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Androgen receptor gene amplification and protein expression in hormone refractory prostate cancer
This study examined androgen receptor (AR) gene amplification and protein expression in 102 matched paired hormone sensitive and resistant tumours from 51 patients. AR gene amplification and X chromosome copy number were assessed by fluorescent in situ hybridisation, and protein expression was asses...
Autores principales: | , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
2003
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2394367/ https://www.ncbi.nlm.nih.gov/pubmed/12888829 http://dx.doi.org/10.1038/sj.bjc.6601127 |
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author | Edwards, J Krishna, N S Grigor, K M Bartlett, J M S |
author_facet | Edwards, J Krishna, N S Grigor, K M Bartlett, J M S |
author_sort | Edwards, J |
collection | PubMed |
description | This study examined androgen receptor (AR) gene amplification and protein expression in 102 matched paired hormone sensitive and resistant tumours from 51 patients. AR gene amplification and X chromosome copy number were assessed by fluorescent in situ hybridisation, and protein expression was assessed by immunohistochemistry. All tumours were stained for PSA protein expression. Significantly more tumours exhibited AR amplification following the development of hormone resistance (20%, 10 out of 49) compared to matched hormone-sensitive tumours from the same patient (2%, one out of 48) (P=0.0085). The level of AR expression was significantly higher in hormone-resistant tumours compared to matched hormone-sensitive tumours from the same patient (130, interquartile range, 55–167 vs 94.5 interquartile range, 55–120, P=0.019). AR expression levels in hormone-resistant tumours with and without AR amplification were not significantly different. However, an increase in AR expression was seen with the development of AR amplification in paired tumours. The rate of AR gene amplification and/or an increase in AR protein expression during androgen resistant is too low to wholly explain the development of androgen resistance. Alternative mechanisms for modulating the function of the AR, or other signalling pathways, must be considered as key factors in the development of hormone-resistant prostate. |
format | Text |
id | pubmed-2394367 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2003 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-23943672009-09-10 Androgen receptor gene amplification and protein expression in hormone refractory prostate cancer Edwards, J Krishna, N S Grigor, K M Bartlett, J M S Br J Cancer Molecular and Cellular Pathology This study examined androgen receptor (AR) gene amplification and protein expression in 102 matched paired hormone sensitive and resistant tumours from 51 patients. AR gene amplification and X chromosome copy number were assessed by fluorescent in situ hybridisation, and protein expression was assessed by immunohistochemistry. All tumours were stained for PSA protein expression. Significantly more tumours exhibited AR amplification following the development of hormone resistance (20%, 10 out of 49) compared to matched hormone-sensitive tumours from the same patient (2%, one out of 48) (P=0.0085). The level of AR expression was significantly higher in hormone-resistant tumours compared to matched hormone-sensitive tumours from the same patient (130, interquartile range, 55–167 vs 94.5 interquartile range, 55–120, P=0.019). AR expression levels in hormone-resistant tumours with and without AR amplification were not significantly different. However, an increase in AR expression was seen with the development of AR amplification in paired tumours. The rate of AR gene amplification and/or an increase in AR protein expression during androgen resistant is too low to wholly explain the development of androgen resistance. Alternative mechanisms for modulating the function of the AR, or other signalling pathways, must be considered as key factors in the development of hormone-resistant prostate. Nature Publishing Group 2003-08-04 2003-07-29 /pmc/articles/PMC2394367/ /pubmed/12888829 http://dx.doi.org/10.1038/sj.bjc.6601127 Text en Copyright © 2003 Cancer Research UK https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Molecular and Cellular Pathology Edwards, J Krishna, N S Grigor, K M Bartlett, J M S Androgen receptor gene amplification and protein expression in hormone refractory prostate cancer |
title | Androgen receptor gene amplification and protein expression in hormone refractory prostate cancer |
title_full | Androgen receptor gene amplification and protein expression in hormone refractory prostate cancer |
title_fullStr | Androgen receptor gene amplification and protein expression in hormone refractory prostate cancer |
title_full_unstemmed | Androgen receptor gene amplification and protein expression in hormone refractory prostate cancer |
title_short | Androgen receptor gene amplification and protein expression in hormone refractory prostate cancer |
title_sort | androgen receptor gene amplification and protein expression in hormone refractory prostate cancer |
topic | Molecular and Cellular Pathology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2394367/ https://www.ncbi.nlm.nih.gov/pubmed/12888829 http://dx.doi.org/10.1038/sj.bjc.6601127 |
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