Prostate Cancer

P2, N=19, Completed, Dana-Farber Cancer Institute | Active, not recruiting --> Completed | Trial completion date: Apr 2026 --> Nov 2025

P2, N=42, Recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2028 --> Dec 2031 | Trial primary completion date: Dec 2027 --> Dec 2030

P=N/A, N=500, Active, not recruiting, Guangxi Medical University | Not yet recruiting --> Active, not recruiting

P=N/A, N=300, Active, not recruiting, University of Pennsylvania | Trial completion date: Aug 2026 --> Dec 2026 | Trial primary completion date: May 2026 --> Oct 2026

These results provide mechanistic information on skeletal metastasis in orthopedic oncology. Dedicated bone metastasis models need to be evaluated.

The developed prognostic model holds clinical relevance, and the identified natural products offer a foundation for designing interventions to potentially mitigate PFAS-associated carcinogenic effects, advancing both mechanistic understanding and preventive strategies. However, the findings are primarily based on computational predictions and a single cell line; further validation in multiple models and experimental systems is required.

GOLPH3, which is overexpressed in PRAD, may enhance glucose metabolic activity in PRAD cells in association with activation of the PI3K/AKT/mTOR pathway, thereby supporting PRAD cell proliferation. These findings provide basic mechanistic evidence for the role of GOLPH3 in PRAD cell metabolism, but further clinical studies are required to determine its prognostic or therapeutic relevance.

It exhibited potent antiproliferative effects on prostate cancer cells. These results indicate that BMX-PROTACs are potential therapeutic candidates for prostate cancer.

The findings indicated that DEHP can influence the development of PCarelated pathways through targeting specific genes and signaling, exhibiting the potential to serve as a biomarker to assess the risk of PCa related to DEHP exposure.

P-PSMA-101 is a first-in-class, stem cell memory T cell-enriched, PSMA-targeting CAR-T therapy. This cellular therapy showed notable clinical activity in two patients; however, PSA50 responses were generally modest. While severe immune effector-related toxicities were observed in some patients, a novel iCasp9 safety switch was largely effective in mitigating toxicity.

In contrast, the distribution pattern of SET oncoprotein immunolabelling was relatively consistent across tumour types, with no statistically significant differences observed. Melanoma, mammary carcinoma, squamous cell carcinoma, prostatic carcinoma, osteosarcoma and transmissible venereal tumour showed the highest immunolabelling intensity patterns, highlighting the importance of SET oncoprotein as a potential therapeutic target and paving the way for future studies on its use in personalized therapy.

P1/2, N=129, Completed, Orion Corporation | Active, not recruiting --> Completed