摘要: Mammalian target of rapamycin (mTOR) is a component signaling pathway (PTEN/PI3K/AKT) that frequently dysregulated in cancer. However, its precise relationship to the MAPK cascade (Ras/Raf/MEK/ERK), another often implicated tumorigenesis, has not been well defined. Recent evidence from tissue specimens obtained patients who have received mTOR inhibitors suggests ERK may be activated response interruption. In this issue JCI, Waugh Kinkade et al. and Carracedo examine between these pathways prostate breast cancer cell model systems (see related articles beginning on pages 3051 3065, respectively). Their findings suggest link inhibition activation, possibly reflecting interruption novel negative S6K1-dependent feedback loop. Significantly, both groups observed simultaneous MEK/ERK resulted substantially enhanced antitumor effects vitro vivo. Together, concurrent complementary warrants further investigation therapy.
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