AIM: To determine, by counting sister chromatid exchange (SCE) frequencies, whether genetic impairment and DNA damage have an effect on the pathogenesis of gastric cancer (GC). METHODS: Analysis of SCE is a cytogenetic technique used to show DNA damage as a result of an exchange of DNA fragments between sister chromatids. We analyzed SCE frequency in 24 patients with GC, 26 patients with chronic atrophic gastritis (CAG), and 15 normal controls. The presence of H pylori was confirmed by urease test, toluidine-blue stain and hematoxylin-eosin stain. RESULTS: SCE was significantly increased in H pylori- negative GC patients, and in H pylori-negative CAG patients compared with controls (7.41 ± 1.36 and 6.92 ± 1.20, respectively, vs 5.54 ± 0.8, P < 0.001). There was no difference in the SCE frequency between H pylori- negative GC patients and H pylori-negative CAG patients (P > 0.05). On other hand, the SCE frequencies in H pylori-positive GC patients were higher than those in H pylori-positive CAG patients (9.20 ± 0.94 vs 7.93 ± 0.81, P < 0.01). Furthermore, H pylori-positive GC patients had a higher SCE frequency than H pylori- negative GC patients (9.20 ± 0.94 vs 7.41 ± 1.36, P < 0.001). Similarly, a significant difference was detected between H pylori-positive CAG patients and H pylori-negative CAG patients (7.93 ± 0.81 vs 6.92 ± 1.20, P < 0.05). CONCLUSION: We suggest the increased SCE in patients reflects a genomic instability that may be operative in gastric carcinogenesis. AIM: To determine, by counting sister chromatid exchange (SCE) frequencies, whether genetic impairment and DNA damage have an effect on the pathogenesis of gastric cancer (GC). METHODS: Analysis of SCE is a cytogenetic technique used to show DNA damage as a The results of an exchange of DNA fragments between sister chromatids. We analyzed SCE frequency in 24 patients with GC, 26 patients with chronic atrophic gastritis (CAG), and 15 normal controls. The presence of H pylori was confirmed by urease test, toluidine-blue stain and hematoxylin-eosin stain. RESULTS: SCE was significantly increased in H pylori-negative GC patients, and in H pylori-negative CAG patients compared with controls (7.41 ± 1.36 and 6.92 ± 1.20, respectively, vs 5.54 ± 0.8, P < 0.001). There was no difference in the SCE frequencies between H pylori-negative GC patients and H pylori-negative CAG patients (P> 0.05). On other hand, the SCE frequencies in H pylori-positive GC patients were higher than those in H pylori-p H pylori-positive GC patients had a higher SCE frequency than H pylori-negative GC patients (9.20 ± 0.94 vs. 7.41 ± 1.36, P <0.001) . Similarly, a significant difference was detected between H pylori-positive CAG patients and H pylori-negative CAG patients (7.93 ± 0.81 vs 6.92 ± 1.20, P <0.05). CONCLUSION: We suggest the increased SCE in patients reflects a genomic instability that may be operative in gastric carcinogenesis.