Defining the role of mTOR in cancer.

By D. Guertin, David M. Sabatini. Cancer Cell, 2007

2,978 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/dc88ff492be1d429b83c4b52ccfa141b17fba937

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Citations in the corpus

Tenets of PTEN tumor suppression. (2008, background): “…a number of tumor suppressor genes directly implicated in human cancer, the mTOR arm of the PTEN/PI3K/AKT pathway is emerging as an effective target for anti-cancer agents, especially in tumors in which the activity of the mTOR pathway is elevated (Faivre et al., 2006; Guertin and Sabatini, 2007).”
The mTOR Signalling Pathway in Human Cancer (2012, neutral): “[1–3]).”
The nuts and bolts of AGC protein kinases (2010, background): “, which consists of the kinase mTOR (also known as FRAP1) bound to the mTOR-interacting proteins rapamycin-insensitive companion of TOR ( RICTOR ), SAPK-interacting protein 1 (Sin1), mLST8, protein observed with RICTOR 1 (PROTOR 1) and PROTOR 2 (Ref”
Epidermal Growth Factor Receptor Cell Proliferation Signaling Pathways (2017, background): “mTOR inhibition is also attractive since it may avoid the side effects associated with inhibition of PI3K-AKT, which have broader biological functions [433].”
Regulation of the mTOR complex 1 pathway by nutrients, growth factors, and stress (2010, background): “…a FRAP-ATM-TTRAP (FAT) domain of poorly understood function. mTOR exists in two distinct complexes called complex 1 (mTORC1) and complex 2 (mTORC2) (Guertin and Sabatini, 2007). mTORC1 is a homodimer (Takahara et al., 2006; Wang et al., 2006; Yip et al., 2010; Zhang et al., 2006), and has four…”
AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity (2011, positive): “mTOR functions in two multiprotein complexes, mTORC1 andmTORC2 (Guertin and Sabatini, 2007).”
Active-Site Inhibitors of mTOR Target Rapamycin-Resistant Outputs of mTORC1 and mTORC2 (2009, background): “]. Two of these molecules, PP242 and PP30, are the first potent, selective, and ATP-competitive inhibitors of mTOR. Unlike rapamycin, these molecules inhibit both mTORC1 and mTORC2, and, unlike PI3K family inhibitors such as LY294002, these molecules inhibit mTOR with a high degree of selectivity re”
DEPTOR is an mTOR Inhibitor Whose Frequent Overexpression in Multiple Myeloma Cells Promotes their Survival (2009, background): “…the mTOR signaling network. mTOR resides in two distinct multiprotein complexes referred to as mTOR complex 1 (mTORC1) and 2 (mTORC2) (reviewed in Guertin and Sabatini, 2007). mTORC1 is composed of the mTOR catalytic subunit and three associated proteins, raptor, PRAS40, and mLST8/GbL. mTORC2…”
Targeting phosphoinositide 3-kinase: moving towards therapy. (2008, result): “Promising results were obtained in mantle cell lymphoma, endometrial cancer and renal cell carcinoma [162].”
The mammalian Target of Rapamycin (mTOR) regulates T helper cell differentiation through the selective activation of mTORC1 and mTORC2 signaling (2011, background): “2005" language="eng" relation="no"> The kinase mTOR is an evolutionarily conserved member of the phosphatidylinositol-3-OH kinase (PI(3)K)-related kinase family that has a central role in the regulation of metabolism, protein synthesis, energy balance, proliferation and surviva”
Dietary and genetic obesity promote liver inflammation and tumorigenesis by enhancing IL-6 and TNF expression (2010, background): “A more relevant player whose contribution merits further and dedicated studies is mTOR, whose activity is elevated in the obese liver (Figure 4A) and which is known to be an important regulator of cell and tumor growth (Guertin and Sabatini, 2007).”
Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells. (2009, background): “In addition, the cannabinoid-induced decrease in p70S6 kinase and S6 phosphorylation, autophagy, and cell death were not evident in Tsc2–/– cells, in which mTORC1 is constitutively active (20) (Figure 4B and Supplemental Figure 6, A and B), further supporting a major role for mTORC1 inhibition in th”
Nutrient-dependent mTORC1 association with the ULK1-Atg13-FIP200 complex required for autophagy. (2009, background): “(m)TOR forms two distinct complexes, (m)TORC1 and (m)TORC2 (Wullschleger et al., 2006; Guertin and Sabatini, 2007; Yang and Guan, 2007).”
The 14-3-3 proteins: integrators of diverse signaling cues that impact cell fate and cancer development (2008, background): “The mammalian target of rapamycin (mTOR) is a key effector in an important growthpromoting pathway that is commonly dysregulated in human cancers [15,16].”