Abstract A024: A plastic, MYC -dependent KRT17 +/ GATA6 + hybrid state drives chemoresistance and therapeutic vulnerability in pancreatic cancer
Pancreatic ductal adenocarcinoma (PDAC) progression is driven by cellular heterogeneity not fully captured by the classical (GATA6+) versus basal-like (KRT17+) model. Intermediary states are linked to aggression, but their characteristics remain unclear. Here, we deconstruct this heterogeneity using a KRT17/GATA6 fra...