Prostate Cancer

P=N/A, N=90, Recruiting, Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins | Not yet recruiting --> Recruiting

P2, N=4, Completed, Weill Medical College of Cornell University | Recruiting --> Completed

TAK-931 treated prostate cancer cells exhibit an abnormal cell cycle profile, suggesting that CDC7 inhibition induces replication stress and promotes apoptosis. Collectively, our findings demonstrate that CDC7 is a regulator of tumor progression in prostate cancer and represents new therapeutic target in advanced prostate cancer.

[68Ga]Ga-OncoACP3-DOTA changed therapeutic management in three of six patients with biochemical recurrence, and in two of 12 patients with known metastases. Although the retrospective comparison is potentially biased, the intense and reliable tumor uptake and the low off-target activity of OncoACP3-DOTA provide a strong rationale for future exploration in trials on PET imaging and radioligand therapy with β- and α-particle emitters.

Although multiple factors can influence symptom severity, genetic variation may play a part. The early identification of men likely to develop severe symptoms during the course of their prostate cancer could theoretically enable symptoms to be managed more aggressively from an early stage. These preliminary findings need to be replicated in a larger cohort of men with CRPC.

In cancer therapy, cisplatin not only amplifies ROS-induced DNA damage but also, as a widely utilized chemotherapeutic agent, induces nuclear DNA (nDNA) lesions via interstrand/intrastrand crosslinking with DNA and disruption of repair mechanisms...This dual-damage strategy overcomes penetration barriers and immunogenic "cold" tumor limitations, achieving robust anti-tumor efficacy in prostate cancer models. Our work not only deciphers the mechanistic interplay of Fe3O4/AIPH/DDP@PLGA as a biomimetic AIM2 activator but also pioneers a transformative paradigm for solid tumor immunotherapy through controlled radical amplification and PANoptosis induction.

P2, N=100, Recruiting, University of Washington | Trial completion date: Jul 2031 --> Jul 2033 | Trial primary completion date: Jul 2026 --> Jul 2028

P1/2, N=292, Active, not recruiting, ImCheck Therapeutics | Trial completion date: Dec 2025 --> Oct 2026 | Trial primary completion date: Sep 2025 --> Oct 2026

P=N/A, N=330, Recruiting, Fujian Medical University Union Hospital | N=664 --> 330

P2, N=250, Not yet recruiting, AHS Cancer Control Alberta

The model also offered robust stratification for patients based on BCR-free survival probability. Our findings underscore the potential of radiogenomic signatures as non-invasive biomarkers to personalized PCa RT decisions and provide a novel clinically explainable predictive model based on radiomic and molecular biomarkers for BCR-free survival and TR of mentioned cancer.