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Tumor tissue samples were obtained from each of ten patients with stomach cancer who had undergone surgery. The simultaneous detection of signals from 17 alpha pericentromeric and 17 p 13.1 loci after hybridization with the appropriate probes was carried out on 100-200 tumor cells in each case. The copy number category (i.e., monosomy, disomy, trisomy, and so on) was defined as described by Waldman et al., and the deletion of a gene of interest was defined as described by Matsumura et al. The copy number category was monosomic in seven and disomic in three out of ten cases. The frequency of the copy number 2 (two centromeric signals per nucleus) was lower in tumor cells than in control cells that comprise normal gastric epithelium cells and cells from a normal fibroblast cell line. The copy numbers 3, 4, 5, and above (polysomy) were more frequent in tumor cells, whereas no normal cells having three or more centromeric signals per nucleus was present in the control. Incidence of p 53 gene deletion in ten patients ranged from 55.4% to 90.0%, and from 1.5% to 30.7% if nuclei having three or more copy numbers were taken into consideration. The mean incidence of the p 53 deletion was significantly higher in the differentiated type than in the undifferentiated type of carcinoma (p &lt; 0.02). Various types in the combination pattern of 17 alpha centromere/17 p 13.1 signals were observed, and the most frequent pattern in the ten cases was a combination of 1/1. The deletion of chromosome 17 p may play an important role in carcinogenesis of the stomach.

Chromosome 17 copy numbers and incidence of p53 gene deletion in gastric cancer cells. Dual color fluorescence in situ hybridization analysis.