High level amplification of 1p32-33 and 2p22-24 in small cell lung carcinomas.
High level amplification of 1p32-33 and 2p22-24 in small cell lung carcinomas.
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DOI：
10.3892/ijo.19.3.451
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发表时间：
2001-09
影响因子：
5.2
通讯作者：
W. Lui;D. Tanenbaum;Catharina Larsson
中科院分区：
文献类型：
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作者：
W. Lui;D. Tanenbaum;Catharina Larsson
小细胞肺癌（SCLC）是一种常见的高度侵袭性肿瘤，临床预后通常较差。为了探讨肿瘤进展背后的遗传机制，使用比较基因组杂交（CGH）进行DNA拷贝数改变的一般筛选。在分析的23例病例系列中，经常检测到CGH改变，在个体肿瘤中的异常范围为9至22个。染色体臂3 p（23/23）、13 q14 -21（23/23）、4p（20/23）、4 q（20/23）和2 q22 -24（18/23）的丢失率最高，而染色体臂19 p（18/23）、19 q（17/23）、1 p31 -35（15/23）、17 q22 -25（11/23）和5 p14 -15.3（9/23）。此外，在3例和2例病例中分别发现染色体臂1 p32 -33和2 p22 -24的高水平扩增。用于这些扩增的候选基因包括I-MYC（1 p32）和n-MYC（2p24.1）癌基因，其先前已被发现在SCLC中过表达。综上所述，研究结果表明SCLC中存在高水平的染色体不稳定性，这与该肿瘤类型的高度恶性表型非常一致。描绘了参与获得和丢失的亚染色体区域，并证明了1 p32 -33和2 p22 -24的扩增，从而为准确表征参与SCLC肿瘤进展的分子事件提供了起点。
Small cell lung cancer (SCLC) is a frequently occurring, highly aggressive tumor with a generally poor clinical outcome. In order to approach the genetic mechanisms behind the tumor progression, a general screen for DNA copy number alterations was performed using comparative genomic hybridization (CGH). In the series of 23 cases analyzed, CGH alterations were frequently detected ranging from 9 to 22 abnormalities in the individual tumors. The most frequent losses were detected on chromosome arms 3p (23/23), 13q14-21 (23/23), 4p (20/23), 4q (20/23), and 2q22-24 (18/23), while gains preferentially involved chromosome arms 19p (18/23), 19q (17/23), 1p31-35 (15/23), 17q22-25 (11/23), and 5p14-15.3 (9/23). In addition, high level amplification at chromosome arms 1p32-33 and 2p22-24 were found in three and two cases, respectively. Candidate genes for these amplifications include the l-MYC (1p32) and n-MYC (2p24.1) oncogenes, which have been previously found to be overexpressed in SCLC. Taken together, the findings demonstrate a high level of chromosomal instability in SCLC, which is well in agreement with the highly malignant phenotype of this tumor type. Subchromosomal regions involved in gains and losses were delineated and the amplifications of 1p32-33 and 2p22-24 were demonstrated, thus providing starting points for the exact characterization of molecular events involved in SCLC tumor progression.