Interactions of PI3K/Akt/mTOR and estrogen receptor signaling in breast cancer

摘要

Endocrine therapies are used to treat estrogen receptor-positive (ER+) breast cancer; however, patients develop resistance in some cases due to hormone-independent activation of ER signaling. Dysregulation of mTOR, a central hub for various signaling pathways regulated by hormones and growth factors, is a mechanism of endocrine therapy resistance. Activation of kinases in these pathways can cause ligand-independent ER signaling. Phosphorylation of ER regulates activity and predicts clinical outcome in ER+ breast cancer.