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Patient-derived organoids reveal ductal dysfunction and CFTR-modulator responses in chronic pancreatitis
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DOI：10.1016/j.stem.2026.06.002.png)
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Abstract
En 中文
• CP PDOs retain epithelial-intrinsic inflammatory disease programs • Transcriptomic analysis defines three CP PDO subtypes independent of etiology • CFTR dysfunction is common in CP PDOs, including wild-type models • CFTR modulators restore ductal function and suppress inflammatory signaling
Keywords:
chronic pancreatitis
patient-derived organoids
CFTR
molecular subtypes
CFTR correctors
CFTR potentiators
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