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A major problem with the use of antiestrogens (AE) is the prevalence of resistance, either at the outset of treatment or after continued use. The underlying mechanisms of AE resistance remain unclear. Estrogen receptor (ER)-mediated actions were identified initially as a pathway that was blocked in AE-treated cells, and inhibition of this pathway has been shown to cause permanent growth arrest/cell death. Reactive oxygen species (ROS), a byproduct of oxidative processes, can induce an irreversible growth arrest similar to selective estrogen receptor modulator (SERM) antiestrogens. SERMs are capable of producing ROS through their metabolic activation. These findings suggest that SERMs may mediate growth arrest by a mechanism involving ROS accumulation. Breast cancer cells have higher amounts of ROS than normal cells, and chronic treatment with tamoxifen or fulvestrant adds additional ROS. Breast cancer cells receiving longterm antiestrogen treatment appear to adapt to this increased, persistent level of ROS. This, in turn, leads to the disruption of reversible redox signaling that involves redoxsensitive phosphatases and protein kinases such as ERK and AKT, and also involves transcription factors such as AP-1 and NF-κB. This has downstream consequences for apoptosis, cell cycle progression, and cell metabolism. This review

Thioredoxin and Jab1 Control Estrogen- and Antiestrogen-Mediated Progression of the Cell Cycle Through p27 Interactions