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. Author manuscript; available in PMC: 2013 Jan 8.
Published in final edited form as: Horm Mol Biol Clin Investig. 2012 Feb;9(2):143–163. doi: 10.1515/hmbci-2011-0004

Figure 8.

Figure 8

Evolution of acquired SERM resistance. After long-term treatment with SERMs (1–2 years in vivo), initially responsive ER-positive tumors become resistant to treatment and are stimulated by SERMs (Phase I of resistance) as well as by E2. After long-term transplantation into SERM-treated animal (5+ years), breast tumor growth is inhibited by E2, though still stimulated by SERMs (Phase II of resistance). A stylized representation of MCF-7 tumor growth is illustrated in Figure 9. This process with SERMs in vivo is replicated with estrogen deprivation with MCF-7 breast cancer cells in vitro; cells initially start to grow spontaneously but estrogen still induces growth (hypersensitivity). This is Phase I. Long-term estrogen deprivation causes spontaneous growth in culture but apoptosis with physiologic estrogens both in vitro and in vivo (Phase II).