The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
AR, the cell cycle, and prostate cancer
Open accessAbstract
The androgen receptor (AR) is a critical effector of prostate cancer development and progression. The dependence of this tumor type on AR activity is exploited in treatment of disseminated prostate cancers, wherein ablation of AR function (achieved either through ligand depletion and/or the use of AR antagonists) is the first line of therapeutic intervention. These strategies are initially effective, and induce a mixed response of cell cycle arrest or apoptosis in prostate cancer cells. However, recurrent, incurable tumors ultimately arise as a result of inappropriately restored AR function. Based on these observations, it is imperative to define the mechanisms by which AR controls cancer cell proliferation. Mechanistic investigation has revealed that AR acts as a master regulator of G1-S phase progression, able to induce signals that promote G1 cyclin-dependent kinase (CDK) activity, induce phosphorylation/inactivation of the retinoblastoma tumor suppressor (RB), and thereby govern androgen-dependent proliferation. These functions appear to be independent of the recently identified TMPRSS2-ETS fusions. Once engaged, several components of the cell cycle machinery actively modulate AR activity throughout the cell cycle, thus indicating that crosstalk between the AR and cell cycle pathways likely modulate the mitogenic response to androgen. As will be discussed, discrete aberrations in this process can alter the proliferative response to androgen, and potentially subvert hormonal control of tumor progression.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
The nuclear receptor superfamily: the second decade
Mangelsdorf, D. J., Thummel, C., Beato, M., Herrlich, P., Schütz, G., Umesono, K., Blumberg, B., Kastner, P., Mark, M., Chambon, P., et al. (1995) · Cell · doi:10.1016/0092-8674(95)90199-x · Cited by 6,964
Sherr, C. J. (1996) · Science · doi:10.1126/science.274.5293.1672 · Cited by 5,379
Recurrent Fusion of TMPRSS2 and ETS Transcription Factor Genes in Prostate Cancer
Tomlins, S. A., Rhodes, D. R., Perner, S., Dhanasekaran, S. M., Mehra, R., Sun, X.-W., Varambally, S., Cao, X., Tchinda, J., Kuefer, R., et al. (2005) · Science · doi:10.1126/science.1117679 · Cited by 3,846
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
Androgen Receptor in Prostate Cancer
Heinlein, C. A., & Chang, C. (2004) · Endocrine Reviews · doi:10.1210/er.2002-0032 · Cited by 1,780
New functional activities for the p21 family of CDK inhibitors.
LaBaer, J., Garrett, M. D., Stevenson, L. F., Slingerland, J. M., Sandhu, C., Chou, H. S., Fattaey, A., & Harlow, E. (1997) · Genes & Development · doi:10.1101/gad.11.7.847 · Cited by 1,402
HDAC6 Regulates Hsp90 Acetylation and Chaperone-Dependent Activation of Glucocorticoid Receptor
Kovacs, J. J., Murphy, P. J. M., Gaillard, S., Zhao, X., Wu, J.-T., Nicchitta, C. V., Yoshida, M., Toft, D. O., Pratt, W. B., & Yao, T.-P. (2005) · Molecular Cell · doi:10.1016/j.molcel.2005.04.021 · Cited by 1,153
Cheng, M., Olivier, P., Diehl, J. A., Fero, M., Roussel, M. F., Roberts, J. M., & Sherr, C. J. (1999) · The EMBO Journal · doi:10.1093/emboj/18.6.1571 · Cited by 1,142 · cited 2×
“This classification may be overly simplistic, as while p21Cip1 can inhibit CDK2 complexes, p21Cip1 is conversely important for promoting formation, activation and nuclear enrichment of CDK4/6-cyclin D complexes [Alt et al., 2002; Cheng et al., 1999; LaBaer et al., 1997; Sherr and Roberts, 1999].”
Living with or without cyclins and cyclin-dependent kinases
Sherr, C. J., & Roberts, J. M. (2004) · Genes & Development · doi:10.1101/gad.1256504 · Cited by 1,089
Cited by
Korpal, M., Korn, J. M., Gao, X., Rakiec, D. P., Ruddy, D. A., Doshi, S., Yuan, J., Kovats, S. G., Kim, S., Cooke, V. G., et al. (2013) · Cancer Discovery · doi:10.1158/2159-8290.cd-13-0142 · Cited by 561
Tailoring to RB: tumour suppressor status and therapeutic response
Knudsen, E. S., & Knudsen, K. E. (2008) · Nature Reviews Cancer · doi:10.1038/nrc2401 · Cited by 344
Self-citationChanges in primary lymphoid organs with aging
Chinn, I. K., Blackburn, C. C., Manley, N. R., & Sempowski, G. D. (2012) · Seminars in Immunology · doi:10.1016/j.smim.2012.04.005 · Cited by 282
Cheng, S.-W. G., Kuzyk, M. A., Moradian, A., Ichu, T.-A., Chang, V. C.-D., Tien, J. F., Vollett, S. E., Griffith, M., Marra, M. A., & Morin, G. B. (2012) · Molecular and Cellular Biology · doi:10.1128/mcb.06267-11 · Cited by 124
Androgen regulation of gene expression.
(2010) · Advances in cancer research · doi:10.1016/s0065-230x(10)07005-3 · Cited by 117
Metadata
- Authors
- Balk, S. P., & Knudsen, K. E.
- Venue
- Nuclear Receptor Signaling
- Publisher
- SAGE Publications
- Published
- 2008-01
- Volume
- 6
- Issue
- 1
- Pages
- e001-e001
- ISSN
- 1550-7629 (ISSN-L)
- OpenAlex
- W2167277055
- Cited by
- 333
- References
- 15
- FWCI
- 24.21
- Type
- journal article
- Language
- en
- Open access
- hybrid
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
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: AR, the cell cycle, and prostate cancer. https://app.cochat.ai/papers/10.1621/nrs.06001
- The paper
- Balk, S. P., & Knudsen, K. E. (2008). AR, the cell cycle, and prostate cancer. Nuclear Receptor Signaling. https://doi.org/10.1621/nrs.06001
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
