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

Lookup NU author(s): Dr Kelly Coffey, Professor Craig Robson, Professor Hing Leung

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Abstract

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 naive 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. British Journal of Cancer (2011) 105, 1362-1369. doi:10.1038/bjc.2011.367 www.bjcancer.com Published online 27 September 2011 (C) 2011 Cancer Research UK


Publication metadata

Author(s): Armstrong K; Robson CN; Leung HY; Ahmad I; Kalna G; Tan SS; Edwards J

Publication type: Article

Publication status: Published

Journal: British Journal of Cancer

Year: 2011

Volume: 105

Issue: 9

Pages: 1362-1369

Print publication date: 01/10/2011

ISSN (print): 0007-0920

ISSN (electronic): 1532-1827

Publisher: Nature Publishing Group

URL: http://dx.doi.org/10.1038/bjc.2011.367

DOI: 10.1038/bjc.2011.367


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