ReviewCellular oncology (Dordrecht, Netherlands)2026
Acinar-ductal metaplasia in pancreatitis and pancreatic ductal adenocarcinoma.
Review in Cellular oncology (Dordrecht, Netherlands), 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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10 authors.
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Abstract
Acinar-ductal metaplasia (ADM) represents a dynamic and reversible cellular adaptation in the pancreas, whereby acinar cells dedifferentiate and transdifferentiate into duct-like cells in response to inflammatory, metabolic, and environmental stressors. While transient ADM facilitates tissue repair after acute injury, persistent stimuli-including chronic pancreatitis, metabolic dysregulation, obesity, diabetes, smoking, and oncogenic KRAS mutations-stabilize ADM and promote progression to pancreatic intraepithelial neoplasia (PanIN) and pancreatic ductal adenocarcinoma (PDAC). ADM is orchestrated by integrated signaling networks involving TGF-β/SMAD, EGFR-KRAS-MAPK, PI3K-AKT-mTOR, Notch, Wnt/β-catenin, and JAK/STAT3, which regulate dedifferentiation, proliferation, survival, and fibrosis. Inflammatory cells, particularly macrophages and eosinophils, and pro-inflammatory cytokines such as IL‑6, IL‑18, and TNF‑α further amplify ADM and create a tumor-promoting microenvironment. Single-cell analyses reveal that ADM encompasses heterogeneous cell states with distinct lineage trajectories, determining reversibility or pre-neoplastic transformation. Pharmacological interventions, including HDAC inhibitors, JAK/STAT3 inhibitors, metformin, and anti-inflammatory agents, show potential in preventing or reversing ADM. Understanding the complex molecular, cellular, and environmental regulation of ADM provides critical insights into pancreatic regeneration and early tumorigenesis and offers a framework for developing targeted strategies for the prevention and treatment of pancreatitis and PDAC.
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