Drug resistance in cancer is often linked to changes in tumor cell state or lineage, but the molecular mechanisms driving this plasticity remain unclear. Here we show using a variety of organoid in vitro models that lineage plasticity can be mimicked and targeted. Using murine organoid and genetically engineered mouse models, we investigated the causes of lineage plasticity in prostate cancer and its relationship to antiandrogen resistance. We found that plasticity initiates in an epithelial population defined by mixed luminal-basal phenotype and that plasticity depends on various context dependent pathways. Here I will discuss several of these critical regulators of lineage plasticity in castration resistant prostate cancer as well as discuss how lineage regulation is relevant for other cancer types as well.<\/p>\n
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