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Upregulated FGFR1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer

BACKGROUND: Prostate cancer (PC) represents a global health issue. Treatment for locally advanced and metastatic PC remains unsatisfactory. The androgen receptor (AR) has been validated in having a key role in both naïve and castrate-resistant PC (CRPC). However, the significance of other signalling...

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Autores principales: Armstrong, K, Ahmad, I, Kalna, G, Tan, S S, Edwards, J, Robson, C N, Leung, H Y
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3241546/
https://www.ncbi.nlm.nih.gov/pubmed/21952621
http://dx.doi.org/10.1038/bjc.2011.367
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author Armstrong, K
Ahmad, I
Kalna, G
Tan, S S
Edwards, J
Robson, C N
Leung, H Y
author_facet Armstrong, K
Ahmad, I
Kalna, G
Tan, S S
Edwards, J
Robson, C N
Leung, H Y
author_sort Armstrong, K
collection PubMed
description BACKGROUND: Prostate cancer (PC) represents a global health issue. Treatment for locally advanced and metastatic PC remains unsatisfactory. The androgen receptor (AR) has been validated in having a key role in both naïve and castrate-resistant PC (CRPC). However, the significance of other signalling pathways in CRPC is less well validated. METHODS: To gain a better insight into the molecular signalling cascades involved in clinical CRPC, we performed gene expression profiling using the Illumina DASL assay and studied matched hormone-naive (HN) and CR prostate tumours (n=10 pairs). Ingenuity Pathways Analysis (IPA) was used to identify potential networks involved, and further validation was performed in in vitro cell models and clinical tumours. RESULTS: Expression of 50 genes was significantly different between HN and CRPC. IPA revealed two networks of particular interest, including AR and FGFR1, respectively. FGFR1 expression was confirmed to be significantly upregulated in CRPC (P⩽0.005), and abnormal FGFR1 expression was associated with shorter time to biochemical relapse in HNPC (P=0.006) and less favourable disease-specific survival in CRPC (P=0.018). CONCLUSION: For the first time, our gene expression profiling experiment on archival tumour materials has identified upregulated FGFR1 expression to be associated with PC progression to the CR state.
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spelling pubmed-32415462012-10-25 Upregulated FGFR1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer Armstrong, K Ahmad, I Kalna, G Tan, S S Edwards, J Robson, C N Leung, H Y Br J Cancer Molecular Diagnostics BACKGROUND: Prostate cancer (PC) represents a global health issue. Treatment for locally advanced and metastatic PC remains unsatisfactory. The androgen receptor (AR) has been validated in having a key role in both naïve and castrate-resistant PC (CRPC). However, the significance of other signalling pathways in CRPC is less well validated. METHODS: To gain a better insight into the molecular signalling cascades involved in clinical CRPC, we performed gene expression profiling using the Illumina DASL assay and studied matched hormone-naive (HN) and CR prostate tumours (n=10 pairs). Ingenuity Pathways Analysis (IPA) was used to identify potential networks involved, and further validation was performed in in vitro cell models and clinical tumours. RESULTS: Expression of 50 genes was significantly different between HN and CRPC. IPA revealed two networks of particular interest, including AR and FGFR1, respectively. FGFR1 expression was confirmed to be significantly upregulated in CRPC (P⩽0.005), and abnormal FGFR1 expression was associated with shorter time to biochemical relapse in HNPC (P=0.006) and less favourable disease-specific survival in CRPC (P=0.018). CONCLUSION: For the first time, our gene expression profiling experiment on archival tumour materials has identified upregulated FGFR1 expression to be associated with PC progression to the CR state. Nature Publishing Group 2011-10-25 2011-09-27 /pmc/articles/PMC3241546/ /pubmed/21952621 http://dx.doi.org/10.1038/bjc.2011.367 Text en Copyright © 2011 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 Diagnostics
Armstrong, K
Ahmad, I
Kalna, G
Tan, S S
Edwards, J
Robson, C N
Leung, H Y
Upregulated FGFR1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer
title Upregulated FGFR1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer
title_full Upregulated FGFR1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer
title_fullStr Upregulated FGFR1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer
title_full_unstemmed Upregulated FGFR1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer
title_short Upregulated FGFR1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer
title_sort upregulated fgfr1 expression is associated with the transition of hormone-naive to castrate-resistant prostate cancer
topic Molecular Diagnostics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3241546/
https://www.ncbi.nlm.nih.gov/pubmed/21952621
http://dx.doi.org/10.1038/bjc.2011.367
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