Although endocrine therapies that block the production or subsequent effects of estrogen have been a bedrock of the treatment for hormonally driven breast cancer for more than 40 years, resistance poses a major threat to their efficacy and has become a focus of ongoing research.
Despite gaps in current knowledge, investigators are already working toward the development of novel treatment strategies to combat the effects of the mutations and wrestle back control of ER-positive tumor growth.
As the cellular orchestrator of the effects of the estrogen hormones, ERs play an important role in a plethora of processes, including its most renowned functions in reproduction and sexual development and in modulating the immune system.1,2
Figure. Key Components of Estrogen Receptor Signaling
Estrogens are steroid hormones that pass freely across the cell membrane and do not need to bind to a membrane-bound receptor to transmit their signal into the cell. Although they can be found in the membranes, ERs predominantly reside in the nucleus, where, after binding to an estrogen ligand, they can act directly as a transcription factor.
ER-Driven Breast Cancer
ER signaling has been shown to be indispensable to mammary gland development,6,7
although the precise mechanisms through which it regulates the proliferation and differentiation of human breast cells is unclear. A relatively small number of cells in the normal mammary gland express ERs.8
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