AR splice variant 7

Pharmacokinetic parameters indicate that α-mangostin is well tolerated and safe in both preclinical and human clinical trials. In summary, understanding the mechanism of action and identifying direct molecular target of α-mangostin is important for development of novel anti-cancer agents and further clinical studies are required to evaluate its efficacy in chemotherapy.

Ili-A inhibited RORC expression, increased malondialdehyde (MDA) content, suppressed glutathione (GSH) production, released free Fe2+, increased reactive oxygen species (ROS), activated the ferroptosis pathway, enhanced enzalutamide sensitivity, and inhibited CRPC cell proliferation. Furthermore, ili-A enhances the interaction between ROR-γ and GPX4.

Advances in screening platforms and the optimization of structure-activity relationships are beginning to address the challenges of targeting disordered protein domains. With agents like EPI-7386 entering clinical evaluation and others advancing through preclinical development, AR NTD-targeted therapies represent a promising avenue to overcome resistance in castration-resistant prostate cancer (CRPC), potentially in combination with existing LBD-directed treatments to achieve more durable disease control.

Ferroptosis-induced immunogenic cell death enables synergy with checkpoint inhibitors, potentially transforming immunologically "cold" prostate tumors. This review establishes ferroptosis targeting as a precision medicine paradigm exploiting the tension between the oxidative requirements of cancer cells and their evolved, yet architecturally vulnerable, defense systems, providing a framework for stage-specific, biomarker-guided interventions.

These findings uncover novel roles for KHDRBS2 and KHDRBS3 in PCa progression, with KHDRBS2 identified as a potential key regulator of AR-V7 expression. Our results provide new insights into AR splice variant regulation and highlight potential therapeutic targets for PCa treatment.

Lutetium-177-PSMA-617 has become the standard radioligand therapy for metastatic castration-resistant prostate cancer, whereas alpha-emitting agents remain under clinical investigation...Integrative models combining imaging, genomic, and liquid biopsy data pave the way toward precision oncology and personalized therapeutic decision-making. Advances in imaging and theragnostics are reshaping prostate cancer management, bridging the gap between molecular biology and clinical practice to enable precision oncology.

Of the thirty-two unique ARVs detected, only AR-V7 (present in 14% of patients) was associated with outcomes after salvage RT+ADT (HR for second biochemical failure, 6.2, 95% CI 2.3-16.5, p=0.0003). These results suggest for the first time that AR-V7 may modulate outcomes for localized in addition to metastatic prostate cancer.

We further show that TRACERs can be modularly reprogrammed to recruit alternative repressors, including PRC2. Collectively, these findings establish TRACERs as a generalizable modality to pharmacologically silence undruggable transcription factors through targeted epigenetic reprogramming, offering a powerful new strategy for treating cancers refractory to existing therapies.

We found no association with prostate cancer outcomes. However, in the group of patients whose PSA became undetectable after treatment, a CTC increase after chemotherapy identified men with a higher risk of cancer progression and death.

In CRPC and enzalutamide-resistant models, ITRI-148 robustly suppresses AR signaling and inhibits cell viability, outperforming enzalutamide...In vivo, ITRI-148 demonstrates potent antitumor efficacy in both castrated and hormone-intact CRPC models, supported by favorable pharmacokinetic properties, stability and safety profiles. These findings position ITRI-148 as a promising next-generation AR-targeting agent capable of degrading resistant AR variants and providing durable inhibition of AR signaling in advanced prostate cancer.

This consensus offers practical guidance for clinical integration of CTCs and outlines strategic research priorities to unlock their full potential in precision oncology.

SCAMP3 and EPS8 cooperatively maintain EGFR stability and signaling in prostate cancer cells, playing a critical role in enzalutamide resistance and metastatic progression. Targeting the SCAMP3-EPS8-EGFR axis offers promising therapeutic opportunities for advanced prostate cancer.