological progression to a higher malignancy grade. Five such rare cases of aggressively recurring meningiomas were present in our departmental cohort of 923 primary meningeal neoplasms operated over a 17-year period. Four other aggressively recurring meningeal tumors with a very similar clinical and histomorphological appearance (three undifferentiated meningeal sarcomas, one hemangiopericytoma) were also included in this study. We investigated whether disease progression can be traced by genetic alterations and whether a pattern of genetic alterations is specific for meningiomas. A total of 40 specimens from primary tumors and multiple recurrences of the nine patients were analyzed with 26 polymorphic allelic markers for deletions on 1p, Iq, 9q, 10q, 14q, and 22q. Loss of heterozygosity (LOH) at 22q was observed in all meningiomas cases at the earliest time point analyzed. Allelic loss at 1p was seen in the original tumor in two cases and upon meningioma recurrence in two others. Deletion on 10q occurred during tumor progression in two cases, and on 9q and 14q in one case. While allelic loss at 22q appears to be an early event in aggressive meningioma disease, there is a clear correlation of further deletions on chromosome arms Ip, Sq, 10q, and 14q with histopathological and clinical progression, as shown in these intraindividual trackings. None of these genetic findings were present in the non-meningiomatous meningeal tumors, indicating that meningothelial cells have their own lineage-specific genetic pathways towards clinical malignancy. (C) Elsevier Science Inc., 1999. All rights reserved.