The Association Between Chronic Helicobacter pylori Infection and the Risk of Gastric Cancer: A Review of Evidence

Abstract

Introduction: In the early 21st century, gastric cancer remained a significant cause of cancer-related mortality globally. During this period, research focus intensified on the role of infectious agents in carcinogenesis, with the bacterium Helicobacter pylori emerging as the primary suspect in the etiology of gastric adenocarcinoma. This review synthesises the pivotal scientific literature published that solidified the causal link between chronic H. pylori infection and the development of gastric cancer.

Literature Review: Large-scale prospective studies published in this decade provided definitive evidence that chronic H. pylori infection was the single most important risk factor for non-cardia gastric cancer. The pathogenic mechanism was elucidated through the Correa cascade, a multi-step pathway of histologic progression from chronic gastritis to atrophy, intestinal metaplasia, dysplasia, and finally carcinoma, with H. pylori acting as the principal trigger. Research identified specific bacterial virulence factors, most notably the oncoprotein CagA, that significantly increase cancer risk by disrupting host cell signaling pathways. Furthermore, landmark intervention trials provided crucial evidence that eradicating the infection could prevent or slow the progression of pre-cancerous lesions, establishing a proof-of-concept for gastric cancer prevention through antimicrobial therapy.

Conclusion: The body of evidence from 2000-2010 transformed the understanding of gastric cancer from an idiopathic disease to an infectious-disease-driven malignancy. H. pylori was unequivocally confirmed as the causative agent, paving the way for primary prevention strategies based on its detection and eradication.