Common gene pathways and families altered by DNA methylation in breast and prostate cancers

    1. Tina Bianco-Miotto1,2
    1. Dame Roma Mitchell Cancer Research Laboratories, Discipline of Medicine, Hanson Institute, Adelaide Prostate Cancer Research Centre, The University of Adelaide, Adelaide, South Australia, Australia
      1School of Paediatrics and Reproductive Health, The Robinson Institute
      2School of Agriculture, Food and Wine, The University of Adelaide, Waite Campus, PMB 1 Glen Osmond, Adelaide, South Australia 5064, Australia
    1. Correspondence should be addressed to T Bianco-Miotto; Email: tina.bianco{at}adelaide.edu.au

    Abstract

    Epigenetic modifications, such as DNA methylation, are widely studied in cancer as they are stable and easy to measure genome wide. DNA methylation changes have been used to differentiate benign from malignant tissue and to predict tumor recurrence or patient outcome. Multiple genome wide DNA methylation studies in breast and prostate cancers have identified genes that are differentially methylated in malignant tissue compared with non-malignant tissue or in association with hormone receptor status or tumor recurrence. Although this has identified potential biomarkers for diagnosis and prognosis, what is highlighted by reviewing these studies is the similarities between breast and prostate cancers. In particular, the gene families/pathways targeted by DNA methylation in breast and prostate cancers have significant overlap and include homeobox genes, zinc finger transcription factors, S100 calcium binding proteins, and potassium voltage-gated family members. Many of the gene pathways targeted by aberrant methylation in breast and prostate cancers are not targeted in other cancers, suggesting that some of these targets may be specific to hormonal cancers. Genome wide DNA methylation profiles in breast and prostate cancers will not only define more specific and sensitive biomarkers for cancer diagnosis and prognosis but also identify novel therapeutic targets, which may be direct targets of agents that reverse DNA methylation or which may target novel gene families that are themselves DNA methylation targets.

    Keywords
    • Revision received 6 June 2013
    • Accepted 28 June 2013
    • Made available online as an Accepted Preprint 1 July 2013
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