Figure 1
From: Targeting oestrogen to kill the cancer but not the patient
The evolution of antihormonal resistance. (A) About 20 years ago, it was believed that oestrogen receptor-positive (ER+) tumours would usually be expected to respond to oestrogen withdrawal or a selective oestrogen receptor modulator (SERM) such as tamoxifen, but eventually resistance would occur because ER− cells would overgrow the tumour. (B) Emerging laboratory and clinical evidence suggests that SERM resistance evolves from acquired resistance (Phase I) to Phase II, where any SERM will maintain growth, whereas, unliganded ER does not provoke growth. However, oestrogen at physiological levels causes rapid apoptosis. In Phase III, tumours are completely resistant to all antihormonal therapies and grow spontaneously. Nevertheless, physiological concentrations of oestrogen causes rapid apoptosis.
