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    Gene expression and epigenetic discovery screen reveal methylation of SFRP2 in prostate cancer.

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    Name:
    Perry et al (IJC-2013) pre-pub ...
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    Authors
    Perry, Antoinette S
    O'Hurley, Gillian
    Raheem, Omer A
    Brennan, Kevin
    Wong, Simon
    O'Grady, Anthony
    Kennedy, Anne-Marie
    Marignol, Laure
    Murphy, Therese M
    Sullivan, Linda
    Barrett, Ciara
    Loftus, Barbara
    Thornhill, John
    Hewitt, Stephen M
    Lawler, Mark
    Kay, Elaine
    Lynch, Thomas
    Hollywood, Donal
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    Affiliation
    Prostate Molecular Oncology, Department of Clinical Medicine, Institute of Molecular Medicine, Trinity College Dublin, Ireland. aperry@tcd.ie
    Issue Date
    2013-04-15
    Keywords
    DNA Methylation
    Epigenesis, Genetic
    Gene Expression Profiling
    Membrane Proteins/genetics
    MeSH
    Adult
    Aged
    Cell Line, Tumor
    DNA Methylation
    Epigenesis, Genetic
    Gene Expression Profiling
    Humans
    Male
    Membrane Proteins
    Middle Aged
    Promoter Regions, Genetic
    Prostatic Neoplasms
    Real-Time Polymerase Chain Reaction
    Reverse Transcriptase Polymerase Chain Reaction
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    Citation
    Perry AS et al. Gene expression and epigenetic discovery screen reveal methylation of SFRP2 in prostate cancer. Int. J. Cancer 2013, 132 (8):1771-80
    Journal
    International journal of cancer. Journal international du cancer
    URI
    http://hdl.handle.net/10147/324052
    DOI
    10.1002/ijc.27798
    PubMed ID
    22915211
    Abstract
    Aberrant activation of Wnts is common in human cancers, including prostate. Hypermethylation associated transcriptional silencing of Wnt antagonist genes SFRPs (Secreted Frizzled-Related Proteins) is a frequent oncogenic event. The significance of this is not known in prostate cancer. The objectives of our study were to (i) profile Wnt signaling related gene expression and (ii) investigate methylation of Wnt antagonist genes in prostate cancer. Using TaqMan Low Density Arrays, we identified 15 Wnt signaling related genes with significantly altered expression in prostate cancer; the majority of which were upregulated in tumors. Notably, histologically benign tissue from men with prostate cancer appeared more similar to tumor (r = 0.76) than to benign prostatic hyperplasia (BPH; r = 0.57, p < 0.001). Overall, the expression profile was highly similar between tumors of high (≥ 7) and low (≤ 6) Gleason scores. Pharmacological demethylation of PC-3 cells with 5-Aza-CdR reactivated 39 genes (≥ 2-fold); 40% of which inhibit Wnt signaling. Methylation frequencies in prostate cancer were 10% (2/20) (SFRP1), 64.86% (48/74) (SFRP2), 0% (0/20) (SFRP4) and 60% (12/20) (SFRP5). SFRP2 methylation was detected at significantly lower frequencies in high-grade prostatic intraepithelial neoplasia (HGPIN; 30%, (6/20), p = 0.0096), tumor adjacent benign areas (8.82%, (7/69), p < 0.0001) and BPH (11.43% (4/35), p < 0.0001). The quantitative level of SFRP2 methylation (normalized index of methylation) was also significantly higher in tumors (116) than in the other samples (HGPIN = 7.45, HB = 0.47, and BPH = 0.12). We show that SFRP2 hypermethylation is a common event in prostate cancer. SFRP2 methylation in combination with other epigenetic markers may be a useful biomarker of prostate cancer.
    Item Type
    Article
    Language
    en
    ISSN
    1097-0215
    ae974a485f413a2113503eed53cd6c53
    10.1002/ijc.27798
    Scopus Count
    Collections
    St. Luke's Radiation Oncology Network, Dublin

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