ArticleBMC medical genomics2026
Decoding the diabetes-pancreatic adenocarcinoma connection: the critical role of PILRA in intermediate monocyte activity.
Article in BMC medical genomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Diabetes is a well-known risk factor for pancreatic adenocarcinoma (PAAD), yet the underlying molecular mechanisms remain unclear. This study employs single-cell sequencing to analyze gene expression patterns and uses Mendelian randomization to assess the association between genetic variations in specific genes and the risk of PAAD. Our findings reveal a significant reduction in the proportion of monocytes in patients with both diabetes and PAAD. Monocytes play a crucial role in the progression of both diseases. Notably, we identified an increase in intermediate monocytes (CD14 + + CD16+) in both conditions. These cells exhibit significant activation of the LGALS9-CD45 receptor, increased metabolic activity, and enhanced involvement in disease pathways. We demonstrate that intermediate monocytes are key cellular players in the link between diabetes and PAAD. Using dual-sample Mendelian randomization, we identified genetic variations in PILRA, a highly variable gene in intermediate monocytes, as a risk factor for PAAD. PILRA + intermediate monocytes show higher metabolic activity and stronger immune cell communication compared to PILRA- cells, suggesting an important role in tumor microenvironment regulation and immune cell activation inhibition. This biological function is associated with cytokine-mediated signaling, focal adhesion, and NOD-like receptor signaling pathways. RT-qPCR validation of PBMC samples indicates a statistically significant, progressive increase in PILRA expression in patients with PAAD, diabetes, and those with both conditions. In summary, this study uncovers the critical role of intermediate monocytes in diabetes-induced PAAD and proposes PILRA as a potential therapeutic target.
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