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Updated: Jun 28, 2025

Cigarette Smoke Exposure in Mice using a Whole-Body Inhalation System
Published on: October 22, 2020
Effect of smoking-related features and 731 immune cell phenotypes on esophageal cancer: a two-sample and mediated
Kaiqi Yang1, Shaoya Li1, Yuchen Ding1
1Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, Beijing Key Laboratory for Precancerous Lesion of Digestive Disease, Beijing, China.
Smoking increases esophageal cancer risk, with specific immune cells like CD62L plasmacytoid dendritic cells and CD27 in CD20-CD38-B cells potentially mediating this effect. Never smoking is protective against esophageal cancer.
Area of Science:
- Oncology
- Immunology
- Genetics
Background:
- Observational studies link smoking to esophageal cancer.
- Causal mechanisms and immune mediators require further investigation.
Purpose of the Study:
- To validate the causal link between smoking traits and esophageal cancer.
- To explore immune cell phenotypes as potential mediators.
Main Methods:
- Bidirectional univariate Mendelian Randomization (MR) analyses.
- Two-step MR and coefficient product method for mediation analysis.
- Sensitivity analyses for reliability.
Main Results:
- Never smoking showed a protective effect (OR=0.10, p=1.82e-05).
- Ever smoking and current smoking promoted esophageal cancer (OR=4.31, p=1.49e-02).
- Two immune phenotypes (CD62L plasmacytoid dendritic cells, CD27 in CD20-CD38-B cells) showed mediating effects.
Conclusions:
- Establishes a causal relationship between smoking and esophageal cancer.
- Identifies specific immune factors potentially mediating this relationship.
- Further clinical studies are recommended.
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