Jude Eze Ogechukwu

Pancreatic ductal adenocarcinoma, the most prevalent form of pancreatic cancer (1), frequently arises from precursor lesions called pancreatic intraepithelial neoplasia (PanIN; ref. 2). Establishment of PanIN is accompanied by expansion of a fibroinflammatory stroma, rich in fibroblasts and immune cells (3–5). In malignant disease, cancer-associated fibroblasts (CAF) represent an abundant and poorly understood cellular component.

Of the estimated 67,440 new patients who will be diagnosed with pancreatic ductal adenocarcinoma (PDAC) in the United States in 2025, about half will have metastatic disease (1). These patients typically respond poorly to standard-of-care chemotherapy, leading to a 5-year survival rate of only 3% (1).

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