Loss of fragile histidine triad and amplification of 1p36.22 and 11p15.5 in primary gastric adenocarcinomas

放大器 生物 比较基因组杂交 遗传学 癌变 癌症 基因 癌症研究 基因组 聚合酶链反应
作者
Yuan Yuan Liu,Hai-Ying Chen,Man Li Zhang,Dan Tian,Shibo Li,Ji Yun Lee
出处
期刊:World Journal of Gastroenterology [Baishideng Publishing Group]
卷期号:18 (33): 4522-4522 被引量:8
标识
DOI:10.3748/wjg.v18.i33.4522
摘要

To investigate the genomic copy number alterations that may harbor key driver genes in gastric tumorigenesis.Using high-resolution array comparative genomic hybridization (CGH), we investigated the genomic alterations of 20 advanced primary gastric adenocarcinomas (seventeen tubular and three mucinous) of Chinese patients from the Jilin province. Ten matching adjacent normal regions from the same patients were also studied.The most frequent imbalances detected in these cancer samples were gains of 3q26.31-q27.2, 5p, 8q, 11p, 18p, 19q and 20q and losses of 3p, 4p, 18q and 21q. The use of high-resolution array CGH increased the resolution and sensitivity of the observed genomic changes and identified focal genetic imbalances, which included 54 gains and 16 losses that were smaller than 1 Mb in size. The most interesting focal imbalances were the intergenic loss/homozygous deletion of the fragile histidine triad gene and the amplicons 11q13, 18q11.2 and 19q12, as well as the novel amplicons 1p36.22 and 11p15.5.These regions, especially the focal amplicons, may harbor key driver genes that will serve as biomarkers for either the diagnosis or the prognosis of gastric cancer, and therefore, a large-scale investigation is recommended.
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