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. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: J Mammary Gland Biol Neoplasia. 2013 May 24;18(2):199–208. doi: 10.1007/s10911-013-9293-5

Figure 6.

Figure 6

Proposed causal links tying BPA exposure, mammary gland development and carcinogenesis: BPA binds to the ERs present in the primary mesenchyme which alters the peri-ductal stroma, increasing peri-ductal collagen deposition and thus tissue rigidity. Increased rigidity is known to block or delay lumen formation. BPA also induces adipocyte differentiation in the primary periductal stroma and fat pad, which in turn causes increased duct elongation and branching. These changes lead to an increased sensitivity to mammotropic hormones such as estrogens and progesterone and likely to prolactin. The solid arrows link observations at E18 with postulated causal links. Dashed arrows link the observed effects at E18 with effects observed during puberty and adulthood. Not represented here are the effects of BPA on the hypothalamus, where it alters the control of ovarian cyclicity and likely the control of prolactin production.