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首页> 外文期刊>Cellular Oncology: Analytical Cellular Pathology >Genomic Alterations in Primary Gastric Adenocarcinomas Correlate with Clinicopathological Characteristics and Survival
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Genomic Alterations in Primary Gastric Adenocarcinomas Correlate with Clinicopathological Characteristics and Survival

机译：原发性胃腺癌的基因组改变与临床病理特征和生存率相关。

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Background & aims: Pathogenesis of gastric cancer is driven by an accumulation of genetic changes that to a large extent occur at the chromosomal level. In order to investigate the patterns of chromosomal aberrations in gastric carcinomas, we performed genome‐wide microarray based comparative genomic hybridisation (microarray CGH). With this recently developed technique chromosomal aberrations can be studied with high resolution and sensitivity.Methods: Array CGH was applied to a series of 35 gastric adenocarcinomas using a genome‐wide scanning array with 2275 BAC and P1 clones spotted in triplicate. Each clone contains at least one STS for linkage to the sequence of the human genome. These arrays provide an average resolution of 1.4 Mb across the genome. DNA copy number changes were correlated with clinicopathological tumour characteristics as well as survival.Results: All thirty‐five cancers showed chromosomal aberrations and 16 of the 35 tumours showed one or more amplifications. The most frequent aberrations are gains of 8q24.2, 8q24.1, 20q13.12, 20q13.2, 7p11.2, 1q32.3, 8p23.1–p23.3, losses of 5q14.1, 18q22.1, 19p13.12–p13.3, 9p21.3–p24.3, 17p13.1–p13.3, 13q31.1, 16q22.1, 21q21.3, and amplifications of 7q21–q22, and 12q14.1–q21.1. These aberrations were correlated to clinicopathological characteristics and survival. Gain of 1q32.3 was significantly correlated with lymph node status (p=0.007). Tumours with loss of 18q22.1, as well as tumours with amplifications were associated with poor survival (p=0.02, both).Conclusions: Microarray CGH has revealed several chromosomal regions that have not been described before in gastric cancer at this frequency and resolution, such as amplification of at 7q21–q22 and 12q14.1–q21.1, as well gains at 1q32.3, 7p11.2, and losses at 13q13.1. Interestingly, gain of 1q32.3 and loss of 18q22.1 are associated with a bad prognosis indicating that these regions could harbour gene(s) that may determine aggressive tumour behaviour and poor clinical outcome.
机译：背景与目的：胃癌的发病机制是由在染色体水平上大量发生的遗传变化积累所驱动。为了研究胃癌中染色体畸变的模式，我们进行了基于全基因组微阵列的比较基因组杂交（微阵列CGH）。使用这项新近开发的技术，可以高分辨率和高灵敏度地研究染色体畸变。方法：使用全基因组扫描阵列，将阵列CGH应用于一系列35例胃腺癌，这些阵列具有一式三份的2275个BAC和P1克隆。每个克隆包含至少一个用于连接人类基因组序列的STS。这些阵列在整个基因组中的平均分辨率为1.4 Mb。 DNA拷贝数的变化与临床病理特征以及生存率相关。结果：所有35例癌症均显示染色体畸变，而35例肿瘤中有16例显示一种或多种扩增。最常见的像差是增益8q24.2、8q24.1、20q13.12、20q13.2、7p11.2、1q32.3、8p23.1–p23.3，损耗5q14.1、18q22.1、19p13 .12–p13.3、9p21.3–p24.3、17p13.1–p13.3、13q31.1、16q22.1、21q21.3，以及7q21–q22和12q14.1–q21.1的放大倍数。这些畸变与临床病理特征和生存率相关。 1q32.3的增益与淋巴结状态显着相关（p = 0.007）。丢失18q22.1的肿瘤以及扩增的肿瘤与较差的生存率相关（两者均为p = 0.02）。结论：微阵列CGH在此频率和分辨率下已揭示了胃癌中以前未描述的几个染色体区域。 ，例如在7q21–q22和12q14.1–q21.1处放大，以及1q32.3、7p11.2处的增益和13q13.1处的损耗。有趣的是，1q32.3的增加和18q22.1的减少与不良预后相关，表明这些区域可能带有可能决定侵袭性肿瘤行为和不良临床预后的基因。

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