Overcoming endocrine resistance due to reduced PTEN levels in estrogen receptor-positive breast cancer by co-targeting mammalian target of rapamycin, protein kinase B, or mitogen-activated protein kinase kinase

@inproceedings{Fu2014OvercomingER,
  title={Overcoming endocrine resistance due to reduced PTEN levels in estrogen receptor-positive breast cancer by co-targeting mammalian target of rapamycin, protein kinase B, or mitogen-activated protein kinase kinase},
  author={Xiaoyong Fu and Chad J Creighton and Nrusingh C. Biswal and Vijetha Kumar and Martin J Shea and Sabrina Herrera and Alejandro Lui{\~n}a Contreras and Carolina Gutierrez and Tao Wang and Sarmistha Nanda and Mario Alberto Giuliano and Gladys D. Morrison and Agostina Nardone and Kristen L. Karlin and Thomas Westbrook and Laura Heiser and Pavana Anur and Paul T. Spellman and Sylvie M. Guichard and Paul David Smith and Barry R. Davies and Teresa C M Klinowska and Adrian V. Lee and Gordon B. Mills and Mothaffar F Rimawi and Susan G. Hilsenbeck and Joe W. Gray and Amit Joshi and Charles Osborne and Rachel Schiff},
  booktitle={Breast Cancer Research},
  year={2014}
}
Activation of the phosphatidylinositol 3-kinase (PI3K) pathway in estrogen receptor α (ER)-positive breast cancer is associated with reduced ER expression and activity, luminal B subtype, and poor outcome. Phosphatase and tensin homolog (PTEN), a negative regulator of this pathway, is typically lost in ER-negative breast cancer. We set out to clarify the role of reduced PTEN levels in endocrine resistance, and to explore the combination of newly developed PI3K downstream kinase inhibitors to… CONTINUE READING