ArticleThe Journal of clinical investigation2022
Androgen receptor activity in prostate cancer dictates efficacy of bipolar androgen therapy through MYC.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
34 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Efficacy and safety of bipolar androgen therapy in castration-resistant prostate cancer following abiraterone or enzalutamide resistance: A systematic review.Frontiers in endocrinology · 2022Pooled it
- Bipolar androgen therapy plus nivolumab for patients with metastatic castration-resistant prostate cancer: the COMBAT phase II trial.Nature communications · 2024Trial
- Development of XYD113 as a potent and highly selective GSPT1 degrader for cancer therapy.Acta pharmacologica Sinica · 2026Article
- HLA Class I Expression Is Associated with Increased Immune Cell Density and PTEN Loss in Prostate Cancer.Molecular cancer research : MCR · 2026Article
- Castration Resistance Accelerates Prostate Cancer Kinetics.The Prostate · 2026Article
- Androgen Receptor Drives Polyamine Synthesis, Creating a Vulnerability for Prostate Cancer.Cancer research · 2026Article
- Emerging therapies to overcome antiandrogen resistance and beyond in lethal prostate cancer.Journal of the National Cancer Center · 2026Review
- Bipolar androgen therapy as platform for personalized medicine in castration-resistant prostate cancer.Discover oncology · 2026Article
- PCAT1 Supports Partial AR-V7 Function and Promotes Enzalutamide Resistance in Prostate Cancer.International journal of general medicine · 2026Article
- Precision Medicine in Prostate Cancer with a Focus on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- The intricate interplay between circadian rhythm, androgen signaling, hormone therapy, and cellular senescence in prostate cancer.Cancer metastasis reviews · 2025Review
- New frontiers in prostate cancer treatment from systemic therapy to targeted therapy.EMBO molecular medicine · 2025Review
- Reprogramming of Androgen Receptor Activity in Castration-resistant Prostate Cancer is Shaped by Truncated Variants.European urology focus · 2025Article
- PSA/testosterone ratio as a potential biomarker to identify early progressors of adaptive therapy in metastatic castration sensitive prostate cancer.medRxiv : the preprint server for health sciences · 2025Article
- Polyamine metabolism in prostate cancer.Current opinion in oncology · 2025Review
- Advances in the application of PD-1/PD-L1 immunotherapy for prostate cancer: a review.Frontiers in immunology · 2025Review
- Apolipoprotein E promotes primary resistance to AR-targeted therapy via inducing TRIM25-mediated AR ubiquitination and sensitizes immunotherapy in prostate cancer.Theranostics · 2025Article
- Targeted Therapy in Salivary Gland Cancer: Prevalence of a Selected Panel of Actionable Molecular Alterations in a German Tertiary Referral Center Patient Cohort.Molecular diagnosis & therapy · 2025Article
- Challenges and opportunities for the diverse substrates of SPOP E3 ubiquitin ligase in cancer.Theranostics · 2025Review
- GG-NER's role in androgen receptor signaling inhibitor response for advanced prostate cancer.Cell communication and signaling : CCS · 2024Article
Corrections and comments
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Authors and funding
25 authors at 1 institution in 1 country.
Funding
Abstract
Testosterone is the canonical growth factor of prostate cancer but can paradoxically suppress its growth when present at supraphysiological levels. We have previously demonstrated that the cyclical administration of supraphysiological androgen (SPA), termed bipolar androgen therapy (BAT), can result in tumor regression and clinical benefit for patients with castration-resistant prostate cancer. However, predictors and mechanisms of response and resistance have been ill defined. Here, we show that growth inhibition of prostate cancer models by SPA required high androgen receptor (AR) activity and were driven in part by downregulation of MYC. Using matched sequential patient biopsies, we show that high pretreatment AR activity predicted downregulation of MYC, improved clinical response, and prolonged progression-free and overall survival for patients on BAT. BAT induced strong downregulation of AR in all patients, which is shown to be a primary mechanism of acquired resistance to SPA. Acquired resistance was overcome by alternating SPA with the AR inhibitor enzalutamide, which induced adaptive upregulation of AR and resensitized prostate cancer to SPA. This work identifies high AR activity as a predictive biomarker of response to BAT and supports a treatment paradigm for prostate cancer involving alternating between AR inhibition and activation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.