R. A. Urrutia

This paper identifies a GATA6-centered gene regulatory network involving HNFs and ΔNp63 that controls plasticity and immune escape in pancreatic cancer, showing GATA6 loss is necessary but not sufficient for the basal phenotype.

This study identifies a metabolic signature in pancreatic adenocarcinoma that predicts clinical outcomes and drug resistance, suggesting metabolic targeting as a therapeutic strategy.

This paper shows that inactivating NUPR1 in pancreatic cancer cells causes ER stress, mitochondrial dysfunction, and necrotic cell death independent of caspases.