ArticleDiscover oncology2025
Immune-related gene expression with colorectal cancer risk: a Mendelian randomization analysis.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Transcriptome-wide Mendelian randomization exploring dynamic CD4+ T cell gene expression in colorectal cancer development.Journal of leukocyte biology · 2025Article
- Druggable Genome Mendelian Randomization and GWAS-sceQTLs MR Analysis Reveal Genetic Associations Between Open-Angle Glaucoma and Immune Cells, and Identify Potential Drugs.Translational vision science & technology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
backgroundThe potential role of immune cells and the precise contributions of genes from various immune cells in the development of colorectal cancer (CRC) remains unclear. We aimed to investigate the potential causal relationships between specific immune cell genes and the development of CRC by performing Mendelian randomization (MR) analysis.
methodsThe cis-expression quantitative trait loci (eQTLs) data for type-specific immune cells were used to perform MR analysis. Outcomes data were obtained from the latest Genome Wide Association Studies (GWAS), comprising 78,473 European ancestry CRC cases and 107,143 controls. A few sensitivity analyses, encompassing pleiotropy and colocalization analyses, along with the application of False Discovery Rate (FDR) correction, were carried out to mitigate potential biases.
resultsA total of 395 genes were found to be associated with CRC. After FDR correction, a total of 47 genes across 14 immune cell types were identified. Notably, the FHL3 gene showed the strongest association with CRC in multiple immune cell types, including CD4 + naïve and central memory T cells (CD4NC), CD4 + T cells with an effector memory or central memory phenotype (CD4ET), CD8 + naïve and central memory T cells (CD8NC), CD8 + T cells with an effector memory phenotype (CD8ET), and NK recruiting cells (NKR). Sensitivity analyses and pleiotropy assessments excluded the bias due to weak instruments and linkage disequilibrium. Additionally, the associations were supported by strong evidence of colocalization with CRC. The expression of FHL3 in normal tissue was higher than that in the tumor tissue at the mRNA expression and single-cell levels, and low mRNA expression of FHL3 was associated with shorter survival time in CRC patients.
conclusionsOur study provides a novel perspective on the potential causal link between the low expression of FHL3 gene and the risk of CRC. More evidence is essential to further reveal the biological mechanisms underlying this association.
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