The DOI matches its Crossref record; 419 of the 419 references it cites were found in a registry or an index.
Androgen Receptor in Prostate Cancer
Abstract
The normal development and maintenance of the prostate is dependent on androgen acting through the androgen receptor (AR). AR remains important in the development and progression of prostate cancer. AR expression is maintained throughout prostate cancer progression, and the majority of androgen-independent or hormone refractory prostate cancers express AR. Mutation of AR, especially mutations that result in a relaxation of AR ligand specificity, may contribute to the progression of prostate cancer and the failure of endocrine therapy by allowing AR transcriptional activation in response to antiandrogens or other endogenous hormones. Similarly, alterations in the relative expression of AR coregulators have been found to occur with prostate cancer progression and may contribute to differences in AR ligand specificity or transcriptional activity. Prostate cancer progression is also associated with increased growth factor production and an altered response to growth factors by prostate cancer cells. The kinase signal transduction cascades initiated by mitogenic growth factors modulate the transcriptional activity of AR and the interaction between AR and AR coactivators. The inhibition of AR activity through mechanisms in addition to androgen ablation, such as modulation of signal transduction pathways, may delay prostate cancer progression.
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In the citing paper
“Upon androgen stimulation, AR translocates into the nucleus, binds to genomic androgen response elements and modulates gene expression of target genes40.”
From Genome-scale CRISPR screens identify PTGES3 as a direct modulator of androgen receptor function in advanced prostate cancer (2025) · cites this paper as [40]
In the citing paper
“The unliganded AR primarily exists in the cytoplasm in a complex with heat shock protein 90 (Hsp90, and tetratricopeptide repeat (TPR) proteins (FK506-binding proteins, FKBP52 and FKBP51, and cyclosporin A-binding protein, Cyp40) (Febbo et al., 2005; Heinlein and Chang, 2004; Periyasamy et al., 2007; Veldscholte et al., 1992a; Veldscholte et al., 1992b).”
From FKBP51 and Cyp40 are positive regulators of androgen-dependent prostate cancer cell growth and the targets of FK506 and cyclosporin A (2010) · cites this paper as Heinlein and Chang, 2004
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Items 401–419 of 419
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Hu, R., Dunn, T. A., Wei, S., Isharwal, S., Veltri, R. W., Humphreys, E., Han, M., Partin, A. W., Vessella, R. L., Isaacs, W. B., et al. (2009) · Cancer Research · doi:10.1158/0008-5472.can-08-2764 · Cited by 1,077
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Interaction of Nuclear Receptors with the Wnt/β-Catenin/Tcf Signaling Axis: Wnt You Like to Know?
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Metadata
- Authors
- Heinlein, C. A., & Chang, C.
- Affiliations
- University of Rochester Medicine (US)
- ORCID
- Chang, Chawnshang
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2004-04-01
- Volume
- 25
- Issue
- 2
- Pages
- 276-308
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- OpenAlex
- W2064293531
- Cited by
- 1,780
- References
- 419
- Citations by year
- 2026: 33 · 2025: 66 · 2024: 69 · 2023: 101 · 2022: 81 · 2021: 99 · 2020: 84 · 2019: 81 · 2018: 71 · 2017: 94 · 2016: 87 · 2015: 93 · 2014: 104 · 2013: 95 · 2012: 88
- FWCI
- 11.47
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Endocrine Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 60948, R01DK060948, R01DK060905, DK60905)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Prostate Cancer Treatment and Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Health Sciences › Medicine › Urology › Prostate Cancer Diagnosis and Treatment
- Keywords
- androgen receptor, prostate cancer, castration-resistant prostate cancer, androgen receptor mutations, ligand specificity, growth factor signaling, endocrine therapy resistance, androgen deprivation therapy, prostate development
- MeSH terms
- Androgen Antagonists, Androgens, Animals, Cell Division, Growth Substances, Humans, Male, Mutation, Prostate, Prostatic Neoplasms, Receptors, Androgen, Repetitive Sequences, Nucleic Acid, Transcription, Genetic, Gene Expression, Genes, Tumor Suppressor, Apoptosis, Prostate-Specific Antigen
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