H. C. Crawford

Tuft cells transdifferentiate to neural-like progenitor cells in the progression of pancreatic cancer

The paper shows that metaplastic tuft cells in pancreatic cancer transdifferentiate into neural-like progenitor cells, driven by Myc activity, and this transition is linked to poor patient survival.

ROR2 regulates cellular plasticity in pancreatic neoplasia and adenocarcinoma

This study identifies ROR2 as a regulator of cellular plasticity in pancreatic neoplasia, showing it promotes an aggressive PDAC phenotype and resistance to KRAS inhibitors.

Glucose-6-phosphate dehydrogenase deficiency accelerates pancreatic acinar-to-ductal metaplasia

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.

Hypoxia promotes an inflammatory phenotype of fibroblasts in pancreatic cancer

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

Extrinsic KRAS signaling shapes the pancreatic microenvironment through fibroblast reprogramming.

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

Progranulin promotes immune evasion of pancreatic adenocarcinoma through regulation of MHCI expression

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.

The Pancreatic Tumor Microenvironment Compensates for Loss of GOT2

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

GOT1 Inhibition Primes Pancreatic Cancer for Ferroptosis through the Autophagic Release of Labile Iron

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

Tissue of Origin Dictates GOT1 Dependence and Confers Synthetic Lethality to Radiotherapy

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.

Macrophage Released Pyrimidines Inhibit Gemcitabine Therapy in Pancreatic Cancer

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.

HNF1A is a Novel Oncogene and Central Regulator of Pancreatic Cancer Stem Cells

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