• Aiyu Guan, Zeming Li, and Xingren Guo.
• Department of Hepatobiliary Surgery, Yuncheng Central Hospital Affiliated to Shanxi Medical University, Yuncheng, Shanxi Province, China.
• Medicine (Baltimore). 2024 Oct 11; 103 (41): e40047e40047.

AbstractIt is unknown what causes pancreatic cancer. We conducted a phenome-wide Mendelian randomization analysis (MR-pheWAS), a bidirectional Mendelian study, and a systematic review of research in order to thoroughly investigate any causal association between pancreatic cancer and Atlas. We used phenome-wide Mendelian randomization analysis to test for associations between pancreatic cancer and 776 phenotypes (n = 452,264) of Atlas in the UK Biobank. Causality is confirmed by two-sample Mendelian randomization (MR) analysis using correlation found by false discovery rate correction. Simultaneously, a comprehensive evaluation of pancreatic cancer MR studies was conducted in order to complement our findings and harmonize the existing evidence. According to the inverse-variance-weighted model, a total of 41 out of 776 phenotypes had a nominal significance level (P < .05) genetic prediction association with pancreatic cancer. Only genetically predicted pancreatic cancer was shown to be linked with elevated eosinophil counts following false discovery rate correction (P = .031) when several tests were taken into account. Pancreatic cancer and eosinophils were shown to be positively causally associated to one another, establishing a self-loop, according to two-sample MR validation in the IEU database (OR = 1.011, 95% CI: 1.002-1.020, P = .010) (OR = 1.229, 95% CI: 1.037-1.458, P = .017). Although MR-pheWAS found a strong causal relationship between eosinophils and pancreatic cancer, it also found a negative exclusion value for each phenotype and a significant number of suggestive association phenotypes that offered guidance for further research.Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.

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