Extended Data Fig. 10: Additional validation of the META-55/META-16 gene signatures and survival analyses.

a, b, Heatmaps of hierarchical consensus clustering analysis used to define tumors with high (brown cluster) and low (green cluster) expression of META-16 in MAYO (n = 235) and JHMI (n = 260) cohorts, as indicated (Supplementary Table 3). Brown vertical bars on the second from top row represent patients that developed distant metastasis. Colors represent row-scaled expression values. c, d, Kaplan-Meier survival analyses comparing patients with low and high overall expression of META-55. The p-values were estimated using a log-rank test. e, Multivariable survival analysis of the META-55 gene signature in the JHMI and MAYO cohorts showing significant association with metastasis-free survival but not with prostate-cancer specific mortality (HR = hazard ratio, CI = confidence interval, p-values estimated from Coxproportional hazards model), adjusted for age, pathological Gleason score/grade at diagnosis, pre-PSA, seminal vesicle invasion (SVI), lymph node invasion (LNI), and extra-prostatic extension (EPE). f, g, Kaplan-Meier survival analyses comparing patients from SU2C cohort with the low and high MYC activity with respect to treatment-associated survival (that is, time from the start of treatment with androgen receptor signaling inhibitor (ARSi) therapy, to death or last follow-up, n = 75 patients) or treatment-associated disease progression (that is, time on treatment with ARSIs, n = 56) as defined in²⁶. The p-values were estimated using a log-rank test.