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      Urine markers and prostate cancer

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          Abstract

          Prostate cancer (PCa) is globally the most common cancer in men, with an estimated prevalence of more than two million cases. Given the poor success rate in treating advanced PCa, intervention in early stages may reduce the progression of a small, localized carcinoma to a large metastatic lesion, thereby reducing disease-related deaths. Urine is readily available and can be used to detect either exfoliated cancer cells or secreted products. The major advantages of urine-based assays are their noninvasive character and ability to monitor PCa with heterogeneous foci. The aim of this review was to summarize the current evidence regarding performance characteristics of tests proposed for urine-based prostate cancer detection.

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          Metabolomic profiles delineate potential role for sarcosine in prostate cancer progression.

          Arun Sreekumar, Laila Poisson, Thekkelnaycke M Rajendiran … (2009)
          Multiple, complex molecular events characterize cancer development and progression. Deciphering the molecular networks that distinguish organ-confined disease from metastatic disease may lead to the identification of critical biomarkers for cancer invasion and disease aggressiveness. Although gene and protein expression have been extensively profiled in human tumours, little is known about the global metabolomic alterations that characterize neoplastic progression. Using a combination of high-throughput liquid-and-gas-chromatography-based mass spectrometry, we profiled more than 1,126 metabolites across 262 clinical samples related to prostate cancer (42 tissues and 110 each of urine and plasma). These unbiased metabolomic profiles were able to distinguish benign prostate, clinically localized prostate cancer and metastatic disease. Sarcosine, an N-methyl derivative of the amino acid glycine, was identified as a differential metabolite that was highly increased during prostate cancer progression to metastasis and can be detected non-invasively in urine. Sarcosine levels were also increased in invasive prostate cancer cell lines relative to benign prostate epithelial cells. Knockdown of glycine-N-methyl transferase, the enzyme that generates sarcosine from glycine, attenuated prostate cancer invasion. Addition of exogenous sarcosine or knockdown of the enzyme that leads to sarcosine degradation, sarcosine dehydrogenase, induced an invasive phenotype in benign prostate epithelial cells. Androgen receptor and the ERG gene fusion product coordinately regulate components of the sarcosine pathway. Here, by profiling the metabolomic alterations of prostate cancer progression, we reveal sarcosine as a potentially important metabolic intermediary of cancer cell invasion and aggressivity.
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            Recurrent gene fusions in prostate cancer.

            Chandan Kumar-Sinha, Scott Tomlins, Arul M Chinnaiyan (2008)
            The discovery of recurrent gene fusions in a majority of prostate cancers has important clinical and biological implications in the study of common epithelial tumours. Gene fusion and chromosomal rearrangements were previously thought to be primarily the oncogenic mechanism of haematological malignancies and sarcomas. The prostate cancer gene fusions that have been identified thus far are characterized by 5' genomic regulatory elements, most commonly controlled by androgen, fused to members of the Ets family of transcription factors, leading to the overexpression of oncogenic transcription factors. Ets gene fusions probably define a distinct class of prostate cancer, and this might have a bearing on diagnosis, prognosis and rational therapeutic targeting.
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              Can urinary exosomes act as treatment response markers in prostate cancer?

              Paul J Mitchell, Joanne Welton, John Staffurth … (2009)
              Background Recently, nanometer sized vesicles (termed exosomes) have been described as a component of urine. Such vesicles may be a useful non-invasive source of markers in renal disease. Their utility as a source of markers in urological cancer remains unstudied. Our aim in this study was to investigate the feasibility and value of analysing urinary exosomes in prostate cancer patients undergoing standard therapy. Methods Ten patients (with locally advanced PCa) provided spot urine specimens at three time points during standard therapy. Patients received 3–6 months neoadjuvant androgen deprivation therapy prior to radical radiotherapy, comprising a single phase delivering 55 Gy in 20 fractions to the prostate and 44 Gy in 20 fractions to the pelvic nodes. Patients were continued on adjuvant ADT according to clinical need. Exosomes were purified, and the phenotype compared to exosomes isolated from the prostate cancer cell line LNcaP. A control group of 10 healthy donors was included. Serum PSA was used as a surrogate treatment response marker. Exosomes present in urine were quantified, and expression of prostate markers (PSA and PSMA) and tumour-associated marker 5T4 was examined. Results The quantity and quality of exosomes present in urine was highly variable, even though we handled all materials freshly and used methods optimized for obtaining highly pure exosomes. There was approx 2-fold decrease in urinary exosome content following 12 weeks ADT, but this was not sustained during radiotherapy. Nevertheless, PSA and PSMA were present in 20 of 24 PCa specimens, and not detected in healthy donor specimens. There was a clear treatment-related decrease in exosomal prostate markers in 1 (of 8) patient. Conclusion Evaluating urinary-exosomes remains difficult, given the variability of exosomes in urine specimens. Nevertheless, this approach holds promise as a non-invasive source of multiple markers of malignancy that could provide clinically useful information.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cent European J Urol
                Journal ID (iso-abbrev): Cent European J Urol
                Journal ID (publisher-id): CEJU
                Title: Central European Journal of Urology
                Publisher: Polish Urological Association
                ISSN (Print): 2080-4806
                ISSN (Electronic): 2080-4873
                Publication date (Electronic): 18 March 2011
                Publication date (Print): 2011
                Volume: 64
                Issue: 1
                Pages: 9-14
                Affiliations
                [1 ]2 nd Clinic of Urology, Medical University of Łódź, Poland
                [2 ]Department of Cytobiochemistry, University of Łódź, Poland
                Author notes
                Correspondence Jacek Wilkosz, 2 nd Clinic of Urology, Medical University of Lódz, M. Kopernik Memorial Hospital, 62, Pabianicka Street, 93-513 Łódź Poland. phone: +48 42 689 52 11. jacek.wilkosz@ 123456gmail.com
                Article
                Publisher ID: 00076
                DOI: 10.5173/ceju.2011.01.art2
                PMC ID: 3921702
                PubMed ID: 24578853
                SO-VID: 23294386-cc62-4b8b-b661-c92bde17b7d8
                Copyright © Copyright by Polish Urological Association
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-Noncommercial 3.0 Unported License, permitting all non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 23 December 2010
                Date revision received : 28 January 2011
                Date accepted : 31 January 2011
                Categories
                Subject: Review Articles

                Keywords: prostate cancer,urine markers,fusion genes,multiplex analysis
                Data availability:
                Keywords: prostate cancer, urine markers, fusion genes, multiplex analysis

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