Prostate Cancer

P=N/A, N=90, Recruiting, Vejle Hospital | Not yet recruiting --> Recruiting

P=N/A, N=100, Suspended, University of Arizona | Trial completion date: Sep 2027 --> Nov 2028 | Trial primary completion date: Sep 2026 --> Nov 2027

P2, N=58, Active, not recruiting, OHSU Knight Cancer Institute | Trial completion date: Jun 2025 --> Jun 2026

P=N/A, N=600, Completed, Wake Forest University Health Sciences | Active, not recruiting --> Completed

P=N/A, N=852, Active, not recruiting, ECOG-ACRIN Cancer Research Group | Trial completion date: Dec 2025 --> Aug 2026 | Trial primary completion date: Dec 2025 --> Aug 2026

P1, N=80, Recruiting, ARTBIO Inc. | Trial completion date: Sep 2033 --> Nov 2028

Our study demonstrates that CHD1L is markedly upregulated in prostate cancer and contributes to tumor progression. Pharmacological inhibition of CHD1L with the selective inhibitor OTI-611 significantly suppresses proliferation, migration, and invasion, while inducing apoptosis in vitro and in vivo. Mechanistically, these effects are mediated through activation of the FOXO3-PUMA axis, as FOXO3 suppression abrogates OTI-611-induced apoptosis. Moreover, OTI-611 exhibits strong synergy with docetaxel, enhancing apoptotic cell death and providing a potential strategy to improve therapeutic efficacy in prostate cancer.

AA induces ER stress, leading to transcriptional downregulation of the AR and suppression of PCa cell viability and proliferation. Targeting the PERK pathway may enhance AA efficacy in AR-driven PCa.

In this study, we propose that an AREG-based signature comprising ACSM3, ACTG2, and DES effectively predicts prognosis and reflects immune microenvironment characteristics in PRAD. Through systematic analysis, we established a prognostic model utilizing these three AREGs, which demonstrates strong potential as a clinical predictor for PRAD patient outcomes.

LNCaP and VCaP cells were treated with enzalutamide (0.1-10 µM) for 1-7 days...Crucially, ER stress markers correlated with PSMA trafficking, suggesting serum-based profiling could enable individualized ARB adjustments. Future studies should validate these biomarkers to establish personalized ARB-RLT strategies for improved clinical outcomes.

In this study, we demonstrated that prolonged exposure of the lungs to submicron silica particles can induce alterations in lipid metabolism in PCa and significantly enhance the proliferation and invasive capacity of PCa cells. Consequently, elucidating the mechanisms underlying silica-induced metabolic imbalance holds substantial clinical significance for enhancing the prognosis of patients with tumors related to exposure.

P=N/A, N=15, Recruiting, Brigham and Women's Hospital | Trial completion date: Aug 2024 --> Jun 2026 | Trial primary completion date: May 2024 --> Jun 2026