Asynchronous evolution of epithelial and stromal components distinguishes pancreatic cancer from precursor lesions, with stromal reprogramming being a key differentiator.
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Pancreatic function and diabetes
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HnRNPK limits memory B-cell and plasma cell differentiation, maintaining germinal center B-cell output by regulating transcription and metabolism.
Inhibiting the Na+ channel gene Scn9a reduces beta cell loss and diabetes incidence in NOD mice, highlighting its potential as a therapeutic target for type 1 diabetes.
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Methodological strategies like pragmatic trials and target trial emulation improve real-world evidence for GLP-1 receptor agonists, addressing key gaps in clinical practice and policy.
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