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The PI3K Pathway is Activated in
Breast Cancer
PI3K/mTOR pathway activation is a hallmark of HR+/HER2– breast cancer
cells that have developed resistance to endocrine therapy
1,2
The ER pathway is upregulated in tumors from patients treated with PI3K
inhibitors
1
Dual blockade of the PI3K/mTOR and ER pathways may therefore restore
sensitivity to endocrine therapy
1,3,4
ER, estrogen receptor; HER2–, human epidermal growth factor receptor 2 negative; HR+, hormone receptor-positive; mTOR, mammalian target of rapamycin;
mTORC, mammalian target of rapamycin complex; PI3K, phosphatidylinositol 3-kinase.
1. Bosch A,
et al. Sci Transl Med.
2015;7:283ra51; 2. Miller TW,
et al. Cancer Discov.
2011;1:338–351; 3. Fox EM, e
t al. Front Oncol
. 2012;2:145;
4. Yardley D,
et al. Adv Ther.
2013;30:870–884.
Growth factor receptor
Protein
synthesis
AKT
mTORC2
PI3K
Buparlisib
Pan-PI3K inhibitor
Tumor growth and progression
Resistance to endocrine therapy
Fulvestrant
Estrogen
ER
mTORC1