000			nab a22 7a 4500
999			_c16634 _d16634
003			PC16634
005			20211102104718.0
008			211028b xxu||||| |||| 00| 0 eng d
040			_cH12O
041			_aeng
100			_91082 _aCiruelos Gil, Eva María _eOncología Médica
245	0	0	_aTargeting the PI3K/AKT/mTOR pathway in estrogen receptor-positive breast cancer. _h[artículo]
260			_bCancer treatment reviews, _c2014
300			_a40(7):862-71.
500			_aFormato Vancouver: Ciruelos Gil EM. Targeting the PI3K/AKT/mTOR pathway in estrogen receptor-positive breast cancer. Cancer Treat Rev. 2014 Aug;40(7):862-71.
501			_a PMID: 24774538
504			_aContiene 121 referencias
520			_aApproximately 70-75% of breast cancers express the estrogen receptor (ER), indicating a level of dependence on estrogen for growth. Endocrine therapy is an important class of target-directed therapy that blocks the growth-promoting effects of estrogen via ER. Although endocrine therapy continues to be the cornerstone of effective treatment of ER-positive (ER+) breast cancer, many patients with advanced ER+ breast cancer encounter de novo or acquired resistance and require more aggressive treatment such as chemotherapy. Novel approaches are needed to augment the benefit of existing endocrine therapies by prolonging time to disease progression, preventing or overcoming resistance, and delaying the use of chemotherapy. The phosphatidylinositol 3-kinase/AKT/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway is a key intracellular signaling system that drives cellular growth and survival; hyperactivation of this pathway is implicated in the tumorigenesis of ER+ breast cancer and in resistance to endocrine therapy. Moreover, preclinical and clinical evidence show that PI3K/AKT/mTOR pathway inhibition can augment the benefit of endocrine therapy in ER+ breast cancer, from the first-line setting and beyond. This article will review the fundamental role of the PI3K/AKT/mTOR pathway in driving ER+ breast tumors, and its inherent interdependence with ER signaling. In addition, ongoing strategies to combine PI3K/AKT/mTOR pathway inhibitors with endocrine therapy for improved clinical outcomes, and methods to identify patient populations that would benefit most from inhibition of the PI3K/AKT/mTOR pathway, will be evaluated.
710			_9303 _aServicio de Oncología Médica
856			_uhttp://pc-h12o-es.m-hdoct.a17.csinet.es/pdf/pc/1/pc16634.pdf _ySolicitar documento
942			_2ddc _cART _n0