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. 2019 May 9;9:385. doi: 10.3389/fonc.2019.00385

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Copyright © 2019 Civenni, Albino, Shinde, Vázquez, Merulla, Kokanovic, Mapelli, Carbone and Catapano.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Prostate cancer progression and cancer stem cells. Prostate cancers initiate as in situ carcinoma called prostatic intraepithelial neoplasia (PIN) and then evolve into invasive carcinomas and later, after androgen deprivation therapy (ADT), progress to metastatic castration-resistant prostate carcinomas (mCRPC). After continuous ADT or treatment with new AR-pathway inhibitors (ARPI), treatment-resistant tumors emerge that either retain adenocarcinoma features with enhanced AR signaling (Adeno-CRPC) or acquire neuroendocrine features with attenuated AR signaling (NE-CRPC). Progression through these stages and development of castration-resistance are driven likely by the expansion and specific behavior of prostate cancer stem cells.