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Abstract Background Several blood proteins might be associated with the development of colorectal cancer (CRC), but many studies on this topic are often biased. By using genetic variation data, which is less influenced by environmental factors, we can better determine the causal relationship between specific blood proteins and the occurrence of colorectal cancer. Methods Data from a genome-wide association study (GWAS) on blood proteins, encompassing 1,478 proteins, and colorectal cancer (CRC) GWAS data, covering 637,693 subjects, were collected and organized. Additionally, GWAS data for obesity, diabetes mellitus (DM), and smoking were obtained for further analysis. Single nucleotide polymorphisms (SNPs) significantly associated with the exposure factors (blood proteins) were selected to ensure their independence from other confounding factors and outcomes (CRC onset), and that they only affected outcomes through blood proteins. The causal effects of Mendelian Randomization (MR) were primarily estimated using the inverse variance weighted (IVW) method, with other methods serving as supplementary approaches. The Cochran's Q-test assessed heterogeneity among SNP estimates; the MR Egger method evaluated pleiotropy; and the leave-one-out test examined the sensitivity of individual SNPs. Obesity, DM, and smoking were included in the multivariate MR analysis. Result A total of 31 SNPs and 8 blood protein exposure factors were identified, specifically TNFRSF16 (4 SNPs), RNF8 (4 SNPs), MRM3 (4 SNPs), ST6GALNAC1 (4 SNPs), TIE1 (4 SNPs), CBP (4 SNPs), DNAJB9 (4 SNPs), and EDN2 (3 SNPs). The IVW results showed a significant causal relationship between all 8 exposure factors and colorectal cancer (P |
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