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Introduction <p>Multiple studies suggest a link between ankylosing spondylitis (AS) and endometrial cancer (EC), but causality is uncertain.</p> Method <p>We used genome-wide association studies (GWAS) data in a Mendelian randomization analysis, primarily inverse variance weighting, to investigate if genetically determined AS affects EC risk, with sensitivity analyses for heterogeneity and pleiotropy.</p> Results <p>The IVW results showed a possible causal association between AS and EC (non-endometrioid histology) (OR = 1.05, 95% CI 1.01–1.1, P = 0.02), while there was no significant association between AS and the risks of EC (endometrioid histology) (OR = 0.99, 95% CI  0.97–1.01, P = 0.35) with EC (OR = 0.99, 95% CI 0.98–1.01, P = 0.34). The analysis results of MR Egger, weighted median, simple mode and weighted mode for AS and EC (non-endometrioid histology) were insignificant. No statistically significant heterogeneity or horizontal pleiotropy was detected.</p> Conclusions <p>This MR analysis did not reveal a substantial association between AS and overall EC or EC of endometrioid histology. Conversely, a significant causal connection between AS and non-endometrioid histology EC was identified. Additional research to are needed to explore the mechanisms of the relationship between AS and EC with the non-endometrioid subtype.</p>

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The causal association between ankylosing spondylitis and endometrial cancer: a two-sample mendelian randomization study

  • 期刊论文

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  • 发表日期：

    2025年4月30日

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  • Yanpin Gu,
  • Yupei Shao

摘要

Introduction

Multiple studies suggest a link between ankylosing spondylitis (AS) and endometrial cancer (EC), but causality is uncertain.

Method

We used genome-wide association studies (GWAS) data in a Mendelian randomization analysis, primarily inverse variance weighting, to investigate if genetically determined AS affects EC risk, with sensitivity analyses for heterogeneity and pleiotropy.

Results

The IVW results showed a possible causal association between AS and EC (non-endometrioid histology) (OR = 1.05, 95% CI 1.01–1.1, P = 0.02), while there was no significant association between AS and the risks of EC (endometrioid histology) (OR = 0.99, 95% CI  0.97–1.01, P = 0.35) with EC (OR = 0.99, 95% CI 0.98–1.01, P = 0.34). The analysis results of MR Egger, weighted median, simple mode and weighted mode for AS and EC (non-endometrioid histology) were insignificant. No statistically significant heterogeneity or horizontal pleiotropy was detected.

Conclusions

This MR analysis did not reveal a substantial association between AS and overall EC or EC of endometrioid histology. Conversely, a significant causal connection between AS and non-endometrioid histology EC was identified. Additional research to are needed to explore the mechanisms of the relationship between AS and EC with the non-endometrioid subtype.