Abstract
Most recent investigations into cancer etiology have identified a key role played by epigenetics. Specifically, aberrant DNA and histone modifications which silence tumor suppressor genes or promote oncogenes have been demonstrated in multiple cancer models. While the role of epigenetics in several solid tumor cancers such as colorectal cancer are well established, there is emerging evidence that epigenetics also plays a critical role in breast and prostate cancer. In breast cancer, DNA methylation profiles have been linked to hormone receptor status and tumor progression. Similarly in prostate cancer, epigenetic patterns have been associated with androgen receptor status and response to therapy. The regulation of key receptor pathways and activities which affect clinical therapy treatment options by epigenetics renders this field high priority for elucidating mechanisms and potential targets. A new set of methylation arrays are now available to screen epigenetic changes and provide the cutting-edge tools needed to perform such investigations. The role of nutritional interventions affecting epigenetic changes particularly holds promise. Ultimately, determining the causes and outcomes from epigenetic changes will inform translational applications for utilization as biomarkers for risk and prognosis as well as candidates for therapy.
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Acknowledgments
Support from NIH (Grant numbers: NCI U56CA101599-01; CA15083-25S3; U54CA14393; NIMHD U54MD007598; and NCATS CTSI UL1TR000124 to J.V.V., and a NIMHD-CRECD 5MD007610 to Y.W.).
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Wu, Y., Sarkissyan, M., Vadgama, J.V. (2015). Epigenetics in Breast and Prostate Cancer. In: Verma, M. (eds) Cancer Epigenetics. Methods in Molecular Biology, vol 1238. Humana Press, New York, NY. https://doi.org/10.1007/978-1-4939-1804-1_23
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DOI: https://doi.org/10.1007/978-1-4939-1804-1_23
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