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Updated: Sep 17, 2025
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Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
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Causal relationship between infection and gastrointestinal cancers: a multivariable Mendelian randomization study
Ruopeng Zhang1, Yinghe Li2, Yuqian Huang2
1Department of Gastric Surgery, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Guangzhou, China.
Chinese Clinical Oncology
|June 27, 2025
Summary
This study investigated infections and gastrointestinal cancers using Mendelian randomization. Certain infections, like Epstein-Barr virus (EBV) and H. pylori antibodies, appear protective against these cancers in European populations.
Area of Science:
- Genetics and Epidemiology
- Infectious Diseases and Oncology
Background:
- While associations between infections and gastrointestinal cancers (GICs) are known, direct causal links remain unclear.
- Investigating the role of specific pathogens in GIC development is crucial for understanding cancer etiology.
Purpose of the Study:
- To determine the causal relationship between genetically predicted infections and the risk of gastrointestinal cancers.
- To explore the protective or pathogenic roles of common infectious agents in GIC development.
Main Methods:
- Multivariable Mendelian randomization (MR) analyses were employed.
- Instrumental variables for pathogens like Helicobacter pylori (H. pylori), human papillomavirus (HPV), and herpesviruses were derived from GWAS.
- Summary statistics for GICs in European populations were analyzed using inverse-variance weighted MR and sensitivity analyses.
Main Results:
- No causal link was found between H. pylori infection and gastric cancer (GC) in European ancestry.
- Epstein-Barr virus (EBV) seropositivity and antibody levels showed a negative correlation with GC risk.
- Herpes simplex virus (HSV) infection and H. pylori GroEL antibodies were negatively correlated with colon and colorectal cancer risks, respectively.
Conclusions:
- Infectious pathogens exhibit diverse roles and geographical distribution patterns in relation to GICs.
- Human-pathogen co-evolution appears to influence cancer risk, suggesting complex interactions.
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