Cited by 744Prostate Cancer Treatment and ResearchProstate Cancer Diagnosis and TreatmentCancer, Lipids, and Metabolism

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Androgen Receptor Pathway-Independent Prostate Cancer Is Sustained through FGF Signaling

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Bluemn, Eric G., Coleman, Ilsa M., Lucas, Jared M., Coleman, Roger T., Hernandez-Lopez, Susana, Tharakan, Robin, Bianchi-Frias, Daniella, Dumpit, Ruth F., Kaipainen, Arja, Corella, Alexandra N., Yang, Yu Chi, Nyquist, Michael D., Mostaghel, Elahe, Hsieh, Andrew C., Zhang, Xiaotun, Corey, Eva, Brown, Lisha G., Nguyen, Holly M., Pienta, Kenneth, Ittmann, Michael, Schweizer, Michael, True, Lawrence D., Wise, David, Rennie, Paul S., Vessella, Robert L., Morrissey, Colm, Nelson, Peter S.·2017·Cancer Cell

DOI 10.1016/j.ccell.2017.09.003PMC PMC5750052

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Abstract

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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Background
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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: Coleman, Ilsa M.
Lucas, Jared M.
Dumpit, Ruth F.
Kaipainen, Arja
Corella, Alexandra N.
Yang, Yu Chi
Nyquist, Michael D.
Mostaghel, Elahe
Hsieh, Andrew C.
Corey, Eva
Brown, Lisha G.
Nguyen, Holly M.
Pienta, Kenneth
Ittmann, Michael
Schweizer, Michael
True, Lawrence D.
Wise, David
Morrissey, Colm
Nelson, Peter S.
Venue: Cancer Cell
Publisher: Elsevier BV
Published: 2017-10
Volume: 32
Issue: 4
Pages: 474-489.e6
ISSN: 1535-6108 (ISSN-L)
DOI: 10.1016/j.ccell.2017.09.003
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: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Prostate Cancer Treatment and Research
Health Sciences › Medicine › Urology › 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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Androgen Receptor Pathway-Independent Prostate Cancer Is Sustained through FGF Signaling

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