Prostate Cancer

P2, N=162, Active, not recruiting, Australian and New Zealand Urogenital and Prostate Cancer Trials Group | Trial completion date: Jan 2025 --> Dec 2026

P=N/A, N=100, Terminated, University Hospital, Montpellier | Trial completion date: Oct 2025 --> Jun 2026 | Recruiting --> Terminated; Flaw in the analytical technique

P=N/A, N=5000, Active, not recruiting, McMaster University | Recruiting --> Active, not recruiting

P=N/A, N=500, Recruiting, University Health Network, Toronto | Trial completion date: May 2025 --> May 2027 | Trial primary completion date: May 2025 --> May 2027

Exploratory grouping by the model-derived RiskScore revealed differences in pathway and immune infiltration patterns, suggesting an association between the signature and intratumoral molecular heterogeneity. These exploratory findings primarily serve to characterize the biological features related to the model and provide supplementary clues for understanding molecular alterations in prostate cancer; they should be interpreted with caution.

P=N/A, N=300, Recruiting, Memorial Sloan Kettering Cancer Center | Not yet recruiting --> Recruiting

P=N/A, N=60, Active, not recruiting, University Health Network, Toronto | Recruiting --> Active, not recruiting | N=30 --> 60

P=N/A, N=85, Completed, University Health Network, Toronto | Active, not recruiting --> Completed

P=N/A, N=3000, Enrolling by invitation, Xiangya Hospital of Central South University

We demonstrate that TMB is dynamic and rises over time and with select treatment exposures. These findings reinforce how TMB should be interpreted within the broader context and not necessarily viewed as a standalone threshold for initiating immunotherapy in advanced prostate cancer.

The neoplastic cells could grow into the glandular lumen as HGPIN and/or spread into the duct as IDC-P or spread into the stroma as PCa. In conclusion, our data in part support the theory of intraductal carcinoma origin through retrograde glandular colonization.

Altogether, we uncovered a previously unrecognized triad of ERG-driven processes -dedifferentiation, senescence, and inflammation- that may underpin its oncogenic potential and shape PCa initiation and therapeutic response. Implications: Temporal control of ERG expression in prostate cells enabled accurate mapping of ERG-driven processes, identifying dedifferentiation, senescence, and inflammation as candidate contributors to ERG-dependent tumorigenesis and therapeutic response.