Comment on "Helicobacter pylori infection may improve the survival of patients with carcinomas".

Wei Tang Department of Surgery, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan In this short correspondence, the authors hypothesized Helicobacter pylori infection may promote the development of immune response and thus improve survival rates of patients who have received complete resection of their tumors [1]. The authors based their hypothesis on the fact that patients with Helicobacter pylori infection had a high level of cytokine production. However, before considering it as one potential strategy for tumor therapy, we thought some issues need to be discussed. Firstly, the Helicobacter pylori is a class I carcinogen and is associated with increased risk of gastric cancer while bacterial eradication substantially decreases incidence of gastric cancer [2]. If Helicobacter pylori conduce to outgrowth of gastric cancer which may represent the failure of immune surveillance but trigger an effective anti-tumor immunity which might improve the prognosis after the tumor resection, what might be the underlying mechanism responsible for this conversion? Secondly, even though the cytokines may promote immune response, the negative effect of Helicobacter pylori product on anti-tumor immunity [3] should not be neglected. Lastly, as for the production of cytokines, cytokine gene polymorphisms directly influence interindividual variation in the magnitude of cytokine response, and this clearly contributes to an individual’s ultimate clinical outcome (duodenal ulcer phenotype, gastritis phenotype, or gastric cancer phenotype) [4]. If the cytokine imbalance might be responsible for disease progression and may decide about the disease outcome after Helicobacter pylori infection, whether it had effect on the intensity of anti-tumor immunity and the prognosis of gastric cancer after tumor resection? In fact, we speculate that it is difficult to evaluate the impact of Helicobacter pylori infection on