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. 2022 Jul 21;13(7):632. doi: 10.1038/s41419-022-05084-1

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — The partial agonist role of second-generation AR antagonists induces the expression of cancer-related genes including GR. GR in turn regulates the expression of a set of genes that overlaps with AR downstream pathways. AR alterations can include alternative splicing, point mutation and overexpression. Other AR signaling-independent mechanisms such as PTEN/TP53/RB1 loss of function and MYCN/SOC2 activation can mediate CRPC progression and contribute to AR antagonist resistance in CRPC.