Epigenetics of breast cancer: Modifying role of environmental and bioactive food compounds. Issue 6 (8th June 2016)

• Record Type: Journal Article
• Authors: Romagnolo, Donato F.; Daniels, Kevin D.; Grunwald, Jonathan T.; Ramos, Stephan A.; Propper, Catherine R.; Selmin, Ornella I.
• Is Part Of: Molecular nutrition & food research. Volume 60:Issue 6(2016)
• Page Start: 1310
• Page End: 1329
• Publication Date: 2016-06-08
• Subjects: Breast cancer -- Cancer prevention -- Endocrine disruptors -- Epigenetics -- Tumor suppressor genes; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201501063
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : Agonists of the aromatic hydrocarbon receptor (AHR), bisphenol A (BPA), and arsenic (As) compounds induce epigenetic alterations associated with the development of sporadic breast cancer. Bioactive food components that target epigenetic mechanisms may protect against sporadic breast tumorigenesis. Characterizing the overlap between epigenetic signatures elicited in tumor suppressor genes by endocrine disruptors may afford new strategies for breast cancer prevention with specific bioactive food components. Abstract : Scope: Reduced expression of tumor suppressor genes (TSG) increases the susceptibility to breast cancer. However, only a small percentage of breast tumors is related to family history and mutational inactivation of TSG. Epigenetics refers to non‐mutational events that alter gene expression. Endocrine disruptors found in foods and drinking water may disrupt epigenetically hormonal regulation and increase breast cancer risk. This review centers on the working hypothesis that agonists of the aromatic hydrocarbon receptor (AHR), bisphenol A (BPA), and arsenic compounds, induce in TSG epigenetic signatures that mirror those often seen in sporadic breast tumors. Conversely, it is hypothesized that bioactive food components that target epigenetic mechanisms protect against sporadic breast cancer induced by these disruptors. Methods and results: This review highlights (i) overlaps between epigenetic signatures placed in TSG by AHR‐ligands, BPA, and arsenic with epigenetic alterations associated with sporadic breast tumorigenesis; and (ii) potential opportunities for the prevention of sporadic breast cancer with food components that target the epigenetic machinery. Conclusions: Characterizing the overlap between epigenetic signatures elicited in TSG by endocrine disruptors with those observed in sporadic breast tumors may afford new strategies for breast cancer prevention with specific bioactive food components or diet.