Giuliani et al provide incremental information suggesting that HP infection is an integral factor in the development of GCPLs and, maybe, subsequent gastric cancer. This association was present regardless of whether the indication for gastric resection was ulcer disease or gastric cancer. Thus, the mere presence of a mucosal field defect in patients who underwent resection for cancer cannot explain the propensity toward malignant transformation. Although the data suggest that patients with HP infection are indeed at risk for the development of premalignant lesions, it is also clearly evident that HP-negative patients were at significant risk of GCPLs and thus, likely, gastric cancer. Hence, the development of gastric cancer does not necessarily follow the sequential progression of HP infection, chronic inflammation, GCPL development, and, finally, gastric cancer. Therefore, if a field defect does not explain cancer development and the presence of HP infection is not solely explanatory, what are the key elements of gastric cancer development in this setting? Perhaps chronic inflammation is the common denominator. Although the associations identified by the authors are helpful, simple treatment for HP infection and/or a surveillance program clearly will not eliminate the development of gastric cancer in the remnant stomach. As the authors point out, the investigative community must perform more in-depth studies to identify not only clinical associations but also mechanistic causality through rigorous basic science studies. In recent years, the surgical community has gravitated toward important but limited clinical studies to identify clinical associations of disease development. This study highlights the potential benefits derived from such clinical work but also is a clear reminder that, as a surgical investigative community, we must perform hypothesis-driven basic science that seeks further understanding of the underlying mechanisms of cancer development and the role of HP infection and chronic inflammation.
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