Survival signalling by Akt and eIF4E in oncogenesis and cancer therapy

By H. Wendel, E. Stanchina, J. Fridman, A. Malina, S. Ray, S. Kogan, C. Cordon-Cardo, J. Pelletier, Scott W. Lowe. Nature, 2004

1,001 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/1b6d4ee4f26a1032e77f8746d85aaaffbb6ce9ee

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In Molecular Biology

1. David M. Sabatini
2. R. Shaw
3. Lewis C. Cantley
4. Nahum Sonenberg
5. N. Hay
6. Roberto Zoncu
7. A. Efeyan
8. B. Kaina

In Pathology and Forensic Medicine

1. David M. Sabatini
2. B. Kaina
3. W. Roos
4. C. Sawyers
5. R. Shaw

Citations in the corpus

• mTOR: from growth signal integration to cancer, diabetes and ageing (2010, background): “Indeed, eIF4E promoted cell survival in in vivo mouse models of lymphoma by upregulating the translation of the anti-apoptotic protein myeloid leukaemia cell differentiation 1 (MCL1”
• Activation of Akt and eIF4E survival pathways by rapamycin-mediated mammalian target of rapamycin inhibition. (2005, background): “Because Akt and eIF4E are often associated with cell survival and resistance to cancer therapy (4, 14), our findings imply that the activation of Akt and eIF4E through mTOR inhibition may counteract mTOR inhibitors’ anticancer efficacy and confers resistance to mTOR-targeted cancer therapy.”
• Ras, PI(3)K and mTOR signalling controls tumour cell growth (2006, background): “However, they found that overexpression of eIF4E (the binding partner of the mTORC1-regulated protein 4EBP1) avoided the rapamycin inhibition of growt”
• Upstream and downstream of mTOR. (2004, background): “Therefore, Wendel et al. (2004) postulated that a downstream target of mTOR mediates anti-apoptotic drug resistance, and they could restore drug resistance by expression of eIF4E.”
• Regulation of cap-dependent translation by eIF4E inhibitory proteins (2005, background): “, but also promotes tumour formation in transgenic mic”
• 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).”
• Suppression of anoikis and induction of metastasis by the neurotrophic receptor TrkB (2004, background): “One of the critical downstream targets of the PI(3)K/PKB pathway is p70S6K, a kinase implicated both in anoikis and lymphomagenesi”
• Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis (2006, background): “Also, overexpression of PKB in a murine lymphoma model induces rapamycin-sensitive tumorigenesis and drug resistance that can be phenocopied by over-expression of EIF4”
• DNA damage-induced cell death: from specific DNA lesions to the DNA damage response and apoptosis. (2013, background): “This inhibition of apoptosis by Akt has been characterized in many cancer cell systems [161–164].”
• 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).”