Seventy percent of breast tumors are estrogen receptor (ER) positive. Although endocrine therapy is successful for the majority of patients with ER-positive tumors, approximately 30% show de novo or acquired resistance and the underlying molecular mechanisms and biomarkers that predict such resistance remain elusive. Two recent papers report that hyperactivation of the phosphatidylinositol 3-kinase (PI3K) pathway produces resistance to tamoxifen. This raises the possibility that combining endocrine therapy and PI3K inhibition may be more effective than monotherapy for treating ER-positive breast tumors, either as first-line therapy for tumors with high PI3K activity or after the development of resistance to endocrine therapy. © 2010 BioMed Central Ltd.
CITATION STYLE
Meyer, D. S., & Bentires-Alj, M. (2010). Can phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibition ERase them all? Breast Cancer Research, 12(5). https://doi.org/10.1186/bcr2718
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