Allelic loss on chromosomes 1p32, 9p21, 13q14, 16q22, 17p, and 22q12 in meningiomas associated with meningioangiomatosis and pure meningioangiomatosis
Allelic loss on chromosomes 1p32, 9p21, 13q14, 16q22, 17p, and 22q12 in meningiomas associated with meningioangiomatosis and pure meningioangiomatosis
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DOI：
10.1007/s11060-009-9879-3
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发表时间：
2009-09-01
影响因子：
3.9
通讯作者：
Suh, Yeon-Lim
中科院分区：
文献类型：
--
作者：
Kim, Na Rae;Cho, Seong Jin;Suh, Yeon-Lim
脑膜血管瘤病（MA）是一种罕见的病变，偶尔出现或作为神经纤维瘤病2的一部分。MA引起的脑膜瘤（MA-M）的发生引起了对MA起源于错构瘤的传统概念的怀疑。由于MA的罕见性，对MA（伴或不伴脑膜瘤）的细胞遗传学或分子生物学研究受到限制。本研究对7例MA-M和2例单纯MA的杂合性缺失（洛）进行了研究。六条染色体上的洛缺失利用D1 S193、D1 S463、D22 S193、D22 S929、D22 S282、TP 53、D17 S796、D16 S421、D16 S512、D13 S118、D13 S153、D9 S162、D9S104使用每个标记进行PCR，并通过银染色完成多态性分析。采用半定量手工计数法测定Ki-67标记指数。MA-Ms脑膜瘤部分在染色体22 q12、9 p21和1 p32上的洛分别为57.1%（4/7）、28.6%（2/7）和28.6%（2/7）。28.6%（2/7）的MA-M的MA部分在22 q12位点有一个洛，而每个纯MA在染色体22 q12或9 p21上都有一个洛。脑膜瘤中MA-Ms的增殖指数明显高于MA组分。我们的数据表明，脑膜瘤和MA都经历了相同的重叠克隆过程，MA-M同时经历了额外的遗传改变，赋予更大的增殖潜力。
Meningioangiomatosis (MA) is a rare lesion appearing sporadically or as a part of neurofibromatosis 2. The occurrences of meningiomas arising from MA (MA-M) have raised doubts about the traditional concept of a hamartomatous origin for MA. Cytogenetic or molecular studies on MA, with or without meningiomas, are limited because of the rarity of MA. The current study was to evaluate the loss of heterozygosity (LOH) in seven cases of MA-M and two cases of pure MA. LOH on six chromosomes (1p32, 9p21, 13q14, 16q22, 17p, and 22q12) were investigated using 13 sets of microsatellite markers, including D1S193, D1S463, D22S193, D22S929, D22S282, TP53, D17S796, D16S421, D16S512, D13S118, D13S153, D9S162, and D9S104. PCR was performed using each marker and polymorphic analysis was accomplished by silver staining. Immunohistochemical stain for Ki-67 was carried out and labeling index was measured by using a semiquantitative manual counting method. The meningioma portions of MA-Ms showed LOH for loci on chromosomes 22q12, 9p21, and 1p32 in 57.1% (4/7), 28.6% (2/7), and 28.6% (2/7) of cases, respectively. The MA portions of MA-M had a LOH for loci on 22q12 in 28.6% (2/7) of cases, whereas each pure MA harbored one LOH on either chromosome 22q12 or 9p21. The proliferation indices of MA-Ms were significantly higher in the meningioma than in the MA components. Our data suggest that both the meningioma and the MA undergo the same overlapping clonal process, with the MA-M while undergoing additional genetic alterations that confer a greater proliferative potential.