Resumen
Endocrine therapy targeted against estrogen and the estrogen receptor is the main treatment modality for luminal breast cancer. Although a majority of patients respond to this treatment, one-third of all patients are resistant to this therapy. Hyperactive estrogen receptor along with alternative drivers such as mutations in the major tumor suppressor named p53 are known to contribute to resistance to therapy. The current study shines light on some of the mechanisms underlying the functioning of these players. A better understanding of these mechanisms will have important therapeutic implications by facilitating development of strategies to overcome therapeutic resistance by identifying novel targets and by combining drugs to effectively combat luminal breast cancer.