DNA Copy Number Changes in Gastric Adenocarcinomas: High Resolution–Comparative Genomic Hybridization Study in Turkey

Background and Aims le genetic alterations are responsible for development and progression of gastric cancer which is one of the leading causes of cancer-related deaths worldwide. The aim of this study was to identify the genomic imbalances of gains and/or losses in gastric adenocarcinomas from Turkish patients and to investigate their association with development and progression of this type of cancer. s three patients with gastric adenocarcinoma were enrolled in this study and genomic imbalances were analyzed by high-resolution–comparative genomic hybridization (HR–CGH). s 43 cases (84%) of gastric adenocarcinomas, genomic imbalances have involved all chromosomes in various combinations. The mean number of gains was 3.95 ± 4.19 and the most common gains observed were 7q (35%), 8q (35%), 7 p (28%), 1q (26%), 13q (26%), and 20q (21%). The calculated mean number of losses was 3.65 ± 3.55 and the most common losses were found on arms 18q (26%), 5q (21%), and 14q (21%). High-level amplifications involved chromosomes 1, 7, 8, 9, 13, and 16. No significant differences in chromosomal imbalances were observed in different tumor stages, tumor grades, and Helicobacter pylori infection status groups. The most striking result in this study was the involvement of the 13q gains with increased lymph node metastasis (p = 0.046). Late-stage tumors displayed a somewhat significantly higher number of losses than early-stage tumors (p = 0.053). sions es of gains, losses and amplifications concerned with gastric adenocarcinoma identified in this study are presented in detail. In particular, 13q21–q32 was prominent because it has been linked to increased lymph node metastasis.