Summary
Lineage plasticity (LP)—most commonly exemplified by loss of androgen receptor (AR) signaling and switch from a luminal to an alternate differentiation program—is now recognized as a critical determinant of lethality. Most efforts in the field are focused on factors that promote terminal differentiation of specific LP subtypes such as neuroendocrine prostate cancer (NEPC). However, LP is a continuum, ranging from AR activity-low tumors with persistent AR expression but low AR signaling to those with alternate differentiation programs. Factors involved in the initiation and progression of LP ha
