Original Article
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Sep 7, 2012; 18(33): 4522-4532
Published online Sep 7, 2012. doi: 10.3748/wjg.v18.i33.4522
Loss of fragile histidine triad and amplification of 1p36.22 and 11p15.5 in primary gastric adenocarcinomas
Yuan-Yuan Liu, Hai-Ying Chen, Man-Li Zhang, Dan Tian, Shibo Li, Ji-Yun Lee
Yuan-Yuan Liu, Man-Li Zhang, Dan Tian, Department of Internal Medicine, The First Teaching Hospital of Jilin University, Changchun 130021, Jilin Province, China
Hai-Ying Chen, Department of Infectious Diseases, The First Teaching Hospital of Jilin University, Changchun 130021, Jilin Province, China
Shibo Li, Ji-Yun Lee, Department of Pediatrics, The University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, United States
Ji-Yun Lee, Department of Pathology, College of Medicine, Korea University, Seoul 136-705, South Korea
Author contributions: Liu YY performed the data analysis; Chen HY performed the data collection; Zhang ML and Tian D collected the samples; Li S designed the study and provided financial support; Lee JY designed the study and wrote the manuscript.
Correspondence to: Ji-Yun Lee, PhD, Department of Pathology, College of Medicine, Korea University, 5-1 Anam-Dong, Seoungbuk-Gu, Seoul 136-705, South Korea. jiyun-lee@korea.ac.kr
Telephone: +82-2-9206141 Fax: +82-2-9533130
Received: December 19, 2011
Revised: February 1, 2012
Accepted: April 13, 2012
Published online: September 7, 2012
Abstract

AIM: To investigate the genomic copy number alterations that may harbor key driver genes in gastric tumorigenesis.

METHODS: 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.

RESULTS: 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.

CONCLUSION: 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.

Keywords: Array comparative genomic hybridization, Amplicon, Gastric adenocarcinoma, Oncogene, Fragile histidine triad