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7号染色体三体和性染色体缺失不一定代表恶性胶质瘤中的肿瘤实质细胞。

Trisomy 7 and sex chromosome loss need not be representative of tumor parenchyma cells in malignant glioma.

作者信息

Lindström E, Salford L G, Heim S, Mandahl N, Strömblad S, Brun A, Mitelman F

机构信息

Department of Clinical Genetics, University Hospital, Lund, Sweden.

出版信息

Genes Chromosomes Cancer. 1991 Nov;3(6):474-9. doi: 10.1002/gcc.2870030610.

DOI:10.1002/gcc.2870030610
PMID:1663782
Abstract

We describe the cytogenetic findings in short-term cultures from 40 malignant gliomas, all of which had at least one clone with a simple numerical chromosome aberration. More than one aberrant clone was found in 17 tumors. The most frequent changes were loss of a gonosome (sole aberration in 38 clones), trisomy 7 (sole aberration in four clones), and combinations thereof (the aberrations +7 and -X or -Y were found together as the only changes in four clones). Clones with solitary trisomies for other autosomes--3, 5, 6, and 18--were seen in five tumors. Clones with structural rearrangements were found in nine tumors. The bands most commonly involved were lp36, 7p22, 9p22, 17p13, and 19q13. An extra copy of chromosome 7 was seen as part of a structurally abnormal clone in five tumors. In one case, trisomy 7 and even tetrasomy 7 were found in clones with simple numerical changes, but not in the clone with structural rearrangements. Likewise, the clonal loss of a gonosome was in six tumors, with structural abnormalities not present in the structurally aberrant clones; on the other hand, in two clones with structural aberrations a sex chromosome had been lost. The combined findings indicate that loss of a sex chromosome and trisomy 7 should not be seen as tumor-specific aberrations in gliomas. Instead, both glioma parenchyma cells and nonneoplastic cells in brain tumors may have a propensity to acquire extra copies of chromosome 7 and to lose gonosomes.

摘要

我们描述了40例恶性胶质瘤短期培养中的细胞遗传学发现,所有这些肿瘤都至少有一个具有简单染色体数目畸变的克隆。在17例肿瘤中发现了不止一个异常克隆。最常见的变化是性染色体丢失(38个克隆中的唯一畸变)、7号染色体三体(4个克隆中的唯一畸变)以及二者的组合(+7和-X或-Y畸变一起作为4个克隆中的唯一变化被发现)。在5例肿瘤中发现了其他常染色体——3、5、6和18号染色体——的孤立三体克隆。在9例肿瘤中发现了具有结构重排的克隆。最常涉及的带区是1p36、7p22、9p22、17p13和19q13。在5例肿瘤中,额外的一条7号染色体被视为结构异常克隆的一部分。在1例中,在具有简单数目变化的克隆中发现了7号染色体三体甚至四体,但在具有结构重排的克隆中未发现。同样,6例肿瘤中存在性染色体的克隆性丢失,在结构异常的克隆中不存在结构异常;另一方面,在2个具有结构畸变的克隆中丢失了一条性染色体。综合这些发现表明,性染色体丢失和7号染色体三体不应被视为胶质瘤中肿瘤特异性的畸变。相反,脑肿瘤中的胶质瘤实质细胞和非肿瘤细胞都可能有获得额外7号染色体拷贝和丢失性染色体的倾向。

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1
Trisomy 7 and sex chromosome loss need not be representative of tumor parenchyma cells in malignant glioma.7号染色体三体和性染色体缺失不一定代表恶性胶质瘤中的肿瘤实质细胞。
Genes Chromosomes Cancer. 1991 Nov;3(6):474-9. doi: 10.1002/gcc.2870030610.
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引用本文的文献

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Deletions on Chromosome Y and Downregulation of the Gene in Tumor Tissue Are Associated with Worse Survival of Glioblastoma Patients.Y染色体缺失及肿瘤组织中该基因的下调与胶质母细胞瘤患者较差的生存率相关。
Cancers (Basel). 2021 Mar 31;13(7):1619. doi: 10.3390/cancers13071619.
2
Genomic changes in glioblastoma cell lines detected by comparative genomic hybridization.通过比较基因组杂交检测胶质母细胞瘤细胞系中的基因组变化。
J Neurooncol. 1998 Jan;36(2):141-8. doi: 10.1023/a:1005859318971.
3
Therapy-related chromosomal changes and cytogenetic heterogeneity in human gliomas.
人类胶质瘤中与治疗相关的染色体变化及细胞遗传学异质性
J Neurooncol. 1997 Mar;32(1):7-17. doi: 10.1023/a:1005794815663.
4
Nonrandom gain of chromosome 7 in central neurocytoma: a chromosomal analysis and fluorescence in situ hybridization study.中枢神经细胞瘤中7号染色体的非随机增加:一项染色体分析和荧光原位杂交研究
Virchows Arch. 1997 Jan;430(1):47-51. doi: 10.1007/BF01008016.
5
Comparative genomic hybridization of human malignant gliomas reveals multiple amplification sites and nonrandom chromosomal gains and losses.人类恶性胶质瘤的比较基因组杂交揭示了多个扩增位点以及非随机的染色体增加和缺失。
Am J Pathol. 1994 Jun;144(6):1203-18.
6
Molecular genetic analysis of oligodendroglial tumors shows preferential allelic deletions on 19q and 1p.少突胶质细胞瘤的分子遗传学分析显示,19号染色体长臂(19q)和1号染色体短臂(1p)存在优先等位基因缺失。
Am J Pathol. 1994 Nov;145(5):1175-90.
7
Cytogenetics of cranial base tumors.颅底肿瘤的细胞遗传学
J Neurooncol. 1994;20(3):241-54. doi: 10.1007/BF01053042.