@article {Van Tine287, author = {Van Tine, Brian A. and Crowder, Robert J. and Ellis, Matthew J.}, title = {ER and PI3K Independently Modulate Endocrine Resistance in ER-Positive Breast Cancer}, volume = {1}, number = {4}, pages = {287--288}, year = {2011}, doi = {10.1158/2159-8290.CD-11-0192}, publisher = {American Association for Cancer Research}, abstract = {Endocrine therapy{\textendash}resistant estrogen receptor{\textendash}positive (ER+) 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. Cancer Discovery; 1(4): 287{\textendash}8. {\textcopyright}2011 AACR. Commentary on Miller et al., p. 338.}, issn = {2159-8274}, URL = {https://cancerdiscovery.aacrjournals.org/content/1/4/287}, eprint = {https://cancerdiscovery.aacrjournals.org/content/1/4/287.full.pdf}, journal = {Cancer Discovery} }