The emerging role of non-Helicobacter pylori microbiome in gastric carcinogenesis: a comprehensive review of pathogenic mechanisms and clinical implications.

Gastric cancer remains a leading global health concern, with its etiology shaped by complex interactions between the host and its microbiome. The primary etiological role of Helicobacter pylori (H.pylori) has been well-established, but recent research has pointed to the significant contributions of non-H.pylori pathogens in the onset and progression of gastric cancer. These pathogens contribute to gastric tumorigenesis by directly compromising the gastric epithelial barrier and invading gastric epithelial cells, affecting long-range processes, disrupting microbial balance, and influencing the host's immune microenvironment. In the following, we comprehensively elucidated the potential mechanisms by which Streptococcus anginosus, Methylobacterium, Prevotella, Candida albicans, and Epstein-Barr virus actively participate in gastric tumorigenesis. Beyond this, ongoing investigations seek to identify additional microorganisms that may contribute to gastric cancer development, offering new insights into the multifactorial nature of the disease. Collectively, these findings highlight the critical involvement of diverse non-H.pylori microorganisms at various stages of gastric cancer progression, advancing our understanding of microbe-driven carcinogenesis.