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The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

PTEN and the PI3-Kinase Pathway in Cancer

Open access
Chalhoub, Nader, Baker, Suzanne J.·2009·Annual Review of Pathology: Mechanisms of Disease

Abstract

PI3-kinase and PTEN are major positive and negative regulators, respectively, of the PI3-kinase pathway, which regulates growth, survival, and proliferation. These key signaling components are two of the most frequently mutated proteins in human cancers, resulting in unregulated activation of PI3K signaling and providing irrefutable genetic evidence of the central role of this pathway in tumorigenesis. PTEN regulates PI3K signaling by dephosphorylating the lipid signaling intermediate PIP 3, but PTEN may have additional phosphatase-independent activities, as well as other functions in the nucleus. In this review, we highlight current work showing cancer-relevant complexities in the regulation of PTEN and PI3K activity, potential novel functions for PTEN, and feedback regulation within the pathway. The significance and complexity of PI3K signaling make it an important but challenging therapeutic target for cancer.

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Metadata

Authors
Chalhoub, N., & Baker, S. J.
Venue
Annual Review of Pathology: Mechanisms of Disease
Published
2009-02-01
Volume
4
Issue
1
Pages
127-150
ISSN
  • 1553-4006 (ISSN-L)
  • 1553-4014
OpenAlex
W2151258296
Cited by
1,245
References
11
FWCI
2.09
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: PTEN and the PI3-Kinase Pathway in Cancer. https://app.cochat.ai/papers/10.1146/annurev.pathol.4.110807.092311
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Chalhoub, N., & Baker, S. J. (2009). PTEN and the PI3-Kinase Pathway in Cancer. Annual Review of Pathology: Mechanisms of Disease. https://doi.org/10.1146/annurev.pathol.4.110807.092311

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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.