Ontology highlight
ABSTRACT: Purpose
The development of endocrine resistance remains a significant challenge in the clinical management of estrogen receptor-positive (ER+) breast cancer. Metabolic reprogramming is a prominent component of endocrine resistance and a potential therapeutic intervention point. However, a limited understanding of which metabolic changes are conserved across the heterogeneous landscape of ER+ breast cancer or how metabolic changes factor into ER DNA binding patterns hinder our ability to target metabolic adaptation as a treatment strategy. This study uses dimethyl fumarate (DMF) to restore tamoxifen (Tam) and fulvestrant (Fulv) sensitivity in endocrine-resistant cell lines and investigates how metabolic changes influence ER DNA-binding patterns.Experi
SUBMITTER: Brechbuhl HM
PROVIDER: S-EPMC11703175 | biostudies-literature | 2024 Dec
REPOSITORIES: biostudies-literature