The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Androgen Receptor Signaling in Androgen-Refractory Prostate Cancer
Abstract
Prostate cancer is the second most prevalent cancer in males in the United States. Standard therapy relies on removing, or blocking the actions of, androgens. In most cases, this therapy results in a regression of the cancer because the prostate and most primary prostate tumors depend on androgens for growth and the avoidance of apoptosis. However, a portion of the cancers eventually relapse, at which point they are termed "androgen refractory" and can no longer be cured by conventional therapy of any type. The precise molecular events that lead from androgen-sensitive prostate cancer to androgen-refractory prostate cancer are, therefore, of great interest. This review seeks to identify specific molecular events that may be linked directly to the progression to androgen-refractory cancer. Some of the mechanisms appear to involve the androgen receptor (AR) directly and include mutations in, or amplification of, the AR gene in a manner that allows the AR to respond to low doses of androgens, other steroids, or antiandrogens. In a less direct manner, coactivators may increase the sensitivity of the AR to androgens and even other nonandrogenic substances through a number of mechanisms. Additional indirect mechanisms that do not result from mutation of the AR may involve activation of the AR by peptide growth factors or cytokines or may involve bypassing the AR entirely via other cellular pathways. Identification of the role of these mechanisms in the progression to androgen-refractory prostate cancer is critical for developing therapies capable of curing this disease.
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In vivo amplification of the androgen receptor gene and progression of human prostate cancer
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A Controlled Trial of Leuprolide with and without Flutamide in Prostatic Carcinoma
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Cited by
Increased Survival with Enzalutamide in Prostate Cancer after Chemotherapy
Scher, H. I., Fizazi, K., Saad, F., Taplin, M.-E., Sternberg, C. N., Miller, K., de Wit, R., Mulders, P., Chi, K. N., Shore, N. D., et al. (2012) · New England Journal of Medicine · doi:10.1056/nejmoa1207506 · Cited by 4,586
Androgen Receptor in Prostate Cancer
Heinlein, C. A., & Chang, C. (2004) · Endocrine Reviews · doi:10.1210/er.2002-0032 · Cited by 1,780
Scher, H. I., & Sawyers, C. L. (2005) · Journal of Clinical Oncology · doi:10.1200/jco.2005.03.4777 · Cited by 1,025
Targeting ligand-activated ErbB2 signaling inhibits breast and prostate tumor growth
Agus, D. B., Akita, R. W., Fox, W. D., Lewis, G. D., Higgins, B., Pisacane, P. I., Lofgren, J. A., Tindell, C., Evans, D. P., Maiese, K., et al. (2002) · Cancer Cell · doi:10.1016/s1535-6108(02)00097-1 · Cited by 873
Heemers, H. V., & Tindall, D. J. (2007) · Endocrine Reviews · doi:10.1210/er.2007-0019 · Cited by 753
Self-citation
Metadata
- Authors
- Grossmann, M. E., Huang, H., & Tindall, D. J.
- Venue
- JNCI Journal of the National Cancer Institute
- Publisher
- Oxford University Press (OUP)
- Published
- 2001-11-21
- Volume
- 93
- Issue
- 22
- Pages
- 1687-1697
- ISSN
- 0027-8874 (ISSN-L)
- 1460-2105
- OpenAlex
- W2103177037
- Cited by
- 548
- References
- 7
- FWCI
- 25.92
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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