@article{10.37349/etat.2022.00096,
abstract = {Endocrine resistance is a major hurdle in the treatment of estrogen receptor (ER)-positive breast cancer. When abnormally regulated, molecular signals responsible for cellular proliferation, as well as ER itself, allow for cellular evasion of ER-dependent treatments. Therefore, pharmacological treatments that target these evasion mechanisms are beneficial for the treatment of endocrine-resistant breast cancers. This review summarizes currently understood molecular signals that contribute to endocrine resistance and their crosstalk that stem from mitogen-activated protein kinase (MAPK), phosphoinositol-3 kinase/protein kinase B (PI3K/AKT), mechanistic target of rapamycin (mTOR), cyclin-dependent kinases 4 and 6 (CDK4/6) and aberrant ER function. Recent clinical trials that target these molecular signals as a treatment strategy for endocrine-resistant breast cancer are also highlighted.},
author = {Musheyev, David and Alayev, Anya},
doi = {10.37349/etat.2022.00096},
journal = {Exploration of Targeted Anti-tumor Therapy},
pages = {480--496},
title = {{Endocrine therapy resistance: what we know and future directions}},
url = {https://www.explorationpub.com/Journals/etat/Article/100296},
volume = {3},
year = {2022},
number = {4}
}