Analysis of the differences in structural chromosomal aberrations of the gastric mucosa between H. pylori positive and negative gastric cancer patients: involvement of H. pylori in the onset of gastric cancer and examination of the mechanism in gastric carcinogenesis following H. pylori eradication.

Gene mutations are essential to carcinogenesis. If an evident difference is observed in gastric mucosal chromosomal structure aberrations between H. pylori (Hp)-negative and Hp-positive gastric cancer patients, it may be interpreted as suggesting the involvement of Hp in gene mutations. This study was undertaken to compare chromosomal structural aberrations between Hp-negative and Hp-positive gastric cancer patients and to evaluate the effects of Hp eradication on chromosomal structures in clinical cases. The subjects of this study were 40 patients with gastric cancer divided into four groups: Group A was composed of 12 patients with Hp-negative gastric cancer (well-differentiated gastric cancer in 5 cases and poorly-differentiated in 7 cases), Group B of 8 patients with Hp-negative gastric cancer following Hp eradication (well-differentiated in 4 case and poorly-differentiated in 4 cases), Group C of 13 patients with Hp-positive gastric cancer (well-differentiated in 7 cases and poorly-differentiated in 6 cases) and Group D of 7 patients with gastric cancer (well-differentiated in 5 cases and poorly-differentiated in 2 cases) undergoing Hp eradication at subtotal gastrectomy. In each of the groups A, B and C, the structural chromosomal aberration such as loss of heterozygosity (LOH) and microsatellite instability (MSI) was analyzed. In Group D, changes in structural chromosomal aberrations after Hp eradication as compared to the pre-eradication structures were also analyzed. LOH and MSI were examined by PCR, using DNA extracted from the cancer-affected and intact gastric mucosal tissue specimens from each patient. In A, B and C groups, structural chromosomal aberrations were noted, and these aberrations tended to be more marked in cases of poorly-differentiated gastric cancer in each group. In terms of structural chromosomal aberrations, there was no marked difference between Group A and either Group B or C. Hp eradication resulted in no change in chromosomal structure as compared to the pre-eradication structure in Group D. These results suggest the possibility that Hp eradication does not affect chromosomal structures and Hp is involved in gastric carcinogenesis as an additive environmental factor rather than as a factor acting at the gene level.