DNA Copy Number Changes in Gastric Adenocarcinomas: High Resolution–Comparative Genomic Hybridization Study in Turkey
Received 19 February 2009; accepted 25 June 2009.
Background and Aims
Multiple 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.
Methods
Forty three patients with gastric adenocarcinoma were enrolled in this study and genomic imbalances were analyzed by high-resolution–comparative genomic hybridization (HR–CGH).
Results
In 36/43 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%), 7p (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).
Conclusions
A series 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.
aDepartment of Medical Biology, Faculty of Medicine, Ankara University, Sihhiye, Ankara, Turkey
cDepartment of Biostatistics, Faculty of Medicine, Ankara University, Sihhiye, Ankara, Turkey
eDepartment of Medical Genetics, Faculty of Medicine, Ankara University, Sihhiye, Ankara, Turkey
bDepartment of Surgical Oncology, Faculty of Medicine, Ankara University, Cebeci, Ankara, Turkey
dDepartment of Molecular Biology, Faculty of Science, Ankara University, Tandogan, Ankara, Turkey
Address reprint requests to: Güvem Gümüs Akay, Department of Medical Biology, Faculty of Medicine, Ankara University, 06100 Sihhiye, Ankara, Turkey; Phone: (+90) (312) 3103010/402; FAX: (+90) (312) 3106370
ABSTRACT