ReviewFrontiers in endocrinology2026
Bidirectional relationship between diabetes and pancreatic cancer: from mechanistic investigation to clinical application.
Review in Frontiers in endocrinology, 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
A well-established bidirectional causal relationship connects type 2 diabetes mellitus (T2DM) and pancreatic ductal adenocarcinoma (PDAC). Long-standing T2DM elevates pancreatic cancer risk approximately 1.8-2.2-fold, whereas 30%-74% of PDAC patients develop new-onset diabetes (NOD) 2-36 months before tumor detection, which mostly corresponds to tumour-originated type 3c pancreatogenic diabetes (T3cDM). Notably, 25%-40% of such patients achieve spontaneous glycemic recovery after R0 curative resection, solidifying the causal nature of PDAC-induced hyperglycemia. Six interrelated molecular mechanisms mediate their reciprocal crosstalk: chronic metabolic abnormality mediated by hyperinsulinemia and AGE-RAGE signaling, sustained inflammatory and macrophage remodeling, KRAS-driven oncogenic and epigenetic modification, pancreatic stellate cell-derived desmoplasia, tumor exosome-mediated β-cell damage, and gut-pancreas microbiome dysbiosis. Specifically, PDAC-secreted exosomes loaded with adrenomedullin, peritumor fibrotic islet destruction and circulating S100A8 peptide collectively lead to insulin deficiency, making T3cDM biochemically distinguishable from insulin-resistant classic T2DM by reduced pancreatic polypeptide and endogenous insulin concentrations. Clinically, END-PAC scoring and emerging machine learning algorithms facilitate risk stratification for early PDAC screening among patients aged 50 years or older with NOD. Nonetheless, prominent challenges remain: conflicting clinical data on the anti-PDAC potential of metformin and GLP-1RAs, ethnic heterogeneity limiting the generalizability of current prediction models, and up to 88% T3cDM misdiagnosis owing to the absence of global unified diagnostic benchmarks. Future translational research will center on prospective validation of multi-omic biomarkers, formulation of standardized T3cDM diagnostic criteria, large-scale screening trials, and rational repurposing of antidiabetic agents for pancreatic cancer prevention and adjuvant therapy.
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