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Background <p>The interaction between immune cells and cancer has been extensively researched. However, little is known about the relationship between B Cells and lung squamous cell carcinoma (LUSC).</p> Methods <p>This study performed a comprehensive two-sample Mendelian randomization (MR) analysis of GWAS summary data to determine the causal relationship between the immune phenotypes of 199 subtypes of B cells and the risk of LUSC. Heterogeneity and horizontal pleiotropy were assessed using several methods, including MR-Egger regression and inverse variance weighting.</p> Results <p>MR analysis showed that an increase in the absolute count number of unswitched memory B cells (UMBC) was causally associated with the risk of LUSC at FDR &lt; 0.05. Reverse MR analysis indicated that LUSC was causally associated with the increased expression of CD27 on IgD<sup>+</sup> CD38<sup>−</sup> UMBCs and CD27 on UMBCs at <i>p</i> &lt; 0.05.</p> Conclusion <p>There is a strong association between the number of UMBCs and the risk of LUSC. These results provide a basis for developing new cancer immunotherapies.</p>

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Mendelian randomization analyses support causal relationships between unswitched memory B cells and lung squamous cell carcinoma

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年9月30日

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  • Hong-Jun Li,
  • Chun-Yu Lin,
  • Dai-Zheng Huang,
  • Zhen-Cheng Chen,
  • Xiao-Jv Chi

摘要

Background

The interaction between immune cells and cancer has been extensively researched. However, little is known about the relationship between B Cells and lung squamous cell carcinoma (LUSC).

Methods

This study performed a comprehensive two-sample Mendelian randomization (MR) analysis of GWAS summary data to determine the causal relationship between the immune phenotypes of 199 subtypes of B cells and the risk of LUSC. Heterogeneity and horizontal pleiotropy were assessed using several methods, including MR-Egger regression and inverse variance weighting.

Results

MR analysis showed that an increase in the absolute count number of unswitched memory B cells (UMBC) was causally associated with the risk of LUSC at FDR < 0.05. Reverse MR analysis indicated that LUSC was causally associated with the increased expression of CD27 on IgD+ CD38− UMBCs and CD27 on UMBCs at p < 0.05.

Conclusion

There is a strong association between the number of UMBCs and the risk of LUSC. These results provide a basis for developing new cancer immunotherapies.