Rugge M, Genta RM, Graham DY, Di Mario F, Vaz Coelho LG, Kim N, Malfertheiner P, Sugano K, Tsukanov V, Correa P. 

Gut. 2016 May;65(5):721-5. doi: 10.1136/gutjnl-2015-310846.



The biological, diagnostic and therapeutic panorama has dramatically changed in the 35 years since the publication of Morson's seminal paper. The discovery of H. pylori has revolutionised practice of gastroenterology and the script of Correa's oncogenic cascade has found its lead actor (figure 1). Lesions and conditions viewed as idiopathic in Morson's times are now known to be caused by H. pylori infection and have become curable. The recent interest in large, even nationwide H. pylori eradication programmes as a mean to eliminate gastric cancer will require implementation of this strategy at the population level and will have to be fully integrated into national healthcare priorities. The revised distinction between early and advanced precancerous lesions and the recognition that the extension of metaplastic atrophy is a reliable marker for gastric cancer risk have made possible more targeted and cost-effective surveillance strategies. These should be implemented using efficient delivery systems with a timely referral for positive test. Such measures, coupled with the wide availability of standardised treatment regimens based on clinical efficacy, side effects, simplicity, duration and cost, could make the near eradication of gastric cancer an achievable goal in many parts of the world.