Steroid hormone synthetic pathways in prostate cancer
While androgen deprivation therapy (ADT) remains the primary treatment for metastatic prostate cancer (PCa) since the seminal recognition of the disease as androgen-dependent by Huggins and Hodges in 1941, therapy is uniformly marked by progression to castration-resistant prostate cancer (CRPC) over...
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| Format: | Online |
| Language: | English |
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AME Publishing Company
2013
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219921/ |
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pubmed-42199212014-11-04 Steroid hormone synthetic pathways in prostate cancer Mostaghel, Elahe A. Review Article While androgen deprivation therapy (ADT) remains the primary treatment for metastatic prostate cancer (PCa) since the seminal recognition of the disease as androgen-dependent by Huggins and Hodges in 1941, therapy is uniformly marked by progression to castration-resistant prostate cancer (CRPC) over a period of about 18 months, with an ensuing median survival of 1 to 2 years. Importantly, castration does not eliminate androgens from the prostate tumor microenvironment. Castration resistant tumors are characterized by elevated tumor androgens that are well within the range capable of activating the AR and AR-mediated gene expression, and by steroid enzyme alterations which may potentiate de novo androgen synthesis or utilization of circulating adrenal androgens. The dependence of CRPC on intratumoral androgen metabolism has been modeled in vitro and in vivo, and residual intratumoral androgens are implicated in nearly every mechanism by which AR-mediated signaling promotes castration-resistant disease. AME Publishing Company 2013-09 /pmc/articles/PMC4219921/ /pubmed/25379460 http://dx.doi.org/10.3978/j.issn.2223-4683.2013.09.16 Text en 2013 Translational Andrology and Urology. All rights reserved. |
| repository_type |
Open Access Journal |
| institution_category |
Foreign Institution |
| institution |
US National Center for Biotechnology Information |
| building |
NCBI PubMed |
| collection |
Online Access |
| language |
English |
| format |
Online |
| author |
Mostaghel, Elahe A. |
| spellingShingle |
Mostaghel, Elahe A. Steroid hormone synthetic pathways in prostate cancer |
| author_facet |
Mostaghel, Elahe A. |
| author_sort |
Mostaghel, Elahe A. |
| title |
Steroid hormone synthetic pathways in prostate cancer |
| title_short |
Steroid hormone synthetic pathways in prostate cancer |
| title_full |
Steroid hormone synthetic pathways in prostate cancer |
| title_fullStr |
Steroid hormone synthetic pathways in prostate cancer |
| title_full_unstemmed |
Steroid hormone synthetic pathways in prostate cancer |
| title_sort |
steroid hormone synthetic pathways in prostate cancer |
| description |
While androgen deprivation therapy (ADT) remains the primary treatment for metastatic prostate cancer (PCa) since the seminal recognition of the disease as androgen-dependent by Huggins and Hodges in 1941, therapy is uniformly marked by progression to castration-resistant prostate cancer (CRPC) over a period of about 18 months, with an ensuing median survival of 1 to 2 years. Importantly, castration does not eliminate androgens from the prostate tumor microenvironment. Castration resistant tumors are characterized by elevated tumor androgens that are well within the range capable of activating the AR and AR-mediated gene expression, and by steroid enzyme alterations which may potentiate de novo androgen synthesis or utilization of circulating adrenal androgens. The dependence of CRPC on intratumoral androgen metabolism has been modeled in vitro and in vivo, and residual intratumoral androgens are implicated in nearly every mechanism by which AR-mediated signaling promotes castration-resistant disease. |
| publisher |
AME Publishing Company |
| publishDate |
2013 |
| url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219921/ |
| _version_ |
1613152166247137280 |