HNF1A, a risk factor gene for pancreatic ductal adenocarcinoma, is critical to maintaining pancreatic cancer stem cell properties through regulating POU5F1 (OCT4) expression, providing a novel role for HNF1A in maintenance of the disease.

Circulating myeloid cells invade the brain during pancreatic cancer, where they accumulate at a unique central nervous system interface and drive anorexia and muscle catabolism.

Single-cell RNA-sequencing analyses and functional studies define heterogeneity within the pancreatic ductal tree and unique properties of subpopulations of duct cells including an epithelial-mesenchymal transcriptomic axis and roles in chronic pancreatic inflammation.

A major consequence of ductal-to-squamous lineage transition in pancreatic cancer cells is to augment inflammation, which may explain the exceptionally poor clinical outcomes of squamous-subtype tumors.

UPF1 mutations were reportedly present at high frequencies in a cohort of pancreatic adenosquamous carcinoma patients, but these lesions are unlikely to be functional drivers of this cancer subtype.

Combinations of transcription factors can convert pancreatic acinar cells into endocrine α-, β- and δ-cells in vivo.

CK21 emerges as a compelling candidate for pancreatic cancer treatment, and its capacity to target the NF-κB pathway, induce mitochondrial-mediated apoptosis, and do so with minimal toxicity is a significant stride in the quest for improved therapies.

Pancreatic α and β cells have different cell autonomous signatures; this explains why α but not β cells can clear infections by potentially diabetogenic viruses.

Deletion of Arginase 1 in myeloid cells delays tumor formation in pancreatic cancer.

New role of P2Y₂-αV integrin interactions in ATP-driven pancreatic cancer cell invasion provides a potential anti-metastatic target for pancreatic cancer.