Androgen Receptor Pathway-Independent Prostate Cancer Is Sustained through FGF Signaling
Open accessAbstract
Androgen receptor (AR) signaling is a distinctive feature of prostate carcinoma (PC) and represents the major therapeutic target for treating metastatic prostate cancer (mPC). Though highly effective, AR antagonism can produce tumors that bypass a functional requirement for AR, often through neuroendocrine (NE) transdifferentiation. Through the molecular assessment of mPCs over two decades, we find a phenotypic shift has occurred in mPC with the emergence of an AR-null NE-null phenotype. These "double-negative" PCs are notable for elevated FGF and MAPK pathway activity, which can bypass AR dependence. Pharmacological inhibitors of MAPK or FGFR repressed the growth of double-negative PCs in vitro and in vivo. Our results indicate that FGF/MAPK blockade may be particularly efficacious against mPCs with an AR-null phenotype.
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The vast majority of mCRPC samples from patients resistant to abiraterone and enzalutamide exhibit robust AR/nuclear AR staining.
“Recent analyses of clinical samples have demonstrated that the vast majority of mCRPC samples from patients resistant to ARSI agents abiraterone and enzalutamide exhibit robust AR/nuclear AR staining20,21.”
From Genome-scale CRISPR screens identify PTGES3 as a direct modulator of androgen receptor function in advanced prostate cancer (2025) · cites this paper as [21]
The Discussion (page not provided) says resistance to AR-directed therapy is usually accompanied by reactivation of AR signaling. But the Results (page not provided) give the 85% AR-active figure for tumors collected before enzalutamide and abiraterone were approved; they do not establish that the vast majority of samples from patients resistant to those drugs have robust AR or nuclear AR staining. (LLM, conf=0.82)
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- Authors
- Bluemn, E. G., Coleman, I. M., Lucas, J. M., Coleman, R. T., Hernandez-Lopez, S., Tharakan, R., Bianchi-Frias, D., Dumpit, R. F., Kaipainen, A., Corella, A. N., Yang, Y. C., Nyquist, M. D., Mostaghel, E., Hsieh, A. C., Zhang, X., Corey, E., Brown, L. G., Nguyen, H. M., Pienta, K., Ittmann, M., Schweizer, M., True, L. D., Wise, D., Rennie, P. S., Vessella, R. L., Morrissey, C., & Nelson, P. S.
- Affiliations
- University of Washington (US)
- Fred Hutch Cancer Center (US)
- Johns Hopkins University (US)
- Baylor College of Medicine (US)
- Memorial Sloan Kettering Cancer Center (US)
- Vancouver Prostate Centre (CA)
- Corresponding author
- Morrissey, Colm
- Nelson, Peter S.
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 32
- Issue
- 4
- Pages
- 474-489.e6
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC5750052
- OpenAlex
- W2762381618
- Cited by
- 744
- References
- 70
- Citations by year
- 2026: 73 · 2025: 96 · 2024: 96 · 2023: 102 · 2022: 84 · 2021: 96 · 2020: 73 · 2019: 69 · 2018: 53 · 2017: 2
- FWCI
- 44.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 373 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- NIH (P50CA097186, P01 CA163227)
- DOD (PC140794, PC160662)
- DF/HCC Mazzone
- Institute for Prostate Cancer Research
- Richard M. Lucas Foundation
- Movember
- Prostate Cancer Foundation
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Treatment and Research
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Prostate Cancer Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Keywords
- androgen receptor signaling, prostate cancer, metastatic prostate cancer, FGF signaling, MAPK signaling, FGFR inhibitors, MAPK inhibitors, neuroendocrine transdifferentiation, treatment resistance
- MeSH terms
- Androgen Antagonists, Animals, Cell Differentiation, Fibroblast Growth Factors, Humans, Male, Neoplasm Metastasis, Prostatic Neoplasms, Receptors, Androgen, Signal Transduction, Receptors, Fibroblast Growth Factor, MAP Kinase Signaling System, Cell Line, Tumor, Mice, Inhibitor of Differentiation Protein 1
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