Review Article

Compensatory Estrogen Signal Is Capable of DNA Repair in Antiestrogen-Responsive Cancer Cells via Activating Mutations

Figure 4

Mechanism of tumor resistance in cancer cells treated with tamoxifen (T). The liganded activation of abundant estrogen receptors (ERs) is completely blocked by T binding, and they are deregulated instead of activation. Compensatory abundant expression of growth factor receptors (GFRs) struggles for the unliganded activation of T-bound ERs, while the T blockade of the liganded pathway inhibits the restoration of ER signaling. GF: growth factor; N: nucleus; red arrow: activation; black arrow: inhibition.