J. L. Iovanna

EHMT2 Inactivation in Pancreatic Epithelial Cells Shapes the Transcriptional Landscape and Inflammation Response of the Whole Pancreas

Adaptation of redox metabolism in drug-tolerant persister cells is a vulnerability to prevent relapse in pancreatic cancer

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.

p97/VCP induces GLI1 to control XBP1-dependent endoplasmic reticulum stress transcriptional response

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.

Metabolomic profiling of pancreatic adenocarcinoma reveals fundamental clinical features

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

NUPR1 protects liver from lipotoxic injury by improving the endoplasmic reticulum stress response

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

Establishment of a pancreatic adenocarcinoma molecular gradient (PAMG) that predicts the clinical outcome of pancreatic cancer

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

The stress-induced protein NUPR1 orchestrates protein translation during ER-stress by interacting with eIF2α

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

Basal-like and Classical cells coexistence in pancreatic cancer revealed by single cell analysis

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

Inactivation of NUPR1 promotes cell death by coupling ER-stress responses with necrosis

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