The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.
Castration-recurrent prostate cancer is not androgen-independent.
Abstract
An American man is diagnosed with prostate cancer (PC) every 3 min and dies from the disease every 17 min. Although androgen receptor (AR) expression is diminished following androgen deprivation therapy (ADT) that induces clinical remission in most patients, castration-recurrent PC expresses levels of AR protein similar to those found in androgen-stimulated PC and benign prostate. This observation suggests that the AR may be as important for growth regulation in castration-recurrent PC, as it is in androgen-stimulated PC and benign hyperplasia. Neither ligand-independence, point mutations, glutamine and/or glycine repeat expansion nor amplification have explained AR activation in most cases of castration-recurrent PC. Castration-recurrent PC tissue has levels of testosterone (T) similar to androgen-stimulated benign prostate and levels of dihydrotestosterone (DHT), the most active androgen for AR activation that are approximately 10% of androgen-stimulated benign prostate. These levels of tissue androgens appear capable of activating the AR since prostate-specific antigen (PSA), the classic androgen-regulated gene, is expressed at similar tissue levels in castration-recurrent and androgen-stimulated PC. These startling findings suggest a paradigm shift; PC that recurs during ADT is not androgen-independent.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“However, a paradigm shift occurred upon reports by a number of groups demonstrating that despite being surgically or chemically castrated, very low levels of androgens are still detectable in the tissues and serum of advanced patients (2,3).”
From Minireview: Alternative Activation Pathways for the Androgen Receptor in Prostate Cancer (2011) · cites this paper as [3]
Citations
Cites
Jemal, A., Siegel, R. L., Ward, E. M., Murray, T., Xu, J., Smigal, C., & Thun, M. J. (2006) · CA A Cancer Journal for Clinicians · doi:10.3322/canjclin.56.2.106 · Cited by 5,309
Huggins, C., & Hodges, C. V. (2002) · The Journal of Urology · doi:10.1016/s0022-5347(05)64820-3 · Cited by 3,856
The development of androgen-independent prostate cancer.
Feldman, B. J., & Feldman, D. (2001) · Nature reviews. Cancer · doi:10.1038/35094009 · Cited by 2,326
Molecular determinants of resistance to antiandrogen therapy
Chen, C. D., Welsbie, D. S., Tran, C., Baek, S. H., Chen, R., Vessella, R., Rosenfeld, M. G., & Sawyers, C. L. (2004) · Nature Medicine · doi:10.1038/nm972 · Cited by 2,278
In vivo amplification of the androgen receptor gene and progression of human prostate cancer
Visakorpi, T., Hyytinen, E., Koivisto, P., Tanner, M., Keinänen, R., Palmberg, C., Palotie, A., Tammela, T., Isola, J., & Kallioniemi, O.-P. (1995) · Nature Genetics · doi:10.1038/ng0495-401 · Cited by 1,484
Mutation of the Androgen-Receptor Gene in Metastatic Androgen-Independent Prostate Cancer
Taplin, M., Bubley, G. J., Shuster, T. D., Frantz, M. E., Spooner, A. E., Ogata, G. K., Keer, H. N., & Balk, S. P. (1995) · New England Journal of Medicine · doi:10.1056/nejm199505253322101 · Cited by 1,243
Stanbrough, M., Bubley, G. J., Ross, K., Golub, T. R., Rubin, M. A., Penning, T. M., Febbo, P. G., & Balk, S. P. (2006) · Cancer Research · doi:10.1158/0008-5472.can-05-4000 · Cited by 1,082
Molecular Biology of the Androgen Receptor
Gelmann, E. P. (2002) · Journal of Clinical Oncology · doi:10.1200/jco.2002.10.018 · Cited by 972
Bilateral orchiectomy with or without flutamide for metastatic prostate cancer.
Eisenberger, M. A., Blumenstein, B. A., Crawford, E. D., Miller, G., McLeod, D. G., Loehrer, P. J., Wilding, G., Sears, K., Culkin, D. J., Thompson, I. M., et al. (1998) · New England Journal of Medicine · doi:10.1056/nejm199810083391504 · Cited by 859
Amplification and overexpression of androgen receptor gene in hormone-refractory prostate cancer.
Linja, M. J., Savinainen, K., Saramäki, O. R., Tammela, T. L. J., Vessella, R. L., & Visakorpi, T. (2001) · PubMed · Cited by 762
Cited by
Sorted by citations
Androgen Signaling in Prostate CancerPreprint
Dai, C. S., Heemers, H. V., & Sharifi, N. (2017) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a030452 · Cited by 432
Schweizer, M. T., Antonarakis, E. S., Wang, H., Ajiboye, A. S., Spitz, A. N., Cao, H., Luo, J., Haffner, M. C., Yegnasubramanian, S., Carducci, M. A., et al. (2015) · Science Translational Medicine · doi:10.1126/scitranslmed.3010563 · Cited by 259
Castration-resistant Prostate Cancer: From New Pathophysiology to New Treatment Targets
Chi, K. N., Bjartell, A., Dearnaley, D. P., Fred Saad, C., Schröder, F. H., Sternberg, C., TOMBAL, B. F., & Visakorpi, T. (2009) · European Urology · doi:10.1016/j.eururo.2009.06.027 · Cited by 252
Buttigliero, C., Tucci, M., Bertaglia, V., Vignani, F., Bironzo, P., Maïo, M. D., & Scagliotti, G. V. (2015) · Cancer Treatment Reviews · doi:10.1016/j.ctrv.2015.08.002 · Cited by 198
Klotz, L. H., O’Callaghan, C. J., Ding, K., Toren, P., Dearnaley, D. P., Higano, C. S., Horwitz, E. M., Malone, S. C., Goldenberg, L., Gospodarowicz, M. K., et al. (2015) · Journal of Clinical Oncology · doi:10.1200/jco.2014.58.2973 · Cited by 168
Metadata
- Authors
- Mohler, J. L.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- Corresponding author
- Mohler, James L.
- ORCID
- Mohler, James L.
- Venue
- Advances in experimental medicine and biology
- Publisher
- Springer New York
- Published
- 2008
- Volume
- 617
- Pages
- 223-234
- ISSN
- 0065-2598 (ISSN-L)
- OpenAlex
- W202356157
- Cited by
- 106
- References
- 57
- Citations by year
- 2025: 1 · 2024: 1 · 2023: 3 · 2022: 3 · 2021: 3 · 2020: 3 · 2019: 4 · 2018: 4 · 2017: 4 · 2016: 9 · 2015: 9 · 2014: 9 · 2013: 15 · 2012: 8
- FWCI
- 62.53
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Advances in experimental medicine and biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Prostate Cancer Treatment and Research
- Health Sciences › Medicine › Urology › Prostate Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal and reproductive studies
- Keywords
- castration-resistant prostate cancer, recurrent prostate cancer, androgen receptor, androgen-independent growth, androgen deprivation therapy, dihydrotestosterone, testosterone, prostate-specific antigen, androgen receptor activation, benign prostatic hyperplasia
- MeSH terms
- Androgens, Humans, Male, Neoplasm Recurrence, Local, Neoplasms, Hormone-Dependent, Orchiectomy, Prostatic Neoplasms, Receptors, Androgen
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
