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

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