Pancreatic cancer articles from across Nature Portfolio

In this phase 2 trial, combination treatment with elraglusib, a cell-permeable ATP-competitive inhibitor of glycogen synthase kinase-3β, and gemcitabine plus nab-paclitaxel (GnP), in patients with previously untreated metastatic pancreatic ductal adenocarcinoma led to prolonged overall survival compared with GnP only.

Upregulated HAS2 promotes pancreatic cancer immune evasion by stabilizing PD-L1 through AKT-dependent repression of the E3 ligase MARCH4. Targeting the HAS2–MARCH4–PD-L1 axis restores T-cell infiltration and slows disease.

Temporal profiling of central carbon metabolism during Kras^G12D-driven acinar-to-ductal metaplasia reveals that disruptions in NADPH-producing enzymes accelerate the formation of pancreatic precancerous lesions.

In the early stages of pancreatic ductal adenocarcinoma (PDAC) development, loss of ALDH1L2 expression elevates reactive oxygen species levels, driving accelerated acinar-to-ductal metaplasia. Decreased ALDH1L2 expression is accompanied by formate overflow, which can be used to monitor PDAC progression.

Some of the highlights in the pancreatic cancer field in 2025 include long-term data on personalized neoantigen vaccine approaches in resected pancreatic adenocarcinoma, detailed clinico-genomic analyses of large clinical trial datasets, and therapeutic strategies for early-stage disease.

Oncogenic KRAS hijacks chromatin remodeling during pancreatitis-induced tissue regeneration to drive tumorigenesis. We found that the chromatin remodeler SMARCA5 cooperates with oncogenic KRAS to maintain the malignant chromatin state; its deletion blocked tumorigenesis while preserving pancreatic tissue repair.

Patients with pancreatic exocrine insufficiency are treated with pancreatic enzyme replacement therapy. However, there are several challenges facing the future of this treatment, including infectious agents and the presence of microplastics and nanoplastics.