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Abstract 1087: The role of fibroblast growth factor 9 in the recurrence after radical prostatectomy
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Abstract
Introduction and Objectives: The aim of this study was to investigate the role of fibroblast growth factor 9 (FGF9) in the recurrence after radical prostatectomy. Methods: Immunohistochemical staining using anti-FGF9 antibody was performed for tissues derived from radical prostatectomy in 133 male patients. Cell viability, apoptosis and invasion of LNCaP and androgen-independent LNCaP (AI-LNCaP) cells were assessed with the MTT assay, Apopercentage apoptosis assay and Matrigel invasion assay, respectively, in the presence or absence of treatment with recombinant FGF9 or anti-FGF9 neutralizing antibody. Results: In immunohistochemical staining, FGF9-positive cells were detected in 20 samples. In cases with a Gleason score of 8 or higher, the incidence of cases with FGF9-positive cells was 34.2%, which was significantly higher than that for those with Gleason scores of 7 or lower (7.3%, p=0.0003), respectively. The 3-year biochemical relapse-free survival rate in cases with FGF9-positive cells was 17.5%, which was significantly lower than that in cases in which FGF9-positive cells were not detectable (76.6%, p<0.0001). In androgen-depleted medium, the cell viability of LNCaP was significantly lower than that of AI-LNCaP, and was enhanced to the same level by treatment with recombinant FGF9. Invasion was significantly enhanced and apoptosis by androgen deprivation was significantly suppressed by treatment of LNCaP cells with recombinant FGF9. Furthermore, these effects were significantly suppressed by treatment with anti-FGF9 neutralizing antibody. Conclusions: These results indicate that FGF9 contributes to postoperative recurrence of prostate cancer through stimulation of cell proliferation and invasion, and induction of an anti-apoptotic effect.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1087. doi:10.1158/1538-7445.AM2011-1087
American Association for Cancer Research (AACR)
Title: Abstract 1087: The role of fibroblast growth factor 9 in the recurrence after radical prostatectomy
Description:
Abstract
Introduction and Objectives: The aim of this study was to investigate the role of fibroblast growth factor 9 (FGF9) in the recurrence after radical prostatectomy.
Methods: Immunohistochemical staining using anti-FGF9 antibody was performed for tissues derived from radical prostatectomy in 133 male patients.
Cell viability, apoptosis and invasion of LNCaP and androgen-independent LNCaP (AI-LNCaP) cells were assessed with the MTT assay, Apopercentage apoptosis assay and Matrigel invasion assay, respectively, in the presence or absence of treatment with recombinant FGF9 or anti-FGF9 neutralizing antibody.
Results: In immunohistochemical staining, FGF9-positive cells were detected in 20 samples.
In cases with a Gleason score of 8 or higher, the incidence of cases with FGF9-positive cells was 34.
2%, which was significantly higher than that for those with Gleason scores of 7 or lower (7.
3%, p=0.
0003), respectively.
The 3-year biochemical relapse-free survival rate in cases with FGF9-positive cells was 17.
5%, which was significantly lower than that in cases in which FGF9-positive cells were not detectable (76.
6%, p<0.
0001).
In androgen-depleted medium, the cell viability of LNCaP was significantly lower than that of AI-LNCaP, and was enhanced to the same level by treatment with recombinant FGF9.
Invasion was significantly enhanced and apoptosis by androgen deprivation was significantly suppressed by treatment of LNCaP cells with recombinant FGF9.
Furthermore, these effects were significantly suppressed by treatment with anti-FGF9 neutralizing antibody.
Conclusions: These results indicate that FGF9 contributes to postoperative recurrence of prostate cancer through stimulation of cell proliferation and invasion, and induction of an anti-apoptotic effect.
Citation Format: {Authors}.
{Abstract title} [abstract].
In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL.
Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1087.
doi:10.
1158/1538-7445.
AM2011-1087.
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