LAUSR

P cancer (PCa) initiation, progression, and therapy resistance involve genetic and epigenetic alterations that l e ad to ab err ant cel l l ine age specification and plasticity.1–3 The vast majority of primary prostate cancers are pathologically defined as luminal cancer with luminal cell expansion and absence of basal cells. The basal or neuroendocrine PCa is extremely rare in primary or untreated PCa. Adeno-to-neuroendocrine PCa lineage plasticity has been identified in advanced PCa following the targeted therapy of AR inhibition.2 However, the underlying mechanisms of PCa cell fate determination and lineage plasticity are still poorly understood. Therefore, systematically defining the genetic, epigenetic, and microenvironment factors in PCa cell lineage determination and plasticity may reveal the underlying molecular mechanisms and stimulate the development of novel therapeutic strategies to prevent or reverse the current therapy resistance of prostate cancers. This special issue, “Prostate Cell Fate and Diseases”, contains six original articles and five reviews to introduce some recent PCa research progress in the field of prostate cell fate determination and lineage plasticity. PCa is one of the most common cancers in men in the world. The normal prostate epithelium consists of luminal cells, basal cells, INVITED EDITORIAL