The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Androgen receptor: A key molecule in the progression of prostate cancer to hormone independence
Abstract
Despite earlier detection and recent advances in surgery and radiation, prostate cancer is second only to lung cancer in male cancer deaths in the United States. Hormone therapy in the form of medical or surgical castration remains the mainstay of systemic treatment in prostate cancer. Over the last 15 years with the clinical use of prostate specific antigen (PSA), there has been a shift to using hormone therapy earlier in the disease course and for longer duration. Despite initial favorable response to hormone therapy, over a period of time these tumors will develop androgen‐independence that results in death. The androgen receptor (AR) is central to the initiation and growth of prostate cancer and to its response to hormone therapy. Analyses have shown that AR continues to be expressed in androgen‐independent tumors and AR signaling remains intact as demonstrated by the expression of the AR regulated gene, PSA. Androgen‐independent prostate cancers have demonstrated a variety of AR alterations that are either not found in hormone naïve tumors or found at lower frequency. These changes include AR amplification, AR point mutation, and changes in expression of AR co‐regulatory proteins. These AR changes result in a “super AR” that can respond to lower concentrations of androgens or to a wider variety of agonistic ligands. There is also mounting evidence that AR can be activated in a ligand independent fashion by compounds such as growth factors or cytokines working independently or in combination. These growth factors working through receptor tyrosine kinase pathways may promote AR activation and growth in low androgen environments. The clinical significance of these AR alterations in the development and progression of androgen‐independent prostate cancer remains to be determined. Understanding the changes in AR signaling in the evolution of androgen‐independent prostate cancer will be key to the development of more effective hormone therapy. © 2003 Wiley‐Liss, Inc.
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Cites
In vivo amplification of the androgen receptor gene and progression of human prostate cancer
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Androgen Receptor (AR) Coregulators: An Overview
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“Laboratory AR constructs containing deletions in the hormone-binding domain are constitutively active [Jenster et al., 1991], however, these types of AR deletion mutations have not been found in human prostate cancers and will not be discussed further.”
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“AR gene amplification has been reported in 25–30% of androgen-independent prostate cancer [Visakorpi et al., 1995; Koivisto et al., 1997; Miyoshi et al., 2000; Linja et al., 2001].”
Background
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Development of a second-generation antiandrogen for treatment of advanced prostate cancer.
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Testosterone and Dihydrotestosterone Tissue Levels in Recurrent Prostate Cancer
Titus, M. A., Schell, M. J., Lih, F. B., Tomer, K. B., & Mohler, J. L. (2005) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-05-0525 · Cited by 488
Schaufele, F., Carbonell, X., Guerbadot, M., Borngraeber, S., Chapman, M. S., Ma, A. A. K., Miner, J. N., & Diamond, M. I. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0408819102 · Cited by 208
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Seaton, A., Scullin, P., Maxwell, P. J., Wilson, C., Pettigrew, J., Gallagher, R., O'Sullivan, J. M., Johnston, P. G., & Waugh, D. J. J. (2008) · Carcinogenesis · doi:10.1093/carcin/bgn109 · Cited by 143
Ai, J., Wang, Y., Dar, J. A., Liu, J., Liu, L., Nelson, J. B., & Wang, Z. (2009) · Molecular Endocrinology · doi:10.1210/me.2009-0188 · Cited by 126
Castration-recurrent prostate cancer is not androgen-independent.
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The novel role of pyrvinium in cancer therapy
Momtazi‐borojeni, A. A., Abdollahi, E., Ghasemi, F., Caraglia, M., & Sahebkar, A. (2018) · Journal of Cellular Physiology · doi:10.1002/jcp.26006 · Cited by 75
Ishiguro, H., Akimoto, K., Nagashima, Y., Kojima, Y., Sasaki, T., Ishiguro-Imagawa, Y., Nakaigawa, N., Ohno, S., Kubota, Y., & Uemura, H. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0907044106 · Cited by 74
Ligand-independent activation of androgen receptors by Rho GTPase signaling in prostate cancer.
Lyons, L. S., Rao, S., Balkan, W., Faysal, J., Maiorino, C. A., & Burnstein, K. L. (2008) · Molecular Endocrinology · doi:10.1210/me.2007-0158 · Cited by 67
Gauthier-Landry, L., Bélanger, A., & Barbier, O. (2015) · The Journal of Steroid Biochemistry and Molecular Biology · doi:10.1016/j.jsbmb.2014.05.009 · Cited by 62
Metadata
- Authors
- Taplin, M., & Balk, S. P.
- Venue
- Journal of Cellular Biochemistry
- Publisher
- Wiley
- Published
- 2003-10-08
- Volume
- 91
- Issue
- 3
- Pages
- 483-190
- ISSN
- 0730-2312 (ISSN-L)
- 1097-4644
- OpenAlex
- W1974810481
- Cited by
- 390
- References
- 5
- FWCI
- 18.26
- Type
- journal article
- Language
- en
- Open access
- closed
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