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Development of Compendium for Esophageal Squamous Cell Carcinoma
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Gut Microbiome-Metabolite Interactions Contribute to Esophageal Cancer Risk: Evidence From Mendelian Randomization

He Yang1, Yi Liu2, Tianyu Zhu3

  • 1Department of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China, suda.edu.cn.

International Journal of Genomics
|June 10, 2026
PubMed
Summary

Gut microbiota (GM) causally influences esophageal cancer (EC) and esophageal adenocarcinoma (EAC). Circulating metabolites mediate these effects, suggesting new targets for microbiome-based therapies.

Keywords:
esophageal cancergut microbiotametabolitemultiomics

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Area of Science:

  • Genetics
  • Microbiology
  • Oncology

Background:

  • Emerging evidence links gut microbiota (GM) to esophageal cancer (EC) development.
  • The causal role of GM and the mediating function of metabolites in EC, particularly across subtypes like esophageal adenocarcinoma (EAC), require further elucidation.

Purpose of the Study:

  • To investigate the causal relationships between GM, circulating metabolites, and EC/EAC using a Mendelian randomization (MR) approach.
  • To determine if specific metabolites mediate the influence of GM on EC and EAC development.

Main Methods:

  • A two-sample Mendelian randomization (MR) framework was employed.
  • Inverse-variance weighted (IVW) method for primary analysis, complemented by other MR techniques and genetic risk score (GRS) validation.
  • Mediation analyses were conducted to assess the role of metabolites in the GM-EC/EAC axis.

Main Results:

  • Significant causal associations were found between 25 GM taxa and EC (11 risk-promoting, 14 protective) and 15 GM taxa and EAC (11 risk-promoting, 4 protective).
  • Five metabolites were linked to EC (2 risk, 3 protective) and six to EAC (5 risk, 1 protective).
  • Mediation analyses confirmed that metabolites partially mediate the GM effects on both EC and EAC.

Conclusions:

  • Genetic evidence supports a causal gut microbiota-metabolite-cancer axis in EC pathogenesis.
  • Circulating metabolites act as intermediaries linking GM to EC and EAC.
  • Findings suggest potential for novel biomarkers and microbiome-targeted interventions for EC and EAC.