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- W2014001512 endingPage "4461" @default.
- W2014001512 startingPage "4452" @default.
- W2014001512 abstract "Although antiestrogen therapies targeting estrogen receptor (ER) α signaling prevent disease recurrence in the majority of patients with hormone-dependent breast cancer, a significant fraction of patients exhibit de novo or acquired resistance. Currently, the only accepted mechanism linked with endocrine resistance is amplification or overexpression of the ERBB2 (human epidermal growth factor receptor 2 [HER2]) proto-oncogene. Experimental and clinical evidence suggests that hyperactivation of the phosphatidylinositol 3-kinase (PI3K) pathway, the most frequently mutated pathway in breast cancer, promotes antiestrogen resistance. PI3K is a major signaling hub downstream of HER2 and other receptor tyrosine kinases. PI3K activates several molecules involved in cell-cycle progression and survival, and in ER-positive breast cancer cells, it promotes estrogen-dependent and -independent ER transcriptional activity. Preclinical tumor models of antiestrogen-resistant breast cancer often remain sensitive to estrogens and PI3K inhibition, suggesting that simultaneous targeting of the PI3K and ER pathways may be most effective. Herein, we review alterations in the PI3K pathway associated with resistance to endocrine therapy, the state of clinical development of PI3K inhibitors, and strategies for the clinical investigation of such drugs in hormone receptor-positive breast cancer." @default.
- W2014001512 created "2016-06-24" @default.
- W2014001512 creator A5043946489 @default.
- W2014001512 creator A5080163243 @default.
- W2014001512 creator A5089113899 @default.
- W2014001512 date "2011-11-20" @default.
- W2014001512 modified "2023-10-13" @default.
- W2014001512 title "Phosphatidylinositol 3-Kinase and Antiestrogen Resistance in Breast Cancer" @default.
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