Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-11044
Kristiansen, G; Fritzsche, F R; Wassermann, K; Jäger, C; Tölle, A; Lein, M; Stephan, C; Jung, K; Pilarsky, C; Dietel, M; Moch, H (2008). GOLPH2 protein expression as a novel tissue biomarker for prostate cancer: implications for tissue-based diagnostics. British Journal of Cancer, 99(6):939-948.
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GOLPH2 is coding the 73-kDa type II Golgi membrane antigen GOLPH2/GP73. Upregulation of GOLPH2 mRNA has been recently reported in expression array analyses of prostate cancer. As GOLPH2 protein expression in prostate tissues is currently unknown, this study aimed at a comprehensive analysis of GOLPH2 protein in benign and malignant prostate lesions. Immunohistochemically detected GOLPH2 protein expression was compared with the basal cell marker p63 and the prostate cancer marker alpha-methylacyl-CoA racemase (AMACR) in 614 radical prostatectomy specimens. GOLPH2 exhibited a perinuclear Golgi-type staining pattern and was preferentially seen in prostatic gland epithelia. Using a semiquantitative staining intensity score, GOLPH2 expression was significantly higher in prostate cancer glands compared with normal glands (P<0.001). GOLPH2 protein was upregulated in 567 of 614 tumours (92.3%) and AMACR in 583 of 614 tumours (95%) (correlation coefficient 0.113, P=0.005). Importantly, GOLPH2 immunohistochemistry exhibited a lower level of intratumoral heterogeneity (25 vs 45%). Further, GOLPH2 upregulation was detected in 26 of 31 (84%) AMACR-negative prostate cancer cases. These data clearly suggest GOLPH2 as an additional ancillary positive marker for tissue-based diagnosis of prostate cancer.British Journal of Cancer (2008) 99, 939-948. doi:10.1038/sj.bjc.6604614 www.bjcancer.com.
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|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Surgical Pathology|
|DDC:||610 Medicine & health|
|Deposited On:||22 Jan 2009 15:46|
|Last Modified:||27 Nov 2013 23:31|
|Publisher:||Nature Publishing Group|
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