The translation factor eIF-4E promotes tumor formation and cooperates with c-Myc in lymphomagenesis
By D. Ruggero, L. Montanaro, Li Ma, W. Xu, P. Londei, C. Cordon-Cardo, P. Pandolfi. Nature Medicine, 2004
620 citations recorded by the source corpus.
Subfields: Cancer Research, Dermatology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/afbef651eab951592e7900d59e8ce9068b3d9560
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In Cancer Research
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Citations in the corpus
- mTOR, translation initiation and cancer (2006, background): “Furthermore, two groups independently demonstrated that eIF4E promotes lymphomagenesis in cooperation with Myc in transgenic mice (Ruggero et al., 2004; Wendel et al., 2004).”
- Active-Site Inhibitors of mTOR Target Rapamycin-Resistant Outputs of mTORC1 and mTORC2 (2009, background): “mTORC1 integrates signals from growth factor receptors with cellular nutritional status and controls the level of cap-dependent mRNA translation by modulating the activity of key translational components such as the cap-binding protein and oncogene eIF4E [5].”
- Perturbations of the AKT signaling pathway in human cancer (2005, background): “For example, eIF4E has been shown to cooperate with c-Myc in B-cell lymphomagenesis (Ruggero et al., 2004; Wendel et al., 2004).”
- Human eIF4E promotes mRNA restructuring by stimulating eIF4A helicase activity (2013, background): “of immortalized cells and tumor formation in mice (9, 10, 12).”
- MYC as a regulator of ribosome biogenesis and protein synthesis (2010, background): “The increased expression of ribosomal proteins has also been associated with increased proliferation and growt”
- With TOR less is more: a key role for the conserved nutrient sensing TOR pathway in aging (2010, neutral): “Overexpression of eIF4E has also been shown to increase cellular senescence in mammalian cells as determined by b-galactosidase staining (Ruggero et al., 2004).”
- mTORC1 controls mitochondrial activity and biogenesis through 4E-BP-dependent translational regulation. (2013, methodology): “…(Laplante and Sabatini, 2012), and eIF4E overexpression is tumorigenic in vitro and in vivo (Avdulov et al., 2004; LazarisKaratzas et al., 1990; Ruggero et al., 2004; Wendel et al., s described in (A) and treated with asTORi for 12 hr (A) and treated with asTORi for 12 hr. Cells were rmined by…”
- Translational Control in Cancer. (2018, background): “eIF4E and eIF4G act as classical oncogenes, their overexpression resulting in transformation in vitro (in cell culture) and in vivo (in animals) (Lazaris-Karatzas et al. 1990; Fukuchi-Shimogori et al. 1997; Ruggero et al. 2004; Silvera et al. 2009).”