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Background <p>Cervical cancer remains a significant global health concern, with immune system regulation potentially playing a crucial role in disease development. This study investigates potential causal relationships between genetic variants associated with immune cell populations and cervical cancer risk.</p> Methods <p>We employed multiple Mendelian randomization (MR) approaches inverse-variance weighted, MR-Egger, simple median, and weighted median methods to evaluate genetic instrumental variables linked to various T-cell and B-cell subtypes. Differential gene expression was analyzed using single-cell RNA sequencing, while forest plots, scatter plots, and funnel plots facilitated comprehensive MR analysis.</p> Results <p>Forest plots consistently demonstrated odds ratios clustered tightly around 1.000 (range: 0.998–1.001), despite some variants reaching statistical significance (p &lt; 0.05). MR analysis of CD69 + LGALS3A + regulatory T-cells, CD8 + T-cell populations, and CD20 + B-cells revealed only weak associations with cervical cancer susceptibility. Comparative analysis across different MR methodologies produced consistent results with minimal horizontal pleiotropy bias.</p> Conclusion <p>While immune cell genetic factors may contribute to cervical cancer development, their causal effects appear modest. These findings suggest that genetic predisposition through immune cell regulation likely plays a supplementary rather than primary role in cervical cancer pathogenesis.</p>

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Mendelian randomization reveals limited causal effects of genetic variants on cervical cancer risk: insights from immune cell populations

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月29日

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  • Zhang Zhang,
  • FuRong Fu,
  • ShaoLi Zhuang

摘要

Background

Cervical cancer remains a significant global health concern, with immune system regulation potentially playing a crucial role in disease development. This study investigates potential causal relationships between genetic variants associated with immune cell populations and cervical cancer risk.

Methods

We employed multiple Mendelian randomization (MR) approaches inverse-variance weighted, MR-Egger, simple median, and weighted median methods to evaluate genetic instrumental variables linked to various T-cell and B-cell subtypes. Differential gene expression was analyzed using single-cell RNA sequencing, while forest plots, scatter plots, and funnel plots facilitated comprehensive MR analysis.

Results

Forest plots consistently demonstrated odds ratios clustered tightly around 1.000 (range: 0.998–1.001), despite some variants reaching statistical significance (p < 0.05). MR analysis of CD69 + LGALS3A + regulatory T-cells, CD8 + T-cell populations, and CD20 + B-cells revealed only weak associations with cervical cancer susceptibility. Comparative analysis across different MR methodologies produced consistent results with minimal horizontal pleiotropy bias.

Conclusion

While immune cell genetic factors may contribute to cervical cancer development, their causal effects appear modest. These findings suggest that genetic predisposition through immune cell regulation likely plays a supplementary rather than primary role in cervical cancer pathogenesis.