Abstract
Theory and empirical evidence suggest that psychological stress and other adverse psychosocial experiences can contribute to cancer progression. Research has begun to explore the potential role of epigenetic changes in these pathways. In basic, animal and human models, exposure to stressors or to the products of the physiological stress response (e.g., cortisol) has been associated with epigenetic changes, such as DNA methylation and microRNA (miR) expression, which may influence tumor growth, progression, metastasis, or chemoresistance. However, the specific biological pathways linking stress, epigenetic changes, and cancer outcomes remain unclear. Numerous opportunities exist to extend the preliminary evidence for the role of epigenetic mechanisms in the biopsychosocial pathways contributing to cancer progression. Such work will improve our understanding of how the psychosocial environment influences cancer risk and survival, potentially leading to improved prevention and treatment strategies.
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Notes
- 1.
Interestingly, maltreated children tended to have elevated methylation levels at sites that had low to moderate methylation, but reduced methylation levels at sites that typically had high methylation, suggesting that maltreatment may contribute to a “flattened” or less variable global methylation pattern.
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- 3.
Interestingly, socially isolated mice in this study were actually less likely to develop mammary tumors, possibly because social isolation was associated with less well-developed mammary tissue [85]. Future work is needed to replicate and extend these findings among mice with normative mammary tissue development, and in humans.
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Litzelman, K., Verma, M. (2015). Epigenetic Regulation in Biopsychosocial Pathways. 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_29
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