The war against pancreatic cancer in 2020-advances on all fronts

Key advances An endocrine-exocrine axis involving cholecystokinin secretion by remodelled beta-cells drives obesity-mediated pancreatic ductal adenocarcinoma (PDAC) progression, and this process can be intercepted through weight loss strategies4. Novel avenues for stromal manipulation to improve PDAC therapy were identified in the form of LCCR15+ cancer-associated fibroblasts, which can be used to predict immunotherapy resistance7. Whole-exosome sequencing of primary tumour and matched autopsy samples from patients with recurrent PDAC demonstrated treatment-induced genetic bottlenecks and intermetastatic seeding leading to subclonal heterogeneity in the recurrent tumours, also identifying potentially targetable genetic signatures in recurrent disease9. In 2020, important advances were made across three major frontiers of pancreatic ductal adenocarcinoma (PDAC) research: risk factors, therapeutic resistance and tumour recurrence. Pathophysiology of obesity-mediated PDAC initiation was elucidated, novel stromal mechanisms of therapeutic resistance were unveiled and the genetic evolution of recurrent PDAC under therapeutic pressures was tracked in human samples.

Automated summary

In 2020, significant progress was made in three major areas of pancreatic ductal adenocarcinoma (PDAC) research: risk factors, therapeutic resistance, and tumor recurrence. The pathophysiology of obesity-mediated PDAC initiation was elucidated, novel stromal mechanisms of therapeutic resistance were unveiled, and the genetic evolution of recurrent PDAC under therapeutic pressures was tracked in human samples.