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. 2019 Feb 7;9:1603. doi: 10.1038/s41598-018-38179-x

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© The Author(s) 2019

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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AR pathway model. (A) Calibration of the AR pathway model on dataset GSE7868, containing samples from LNCaP prostate cancer cells, treated with 100 nM dihydrotestosterone (DHT) for 0, 4 and 16 h. (B–E) Validation on independent GEO datasets. (B) GSE7708, LNCap cells treated with 1 nM DHT with or without bicalutamide (added 2 h before DHT) for 16 h. (C) GSE21887 KUCaP-2 cell grafted in nude mice, androgen-dependent tumour growth (AD), castration-induced tumour regression (CI), and castration-resistant (CR) regrowth. (D) GSE33316, LuCaP35 cells grafted in NOD-SCID mice, AD and CI. (E) GSE32982, biopsy samples from prostate cancer, benign prostate tissue and prostate cancer tissue three days after surgical castration. The activity score is calculated as log2odds; p-values are indicated in the figures.