Amplification of DNA sequences from chromosome 19q13.1 in human pancreatic cell lines
Amplification of DNA sequences from chromosome 19q13.1 in human pancreatic cell lines
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DOI：
10.1006/geno.1998.5405
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发表时间：
1998-10-01
期刊：
影响因子：
4.4
通讯作者：
Muleris, M
中科院分区：
文献类型：
--
作者：
Curtis, LJ;Li, Y;Muleris, M
利用传统细胞遗传学和比较基因组杂交 (CGH) 来鉴定 12 种胰腺腺癌细胞系中反复出现的染色体失衡。在所有细胞系中都观察到了多个缺失和增加。常见影响染色体或染色体臂 9p、13、18q、8p、4 和 10p 的丢失以及涉及染色体臂或条带 19q13.1、20q、5p、7p、11q、3q25-qter、8q24 和 10q 的增益。有趣的是，CGH 发现了 19 个不同的高水平扩增位点。复发部位涉及19q13.1（6例）、5p（3例）、12p和16p（2例）。 KRAS2 的扩增在 2 个细胞系中得到证实，ERBB2 在另一个细胞系中得到扩增。为了进一步确定 19 号染色体扩增的发生，利用 NotI 基因组限制性消化的二维分析以及使用来自条带 19q13.1 的探针进行荧光原位杂交。 3 种细胞系中显示出 19 号染色体 NotI 片段重叠组的高水平扩增，其中 2 种显示 OZF 和 AKT2 基因均扩增，1 种仅显示 AKT2 扩增。在这 3 个细胞系中，19 号染色体序列的扩增与同质染色区域的存在相关。我们的结果提供了 19 号染色体扩增程度的异质性证据，并表明存在可能在胰腺癌发生中发挥作用的未知扩增基因。 (C) 1998 年学术出版社。
Conventional cytogenetics and comparative genomic hybridization (CGH) were utilized to identify recurrent chromosomal imbalances in 12 pancreatic adenocarcinoma cell lines. Multiple deletions and gains were observed in all cell lines. Losses affecting chromosomes or chromosome arms 9p, 13, 18q, 8p, 4, and 10p and gains involving chromosome arms or bands 19q13.1, 20q, 5p, 7p, 11q, 3q25-qter, 8q24, and 10q were commonly observed. Interestingly, 19 distinct sites of high-level amplification were found by CGH. Recurrent sites involved 19q13.1 (6 cases), 5p (3 cases), and 12p and 16p (2 cases). Amplification of KRAS2 was demonstrated in 2 cell lines and that of ERBB2 in another. To define the occurrence of chromosome 19 amplification further, two-dimensional analysis of NotI genomic restriction digests and fluorescence in situ hybridization using probes from band 19q13.1 were utilized. High-level amplification of overlapping sets of chromosome 19 NotI fragments was exhibited in 3 cell lines of which 2 showed amplification of both OZF and AKT2 genes and 1 that of AKT2 alone. In these 3 cell lines, amplification of chromosome 19 sequences was associated with the presence of a homogeneously staining region, Our results provide evidence of heterogeneity in. the extent of chromosome 19 amplification and suggest the existence of yet unknown amplified genes that may play a role in pancreatic carcinogenesis. (C) 1998 Academic Press.