J. L. Iovanna

This study identifies mitochondrial and redox metabolic reprogramming in drug-tolerant persister cells of pancreatic cancer and shows that targeting redox metabolism can prevent relapse.

The paper shows p97/VCP interacts with RUVBL2 and mSin3A-HDAC1/2 to regulate GLI1, which activates XBP1 under ER stress, independent of Hh ligands.

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

This study shows NUPR1 protects the liver from lipotoxic injury by enhancing the endoplasmic reticulum stress response and regulating lipid homeostasis through PPAR- signaling.

This paper develops a transcriptomic gradient (PAMG) to predict pancreatic cancer aggressiveness and treatment response using patient-derived xenografts and clinical data.

This paper identifies NUPR1's role in ER stress response by interacting with eIF2α to regulate protein translation recovery.

The paper uses single-cell transcriptomic analysis to show that basal-like and classical cells coexist in pancreatic cancer tumors, revealing unexpected heterogeneity.

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