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. Author manuscript; available in PMC: 2016 Jan 31.
Published in final edited form as: Endocr Relat Cancer. 2014 Oct 22;22(1):R1–31. doi: 10.1530/ERC-14-0448

Figure 6.

Figure 6

Rules for the change in estrogen receptor (ER) positive breast cancer cell populations as they leave an estrogen rich environment at menopause, adapt to a declining estrogen environment over a 5 year period (referred to as Gap). Estrogen independent clones then grow out that are able to survive in an estrogen austere environment. This is modeled in the laboratory with long term estrogen deprived cells that exhibit acquired hypersensitivity to estrogen for growth (103) and then estrogen induced apoptosis (104, 109). Laboratory studies illustrate that the constituents of conjugated equine estrogen (CEE)(196), the endocrine disruptor bisphenol A (163) and phytoestrogens (143) can trigger cell replication or apoptosis dependent upon the cell populations and its natural estrogen rich or austere environment. Reproduced with permission from (140).