Brittany L. Allen-Petersen

This study identifies and optimizes a chloroacetamide scaffold as a covalent inhibitor for UCHL3, supported by structural and biochemical validation.

This study shows that suppressing PP2A-B56α promotes EMT in EGFR mutant NSCLC by reducing epithelial markers and increasing mesenchymal markers, leading to migratory and invasive phenotypes.

This study shows that activating PP2A-B56 in PDAC increases EGFR signaling and promotes tumor growth, suggesting a new therapeutic target.

This study shows that PP2A activation inhibits macropinocytosis and induces cell death in pancreatic ductal adenocarcinoma, suggesting PP2A activators could be used with metabolic inhibitors as a new therapeutic strategy.

This study develops a novel pancreatic cancer mouse model by expressing Myc and mutant Kras in adult acinar cells, showing metastasis and therapeutic resistance similar to human PDAc.

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.