H. C. Crawford

This study shows that G6PD deficiency accelerates pancreatic acinar-to-ductal metaplasia by enhancing NADPH production for ROS management, highlighting a metabolic role in early tumorigenesis.

This study shows hypoxia drives an inflammatory phenotype in pancreatic cancer-associated fibroblasts, promoting tumor IL1 expression and iCAF formation in hypoxic regions.

This study shows that extrinsic KRAS signaling reprograms pancreatic fibroblasts to create an inflammatory microenvironment that supports tumor growth.

This study shows that tumor-derived progranulin (PGRN) promotes immune evasion in pancreatic ductal adenocarcinoma by reducing MHC class I expression, and blocking PGRN enhances immune response and slows tumor progression.

This study shows that the pancreatic tumor microenvironment compensates for loss of GOT2 by providing pyruvate, maintaining redox homeostasis and tumor growth in vivo.

This study shows that inhibiting GOT1 in pancreatic cancer primes cells for ferroptosis by promoting autophagy-mediated release of labile iron.

The paper shows that pancreatic ductal adenocarcinoma (PDA) is more dependent on GOT1 than colorectal cancer (CRC) and that GOT1 inhibition synergizes with radiotherapy to inhibit PDA growth.

This study shows macrophages in pancreatic cancer release pyrimidines that inhibit gemcitabine therapy by competing with the drug for uptake and metabolism, and reducing macrophage burden improves treatment response.

This study identifies HNF1A as a central regulator of pancreatic cancer stem cells and a novel oncogene in pancreatic ductal adenocarcinoma.