Genome-wide analysis of sixteen chordomas by comparative genomic hybridization and cytogenetics of the first human chordoma cell line, U-CHI
Genome-wide analysis of sixteen chordomas by comparative genomic hybridization and cytogenetics of the first human chordoma cell line, U-CHI
复制标题
DOI：
10.1002/gcc.1184
复制
发表时间：
2001-11-01
影响因子：
3.7
通讯作者：
Möller, P
中科院分区：
文献类型：
--
作者：
Scheil, S;Brüderlein, S;Möller, P
脊索瘤的细胞遗传学信息是初步的，仅限于全球26例的gtg带分析。在这项研究中，我们使用比较基因组杂交（CGH）和荧光原位杂交（FISH）在13例患者的16例脊索瘤（10例骶尾骨，5例蝶枕，1例脊柱）中检测到染色体失衡。平均每个肿瘤检测到3.2个损失和4.2个增益。最常见的DNA拷贝数改变是染色体臂3p（50%）和1p（44%）的丢失。7例原发性脊索瘤中有5例检测到3p缺失。因此，3p的缺失可能是脊索瘤发生的早期事件。最常见的增益包括第7季度（69%）、第20季度（50%）、第5季度（38%）和第12季度（38%）。此外，我们从骶骨脊索瘤的复发中培养了第一个人类脊索瘤细胞系U-CH I。U-CH I和它的母体肿瘤具有几乎相同的CGH特征。根据gtg -显带和多色FISH， U-CH I具有以下克隆染色体异常：der(1)t(1;22), del(4), +del(5), +del(6), +7, del(9), del(10), +der(20)t(10;20), +21。因此，新的永久性人类脊索瘤细胞系U-CH I具有脊索瘤典型的细胞遗传学畸变。我们的数据表明，肿瘤抑制基因或错配修复基因（位于1p31和3p14）和致癌基因（位于7q36）可能参与脊索瘤的发生。(C) 2001 Wiley-Liss, Inc。
Cytogenetic information on chordomas is rudimentary and restricted to GTG-banding analysis of 26 cases worldwide. In this study, we present the chromosomal imbalances detected in a series of 16 chordomas (10 sacrococcyeal, five sphenooccipital, and one spinal) from 13 patients using comparative genomic hybridization (CGH) and fluorescence in situ hybridization (FISH). On average, 3.2 losses and 4.2 gains were detected per tumor. The most common DNA copy number alterations were losses on chromosomal arms 3p (50%) and 1p (44%). Losses of 3p were detected in five of seven primary chordomas. Therefore, the loss of 3p might be an early event in chordoma genesis. The most common gains involved 7q (69%), 20 (50%), 5q (38%), and 12q (38%). Additionally, we raised the first human chordoma cell line, U-CH I, from a recurrence of a sacral chordoma. U-CH I and its parent tumor had almost the same CGH profile. According to GTG-banding and multicolor FISH, U-CH I has the following clonal chromosomal abnormalities: der(1)t(1;22), del(4), +del(5), +del(6), +7, del(9), del(10), +der(20)t(10;20), +21. Thus, the novel permanent human chordoma cell line U-CH I has chordoma-typical cytogenetic aberrations. Our data suggest that tumor suppressor genes or mismatch repair genes (located at 1p31 and 3p14) and oncogenes (located in 7q36) might be involved in chordoma genesis. (C) 2001 Wiley-Liss, Inc.