ArticleEndocrine connections2025
Shared molecular mechanisms between type 2 diabetes and thyroid cancer: integrated bioinformatics insights for prognostic biomarker discovery.
Article in Endocrine connections, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- Flavonoids fromJournal of enzyme inhibition and medicinal chemistry · 2026Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Thyroid cancer (TC) is a prevalent endocrine malignancy with rising global incidence, particularly among women. Emerging evidence suggests a significant association between type 2 diabetes mellitus (T2D) and TC, potentially mediated by hyperinsulinemia, insulin resistance, and chronic inflammation. However, the molecular mechanisms linking these diseases remain poorly understood. Methods: We integrated transcriptomic datasets from the Gene Expression Omnibus (GEO) database (GSE33630, GSE35570, GSE60542 for TC; GSE86468 for T2D) to identify shared differentially expressed genes (DEGs). Functional enrichment, protein-protein interaction networks, and Cox regression analyses were employed to elucidate pathways and prognostic biomarkers. Results: We identified 28 shared DEGs between TC and T2D, with CD44, TGFBI, RUNX2, and GJA1 as key hub genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis highlighted pathways involving cell adhesion, extracellular matrix remodeling, and NF-κB signaling. A risk model incorporating seven genes (e.g., PRDM1 [protective] and ZFPM2 [risk]) stratified TC patients into high- and low-risk groups with distinct survival outcomes (P = 0.017). Conclusion: T2D and TC exhibit overlapping genetic dysregulation, particularly in pathways governing metabolic reprogramming and tumor microenvironment crosstalk. Notably, PRDM1 and ZFPM2 may serve as therapeutic targets for TC in patients with concurrent diabetes.
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