ER and PI3K independently modulate endocrine resistance in ER-positive breast cancer

Brian A. Van Tine, Robert J. Crowder, Matthew J. Ellis

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Endocrine therapy-resistant estrogen receptor-positive (ER1) breast cancer is the most common cause of breast cancer death. Miller and colleagues demonstrate that ligand-independent ER activity promotes the growth of breast cancer cells through CDK4/E2F. As an independent event, the phosphatidylinositol 3-kinase (PI3K) pathway is also upregulated in endocrine therapy-resistant cells. Promising preclinical evidence by several groups for the combination of an inhibitor of ligand-independent ER, fulvestrant, with PI3K inhibition, has led to the activation of trials evaluating this concept.

Original languageEnglish
Pages (from-to)287-288
Number of pages2
JournalCancer discovery
Volume1
Issue number4
DOIs
StatePublished - Sep 2011

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