BACKGROUND/AIMS: cagA gene might be implicated in the carcinogenesis of gastric adenocarcinoma. We studied the cagA status of Helicobacter pylori (H. pylori) isolates from the patients with gastric cancer and benign gastroduodenal diseases to investigate the mosaicism in cagA gene and its role in the carcinogenesis. METHODS: cagA status was determined by polymerase chain reaction (PCR) using 3 different primer sets for cagA gene. The first cagA primer set amplified a 1318 bp fragment from the N-terminal (nucleotide 1059-2377). The second primer set and the third primer set amplified a 297 bp fragment (nucleotide 2288-2585) and a 1518 bp fragment (nucleotide 3086-4604) from the C-terminal of cagA gene, respectively. Western blot analysis was also performed for CagA protein. RESULTS: The expected 297 bp PCR amplicons for cagA gene was identified in most of all H. pylori strains, and this fraction was not related with gastric cancer. The 1318 bp fragment amplified by the PCR was found in 90.3% (28/31 cases) of gastric cancer, 51.7% (15/29 cases) of gastric ulcer, 50.0% (17/34 cases) of duodenal ulcer, and only in 8.3% (3/36 cases) of gastritis. The 1518 bp PCR amplicon was only in 1.5% (2/130 cases) of all cases. The size of CagA protein in cagA positive strains was almost similar. CONCLUSIONS: It is suggested that mosaicism in cagA may exist and particularly, the distinct cagA gene fragment associated with gastric cancer may exist.