The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Mechanisms mediating androgen receptor reactivation after castration
Open accessAbstract
SUMMARY Androgen deprivation is still the standard systemic therapy for metastatic prostate cancer (PCa), but patients invariably relapse with a more aggressive form of PCa termed hormone refractory, androgen independent, or castration resistant PCa (CRPC). Significantly, the androgen receptor (AR) is expressed at high levels in most cases of CRPC, and these tumors resume their expression of multiple AR-regulated genes, indicating that AR transcriptional activity becomes reactivated at this stage of the disease. The molecular basis for this AR reactivation remains unclear, but possible mechanisms include increased AR expression, AR mutations that enhance activation by weak androgens and AR antagonists, increased expression of transcriptional coactivator proteins, and activation of signal transduction pathways that can enhance AR responses to low levels of androgens. Recent data indicate that CRPC cells may also carry out intracellular synthesis of testosterone and DHT from weak adrenal androgens and may be able to synthesize androgens from cholesterol. These mechanisms that appear to contribute to AR reactivation after castration are further outlined in this review.
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Cites
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
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
The Androgen Axis in Recurrent Prostate Cancer
Mohler, J. L., Gregory, C. W., Ford, O. H., Kim, D., Weaver, C. M., Petrusz, P., Wilson, E. M., & French, F. S. (2004) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-1146-03 · Cited by 675
PENNING, T. M., BURCZYNSKI, M. E., JEZ, J. M., HUNG, C.-F., LIN, H.-K., MA, H., MOORE, M., PALACKAL, N., & RATNAM, K. (2000) · Biochemical Journal · doi:10.1042/bj3510067 · Cited by 649
Holzbeierlein, J., Lal, P., LaTulippe, E., Smith, A., Satagopan, J., Zhang, L., Ryan, C., Smith, S., Scher, H., Scardino, P., et al. (2004) · The American Journal of Pathology · doi:10.1016/s0002-9440(10)63112-4 · Cited by 577
A role for estrogen receptor β in the regulation of growth of the ventral prostate
Weihua, Z., Mäkelä, S., Andersson, L. C., Salmi, S., Saji, S., Webster, J. I., Jensen, E. V., Nilsson, S., Warner, M., & Gustafsson, J.-Å. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.111150898 · Cited by 440
Regulation of androgen receptor activity by tyrosine phosphorylation.
Guo, Z., Dai, B., Jiang, T., Xu, K., Xie, Y., Kim, O., Nesheiwat, I., Kong, X., Melamed, J., Handratta, V. D., et al. (2006) · Cancer Cell · doi:10.1016/j.ccr.2006.08.021 · Cited by 364
Mellinghoff, I. K., Vivanco, I., Kwon, A., Tran, C., Wongvipat, J., & Sawyers, C. L. (2004) · Cancer Cell · doi:10.1016/j.ccr.2004.09.031 · Cited by 344
Cited by
Ribas, J., Ni, X., Haffner, M., Wentzel, E. A., Salmasi, A. H., Chowdhury, W. H., Kudrolli, T. A., Yegnasubramanian, S., Luo, J., Rodriguez, R., et al. (2009) · Cancer Research · doi:10.1158/0008-5472.can-09-1448 · Cited by 416
Hsieh, C.-L., Fei, T., Chen, Y., Li, T., Gao, Y., Wang, X., Sun, T., Sweeney, C. J., Lee, G.-S. M., Chen, S., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1324151111 · Cited by 398
Self-citationA Gain-of-Function Mutation in DHT Synthesis in Castration-Resistant Prostate Cancer
Chang, K.-H., Li, R., Kuri, B., Lotan, Y., Roehrborn, C. G., Liu, J., Vessella, R., Nelson, P. S., Kapur, P., Guo, X., et al. (2013) · Cell · doi:10.1016/j.cell.2013.07.029 · Cited by 312
Peptidomimetic targeting of critical androgen receptor–coregulator interactions in prostate cancer
Ravindranathan, P., Lee, T.-K., Yang, L., Centenera, M. M., Butler, L., Tilley, W. D., Hsieh, J.-T., Ahn, J.-M., & Raj, G. V. (2013) · Nature Communications · doi:10.1038/ncomms2912 · Cited by 257
Pretorius, E., Africander, D. J., Vlok, M., Perkins, M. S., Quanson, J., & Storbeck, K.-H. (2016) · PLOS ONE · doi:10.1371/journal.pone.0159867 · Cited by 148
Metadata
- Authors
- Yuan, X., & Balk, S. P.
- Venue
- Urologic Oncology: Seminars and Original Investigations
- Publisher
- Elsevier BV
- Published
- 2009-01
- Volume
- 27
- Issue
- 1
- Pages
- 36-41
- ISSN
- 1078-1439 (ISSN-L)
- OpenAlex
- W2024304133
- Cited by
- 204
- References
- 19
- FWCI
- 16.42
- Type
- journal article
- Language
- en
- Open access
- green
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