Epigenetic plasticity cooperates with cell-cell interactions to direct pancreatic tumorigenesis.

Furthermore, a subset of early Kras-mutant cell states exhibit marked similarity to either benign or malignant fates that emerge weeks to months later; for instance, Kras-mutant Nestin-positive progenitor-like cells display accessible chromatin near genes active in malignant tumors. These plastic cell states are enriched for open chromatin near cell-cell communication genes encoding ligands and cell-surface receptors, suggesting an increased propensity to communicate with the microenvironment. [Extracted from the article]