CYTOGENETIC ANALYSIS OF 39 PEDIATRIC CENTRAL-NERVOUS-SYSTEM TUMORS
CYTOGENETIC ANALYSIS OF 39 PEDIATRIC CENTRAL-NERVOUS-SYSTEM TUMORS
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DOI：
10.1016/0165-4608(92)90150-7
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发表时间：
1992-03-01
影响因子：
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通讯作者：
YING, KL
中科院分区：
文献类型：
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作者：
KARNES, PS;TRAN, TN;YING, KL
一致的细胞遗传学异常已经在许多儿童实体肿瘤中被描述，包括尤文氏肉瘤、威尔姆氏肿瘤和神经母细胞瘤。对儿童中枢神经系统（CNS）肿瘤的类似分析一直受到技术问题的阻碍。我们报告39例小儿中枢神经系统肿瘤的染色体结果。11例原始神经外胚层肿瘤中有3例出现17号染色体异常（其中2例出现i(17q)），证实了其他研究者观察到的数据。11例原始神经外胚层肿瘤（PNET）中2例细胞表现出涉及11号染色体的缺失或结构异常。在两个PNETs的细胞中发现7q染色体缺失或远端缺失。由于其他研究者已经发现在大约三分之一的PNET患者中17p杂合性缺失，我们建议染色体区域7q和11是值得进一步研究的儿科PNET患者。21例星形细胞瘤中有6例出现数值异常。4例毛细胞星形细胞瘤中1例表现为高二倍体，13例间变性星形细胞瘤中4例表现为假多倍体。13例间变性星形细胞瘤中有4例存在结构性染色体异常（易位、缺失）。1例颅咽管瘤有复杂的结构异常。脑横纹肌样瘤表现出多重复杂的结构重排，但不表现出在某些横纹肌样瘤中观察到的单体22。低二倍体和22号染色体丢失在临床侵袭性脑膜瘤中被注意到，证实了其他研究者的观察结果。
Consistent cytogenetic abnormalities have been described in many pediatric solid tumors, including Ewing's sarcoma, Wilm's tumor, and neuroblastoma. Similar analysis of pediatric central nervous system (CNS) tumors has been hampered by technical problems. We report chromosome results from 39 pediatric CNS tumors. Abnormalities of chromosome 17 were noted in 3 of 11 primitive neuroectodermal tumors (including i(17q) in 2 tumors), confirming data observed by other investigators. Cells from 2 of 11 primitive neuroectodermal tumors (PNET) exhibited loss or structural abnormalities involving chromosome 11. Loss or distal deletion of chromosomes 7q was noted in cells from two PNETs. Because other investigators have shown loss of heterozygosity on 17p in about one-third of PNET, we propose that chromosome regions 7q and 11 are areas worthy of further study in pediatric PNET. Numerical abnormalities were noted in 6 of 21 astrocytomas. Hyperdiploidy was demonstrated in 1 of 4 pilocytic astrocytomas and pseudopolyploidy was demonstrated in 4 of 13 anaplastic astrocytomas. Structural chromosome abnormalities (translocations, deletions) were noted in 4 of 13 anaplastic astrocytomas.Complex structural anomalies were observed in one craniopharyngioma. A rhabdoid tumor of the brain exhibited multiple complex structural rearrangements but did not exhibit the monosomy 22 observed in some rhabdoid tumors. Hypodiploidy and loss of chromosome 22 were noted in a clinically aggressive meningioma, corroborating observations by other investigators.