Experimental models of endocrine responsive breast cancer: strengths, limitations, and use.

Breast cancers characterized by expression of estrogen receptor-alpha; ESR1) represent approximately 70% of all new cases and comprise the largest molecular subtype of this disease. Despite this high prevalence, the number of adequate experimental models of ER+ breast cancer is relatively limited. Nonetheless, these models have proved very useful in advancing understanding of how cells respond to and resist endocrine therapies, and how the ER acts as a transcription factor to regulate cell fate signaling.

A systems biology approach to discovering pathway signaling dysregulation in metastasis.

Total metastatic burden is the primary cause of death for many cancer patients. While the process of metastasis has been studied widely, much remains to be understood. Moreover, few agents have been developed that specifically target the major steps of the metastatic cascade.

Estrogen-Induced Apoptosis in Breast Cancers Is Phenocopied by Blocking Dephosphorylation of Eukaryotic Initiation Factor 2 Alpha (eIF2α) Protein.

Approximately 30% of aromatase-inhibitor-resistant, estrogen receptor-positive patients with breast cancer benefit from treatment with estrogen. This enigmatic estrogen action is not well understood and how it occurs remains elusive. Studies indicate that the unfolded protein response and apoptosis pathways play important roles in mediating estrogen-triggered apoptosis.