Fig. 5. Divergent MYC and AR transcriptional programs dictate disease progression.

a, b Kaplan–Meier curves (a) and log-rank tests (b) reveal that patients bearing a primary tumor characterized by low AR-activity (AR-A) and concurrent high MYC transcriptional signature (Hallmark) have a shorter time to biochemical recurrence (BCR) within the discovery cohort (TCGA). c, d Kaplan–Meier curves (c), univariable and multivariable analysis (d Cox proportional hazards model) confirms that tumors with concurrent low AR-A and high MYC transcriptional signatures develop BCR after radical prostatectomy more rapidly than low AR-A tumors without an active MYC transcriptional program in the validation cohort (Spratt et al., 2017³⁵; n = 855; HR ± 95% CI). e, f Kaplan–Meier curves (e), univariable and multivariable analyses (f Cox proportional hazards model) reveal that tumors with concurrent low AR-A and high MYC transcriptional signatures are more likely to develop a metastatic disease (n = 855; HR ± 95% CI). PSA: prostate-specific antigen; HR: hazard ratio; CI: confidence interval; GS: Gleason score; ECE: extracapsular extension; SVI: seminal vesicles invasion; LNI: lymph node involvement.