# A Two-way Mendelian randomisation study of inflammatory factors and the risk of meningioma

## TL;DR

This study finds a genetic link between lower FLT3 ligand levels and increased risk of meningioma, suggesting FLT3 signaling plays a role in its development.

## Contribution

Identifies FLT3 ligand as a genetically supported factor with causal associations to meningioma risk through two-way Mendelian randomization.

## Key findings

- FLT3 ligand levels show a clear causal association with meningioma occurrence (OR=0.713).
- Reverse MR analysis links meningioma to lower FLT3 ligand levels (OR=0.936).
- No heterogeneity or pleiotropy detected in MR-Egger intercept tests.

## Abstract

To explore the causal relationship between inflammatory factors and meningioma.

The inverse variance weighting method (IVW), Mendelian Randomisation Egger (MR-Egger) regression, weighted median method, simple mode method, and weighted mode method were used to analyse the potential causal relationship between exposure factors and outcomes.

Preliminary MR analysis showed that 6 inflammatory factors, including C-C motif chemokine 19 levels, osteoprotegerin levels, Fms-related tyrosine kinase 3 (FLT3) ligand levels, matrix metalloproteinase-1 levels, C-C motif chemokine 28 levels, and interleukin-5 levels, were associated with meningiomas. Further screening of inflammatory factors and positive MR analysis showed that FLT3 ligand levels had a clear causal association with the occurrence of meningioma (odds ratio [OR]=0.713, 95 % confidence interval [CI]: 0.598–0.851). The results of reverse MR analysis showed that there was a clear causal association between meningioma and Fms-related tyrosine kinase 3 ligand levels (OR=0.936, 95 % CI: 0.885–0.990). The results of heterogeneity and pleiotropic tests of MR-Egger intercept showed that there was no heterogeneity or pleiotropy in all data.

This study clarified FLT3 as being involved in the pathogenesis of meningioma from a genetic perspective and genetically predicted lower FLT3L to be causally associated with a higher meningioma risk, implicating FLT3 signalling in meningioma pathogenesis. FLT3 as a genetically supported candidate factor associated with meningioma risk.