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Evidence for distinct alterations in the FGF axis in prostate cancer progression to an aggressive clinical phenotype
The Journal of pathology, 2010-03, Vol.220 (4), p.452-460
Murphy, Tania
Darby, Steve
Mathers, Marie E
Gnanapragasam, Vincent J
2010
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Murphy, Tania
Darby, Steve
Mathers, Marie E
Gnanapragasam, Vincent J
Titel
Evidence for distinct alterations in the FGF axis in prostate cancer progression to an aggressive clinical phenotype
Ist Teil von
The Journal of pathology, 2010-03, Vol.220 (4), p.452-460
Ort / Verlag
Chichester, UK: John Wiley & Sons, Ltd
Erscheinungsjahr
2010
Quelle
Wiley Online Library Journals Frontfile Complete
Beschreibungen/Notizen
Multiple fibroblast growth factor (FGF) axis alterations are known to occur in prostate cancer. Here we simultaneously profiled key components of this axis to determine their relevance in disease progression. An optimized immunohistochemistry protocol was used in expression analysis of FGF2, FGF8, FGFR1, FGFR4, and Sef (similar expression to FGF) in a single TMA of prostate cancer. FGF ligands and receptors were overexpressed in cancers compared to benign samples (p < 0.0001), while Sef expression was reduced (p < 0.0001). There was a positive association between higher grades and increased FGFR4 (p = 0.02), FGF2, and FGF8 (p = 0.002 and p < 0.0001). Sef expression was progressively lower with increasing grade (p = 0.005). Clinical stage was positively associated with FGF2, FGF8, and FGFR4 expression (p = 0.005, 0.03, and 0.012) but not with FGFR1 or Sef expression. Only reduced Sef was associated with bone metastasis (p = 0.02) and was also predictive of subsequent metastasis in initially localized tumours (p = 0.004). Down-regulation of Sef and increased FGFR4 were also the only independent variables associated with disease-specific survival (HR 1.73, p = 0.04 and HR 0.56, p = 0.01). In in vitro studies, silencing Sef enhanced the cell response to FGFs (p < 0.001) and substantially mitigated the effectiveness of an FGFR1 inhibitor. Conversely, increased Sef blocked the response to FGFs and had a comparable suppressive effect to the inhibitor. This study demonstrates that increased FGFR4 and reduced Sef may be critical FGF alterations associated with prostate cancer progression. Sef may also have a role in the tumour response to FGFR inhibition and warrants further investigation in this context. Copyright © 2009 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Sprache
Englisch
Identifikatoren
ISSN: 0022-3417
eISSN: 1096-9896
DOI: 10.1002/path.2657
Titel-ID: cdi_proquest_miscellaneous_733811123
Format
–
Schlagworte
Benign
,
Biological and medical sciences
,
Biomarkers, Tumor - metabolism
,
Bone Neoplasms - secondary
,
Disease Progression
,
FGF ligand
,
FGF receptor
,
Fibroblast growth factor
,
Fibroblast growth factor 2
,
Fibroblast growth factor 8
,
Fibroblast growth factor receptor 1
,
Fibroblast growth factor receptor 4
,
Fibroblast growth factor receptors
,
Fibroblast Growth Factors - metabolism
,
Gynecology. Andrology. Obstetrics
,
Humans
,
Immunohistochemistry
,
Investigative techniques, diagnostic techniques (general aspects)
,
Ligands
,
Male
,
Male genital diseases
,
Medical sciences
,
Metastases
,
Neoplasm Invasiveness
,
Neoplasm Proteins - metabolism
,
Nephrology. Urinary tract diseases
,
Oligonucleotide Array Sequence Analysis - methods
,
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
,
Phenotype
,
Prostate cancer
,
Prostatic Neoplasms - metabolism
,
Prostatic Neoplasms - pathology
,
Receptors, Fibroblast Growth Factor - antagonists & inhibitors
,
Receptors, Fibroblast Growth Factor - metabolism
,
Receptors, Interleukin - metabolism
,
Similar expression to FGF
,
Survival Analysis
,
Tumor Cells, Cultured
,
Tumors
,
Tumors of the urinary system
,
Urinary tract. Prostate gland
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