FIGURE 3.

Differential response to ADT therapy across prostate cancer (PCa) genomic subtypes. (A) Activity status of 23 transcription factors and chromatin remodelling regulators. (B) Activation of the AR signalling pathway evaluated by AR‐A score and (C) AR activation signature among three prostate cancer multi‐omics classification (PMOC) subtypes in TCGA‐PRAD cohort, Kruskal‐Wallis test. (D) Differentially activated specific pathways in PMOC2 and PMOC3 validated in patients in the Abida cohort. (E) Patients in the PMOC3 subtype benefit more from ADT therapy. (F) Patients in the PMOC3 subtype were more suitable for bicalutamide treatment. (G) Representing the PMOCs in the AHMU‐PC cohort. (H) Distribution of AR activation signature among three PMOCs in AHMU‐PC cohort, Kruskal‐Wallis test; (I) Patients in the AHMU‐PC PMOC3 subtype were more suitable for bicalutamide treatment, Kruskal‐Wallis test. (J) Differential recurrence‐free survival outcome in reproduced PMOCs of external cohorts, log‐rank test