Lineage plasticity in prostate  cancer depends on JAK/STAT inflammatory signaling

Plasticity can be quantified at single-cell level to gain insight into underlying machinery. This strategy identified FGFR and JAK/STAT inflammation as a driver of plasticity in prostate cancer with combined FGFR and JAK inhibition reversing early stages of plasticity and restoring androgen sensitivity, but only prior to full neuroendocrine transformation.