John P. Morris

In mouse pancreatic cancer models, p53, CDKN2A and SMAD4 programs converge on a rare Kras-mutant progenitor-like state whose niche KRAS inhibition collapses and p53 loss expands.

This study shows that p53 and YAP/TAZ-TEAD activities regulate metaplastic heterogeneity in pancreatic cancer by influencing differentiation states and molecular subtypes.

This study identifies the menin-MLL1 complex as essential for HCC survival and shows it cooperates with NF-Y to regulate oncogenic gene transcription.

The paper shows that p53 activity regulates YAP/TAZ-TEAD complexes to shape transcriptional landscapes during tumorigenesis by altering TEAD binding and gene regulatory networks.

This paper shows that mutant IDH disrupts p53 target gene regulation by altering chromatin states, disabling tumor suppression, and that this effect can be reversed with IDH inhibition.