Oral-to-Gut Bacterial Migration Identified as Primary Driver and Diagnostic Marker for Early Gastric Cancer

BGI Genomics identifies oral-to-gut bacterial migration as a driver of gastric cancer. New saliva-based markers show 87% accuracy in early detection.

By: AXL Media

Published: Apr 21, 2026, 4:42 AM EDT

Source: Information for this report was sourced from BGI Genomics

The Discovery of the Oral-Gut Translocation Pathway

Recent metagenomic research has uncovered a definitive link between the oral microbiome and the development of gastric cancer. By analyzing 404 samples using high-precision sequencing, a team led by BGI Genomics and academician Fang Jingyuan identified 28 bacterial species that differ significantly in patients with malignancy. Of these, 20 species typically found in the mouth were found thriving in the gut of cancer patients. Using strain-level genetic analysis (popANI), the researchers confirmed that these oral and gut strains shared over 99.9% genetic similarity, providing irrefutable evidence that bacteria are migrating from the oral cavity to colonize the stomach and intestines.

Metabolic Mechanisms of Tumor Promotion

Once these oral lactic acid bacteria (LAB) reach the gut, they form a resilient co-abundance network capable of surviving harsh gastric acids and bile salts. This microbial consortium triggers a metabolic shift characterized by increased lactic acid fermentation, which significantly acidifies the tumor microenvironment. This localized acidification serves as a catalyst for oncogenic pathways, activating matrix metalloproteinases that facilitate tissue remodeling, tumor invasion, and the growth of new blood vessels. Furthermore, this acidic sanctuary recruits immunosuppressive cells, allowing the developing tumor to effectively evade the host’s natural immune response.

A New "Initiator-Promoter" Model for Carcinogenesis

The findings have led to a revised framework for understanding gastric cancer development. In this "initiator-promoter" model, Helicobacter pylori (Hp) acts as the initiator by causing chronic inflammation and compromising the stomach’s protective mucosal barrier. Once the epithelium is weakened, oral lactic acid bacteria step in as promoters, colonizing the damaged tissue and fueling disease progression through biofilm formation and immune modulation. This paradigm explains why gastric cancer can still develop in Hp-negative patients or in individuals where the primary infection has been successfully eradicated.