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Cited by 332

The DOI matches its Crossref record; 113 of the 113 references it cites were found in a registry or an index.

Common corruption of the mTOR signaling network in human tumors

Open access
Menon, S, Manning, B D·2008·Oncogene

Abstract

The mammalian target of rapamycin (mTOR) is responsive to numerous extracellular and intracellular cues and, through the formation of two physically and functionally distinct complexes, has a central role in the homeostatic control of cell growth, proliferation and survival. Through the aberrant activation of mTOR signaling, the perception of cellular growth signals becomes disconnected from the processes promoting cell growth, and this underlies the pathophysiology of a number of genetic tumor syndromes and cancers. Here, we review the oncogenes and tumor suppressors comprising the regulatory network upstream of mTOR, highlight the human cancers in which mTOR is activated and discuss how dysregulated mTOR signaling provides tumors a selective growth advantage. In addition, we discuss why activation of mTOR, as a consequence of distinct oncogenic events, results in diverse clinical outcomes, and how the complexity of the mTOR signaling network might dictate therapeutic approaches.

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Metadata

Authors
Menon, S., & Manning, B. D.
Venue
Oncogene
Published
2008-12
Volume
27
Issue
S2
Pages
S43-S51
ISSN
  • 0950-9232 (ISSN-L)
  • 1476-5594
OpenAlex
W2053874502
Cited by
332
References
113
FWCI
5.09
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Common corruption of the mTOR signaling network in human tumors. https://app.cochat.ai/papers/10.1038/onc.2009.352
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Menon, S., & Manning, B. D. (2008). Common corruption of the mTOR signaling network in human tumors. Oncogene. https://doi.org/10.1038/onc.2009.352

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.