Bisphenol A and hormone-associated cancers: current progress and perspectives
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Updated: Apr 18, 2026

Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Hui Gao1, Bao-Jun Yang, Nan Li
1From the Department of Obstetrics & Gynecology (HG, B-JY, LMF, X-YS, W-HZ), Beijing TianTan Hospital, Capital Medical University, Beijing 100050, China; Department of Gynecology (NL), Cancer Institute and Hospital, Chinese Academy of Medical Sciences (CAMS), Beijing 100021, China; State Key Laboratory of Environmental Chemistry and Ecotoxicology (S-JL), Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China.
Abstract:
Bisphenol A (BPA), a carbon-based synthetic compound, exhibits hormone-like properties and is present ubiquitously in the environment and in human tissues due to its widespread use and biological accumulation. BPA can mimic estrogen to interact with estrogen receptors α and β, leading to changes in cell proliferation, apoptosis, or migration and thereby, contributing to cancer development and progression. At the genetic level, BPA has been shown to be involved in multiple oncogenic signaling pathways, such as the STAT3, MAPK, and PI3K/AKT pathways. Moreover, BPA may also interact with other steroid receptors (such as androgen receptor) and plays a role in prostate cancer development. This review summarizes the current literature regarding human exposure to BPA, the endocrine-disrupting effects of BPA, and the role of BPA in hormone-associated cancers of the breast, ovary, and prostate.
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