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Genomic alterations in primary gastric cancers analyzed by comparative genomic hybridization and clinicopathological
M Nakanishi1, C Sakakura, Y Fujita
1Department of Hygiene, Kyoto Prefetural University of Medicine, Japan. nakanishi@1surg.kpu-m.ac.jp
Background/Aims:
Genetic changes during the oncogenesis and progression of gastric cancer remain unclear. The aim of our study was to analyze chromosomal aberrations in primary gastric cancers.
Methodology:
Using comparative genomic hybridization, we screened 47 primary gastric cancers for changes in the number of copies of DNA sequences.
Results:
Gains of chromosome arms 20q (55%), 20p (36%), 17q (32%), 19q (30%) and 16p (30%), and losses of chromosome arms 4q (40%), 17p (40%), 5q (38%), 18q (30%) and 4p (28%) were detected most frequently. In addition, a high level of amplification was observed at 3q21 (2%), 6p21 (4%), 7q31 (6%), 8q23-24 (2%), 19q12-13 (2%), and 20q13 (2%). Among these alterations, the gain of 20q was the most frequent change. We then compared these changes with clinicopathological factors and identified signet ring cell carcinomas in 6 cases. Our study demonstrated no amplification of chromosome 20q in signet ring cell carcinoma in contrast to that in the other histologic types of gastric cancer.
Conclusions:
Our findings may be related to the morphologic and clinical features of signet ring cell carcinoma, and several oncogenes mapped on 20q may play an important role as determinants of the clinical and histologic features of gastric cancer.