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CagA status of Helicobacter pylori infection and p53 gene mutations in gastric adenocarcinoma.

We read with great interest the research findings of Dr Shibata et al. (1) regarding the association between p53 mutation and CagA Helicobacter pylori infection. The authors searched for p53 gene mutations by SSCP and, when necessary, by direct sequencing of DNA samples obtained from tumor specimens of patients with gastric adenocarcinoma. Helicobacter pylori infection and CagA status were investigated by ELISA for serum IgG antibodies. Undoubtedly, the use of sera obtained prior to cancer diagnosis greatly improves the sensitivity of H.pylori detection and CagA status investigation. However, it should be pointed out that the interval between serum collection and cancer diagnosis was extremely variable, from 2 years to more than three decades, which makes possible that some patients have already had premalignant lesions, such as atrophy, an adverse condition for H.pylori survival, when serum was obtained. The fact that some samples were drawn many years before carcinoma diagnosis increases the chance of acquiring infection with other H.pylori strains, including CagA ones. Also, it must be mentioned the possibility of changing the bacterium CagA status, what may be achieved by selective loss of parts of the cag pathogenicity island (2). It may be added that the combination of H.pylori– and CagA–/H. pylori groups for statistical analysis could lead to a biased result.