Genome-wide Mendelian Randomization analysis reveals specific inflammatory traits as causal risk factors for oral cancer

Abstract

Abstract Purpose Previous research has suggested a potential connection between persistent inflammation and the risk of developing oral cancer. However, the causal relationships between inflammatory traits and oral cancer are not yet fully understood. Methods To delve deeper into this inquiry, we implemented a two-sample Mendelian randomization (MR) analysis, utilizing genetic data from previous genome-wide association studies (GWAS). In this analysis, we explored several inflammatory traits as potential exposures, while considering oral cancer as the outcome. To ensure the robustness of our findings, we employed the inverse variance weighted (IVW) method as the primary analytical approach, alongside tests for pleiotropy and heterogeneity. Results The IVW method identified two immune-mediated inflammatory diseases that showed associations with an increased risk of oral cancer. In particular, inflammatory bowel disease was found to be correlated with a higher risk of oral cancer (p < 0.001), as well as its subtypes such as Crohn's disease (p = 0.026). Additionally, elevated levels of Interleukin-10 (IL-10) were found to be potentially associated with an increased risk of oral cancer (p = 0.048), while higher levels of IL-18 showed a protective effect on oral cancer (p = 0.011). Conclusion The results of this study offer compelling evidence supporting a causal link between distinct inflammatory traits and the susceptibility to oral cancer. These findings hold significant implications for the clinical management of oral cancer, spanning various aspects such as prevention, diagnosis, and treatment strategies.