Truncation and constitutive activation of the androgen receptor by diverse genomic rearrangements in prostate cancer
Open accessAbstract
Molecularly targeted therapies for advanced prostate cancer include castration modalities that suppress ligand-dependent transcriptional activity of the androgen receptor (AR). However, persistent AR signalling undermines therapeutic efficacy and promotes progression to lethal castration-resistant prostate cancer (CRPC), even when patients are treated with potent second-generation AR-targeted therapies abiraterone and enzalutamide. Here we define diverse AR genomic structural rearrangements ( AR -GSRs) as a class of molecular alterations occurring in one third of CRPC-stage tumours. AR -GSRs occur in the context of copy-neutral and amplified AR and display heterogeneity in breakpoint location, rearrangement class and sub-clonal enrichment in tumours within and between patients. Despite this heterogeneity, one common outcome in tumours with high sub-clonal enrichment of AR -GSRs is outlier expression of diverse AR variant species lacking the ligand-binding domain and possessing ligand-independent transcriptional activity. Collectively, these findings reveal AR -GSRs as important drivers of persistent AR signalling in CRPC.
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Tumor alterations that reactivate AR signaling during treatment with an ARSI have been identified.
“We and other groups have identified tumor alterations that reactivate AR signaling during treatment with an ARSI2,22–29.”
From Genome-scale CRISPR screens identify PTGES3 as a direct modulator of androgen receptor function in advanced prostate cancer (2025) · cites this paper as [27]
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- Authors
- Henzler, C., Li, Y., Yang, R., McBride, T., Ho, Y., Sprenger, C., Liu, G., Coleman, I., Lakely, B., Li, R., Ma, S., Landman, S. R., Kumar, V., Hwang, T. H., Raj, G. V., Higano, C. S., Morrissey, C., Nelson, P. S., Plymate, S. R., & Dehm, S. M.
- Affiliations
- University of Minnesota (US)
- University of Washington (US)
- Fred Hutch Cancer Center (US)
- The University of Texas Southwestern Medical Center (US)
- Corresponding author
- Dehm, Scott M.
- ORCID
- Venue
- Nature Communications
- Published
- 2016-11-29
- Volume
- 7
- Issue
- 1
- Pages
- 13668-13668
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC5141345
- OpenAlex
- W2559738633
- Cited by
- 173
- References
- 53
- Citations by year
- 2026: 9 · 2025: 11 · 2024: 11 · 2023: 20 · 2022: 17 · 2021: 18 · 2020: 19 · 2019: 28 · 2018: 20 · 2017: 19 · 2016: 1
- FWCI
- 20.28
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- U.S. Department of Defense (W81XWH-15–1-, W81XWH1510430, W81XWH)
- U.S. Department of Veterans Affairs (I01 BX003324)
- Lucas Foundation
- University of Minnesota
- University of Washington
- National Institutes of Health (W81XWH, PO1CA163227)
- National Cancer Institute (P01CA085859, P01CA163227, P50CA097186, R01CA174777)
- National Institute of General Medical Sciences (T32GM008244)
- DOD Prostate Cancer Research Program (P50CA97186, W81XWH-15)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- androgen receptor, castration-resistant prostate cancer, truncation, constitutive activation, copy number amplification, subclonal heterogeneity, abiraterone, enzalutamide, ligand-binding domain
- MeSH terms
- Alleles, Chromosomes, Human, Pair 11, Clone Cells, Exons, Humans, Male, Neoplasm Metastasis, Receptors, Androgen, RNA, Messenger, Gene Rearrangement, Genome, Human, Gene Expression Regulation, Neoplastic, Gene Dosage, Cell Line, Tumor, Prostatic Neoplasms, Castration-Resistant
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