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Cited by 206

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Putting the Rap on Akt

Open access
Thompson, James E., Thompson, Craig B.·2004·Journal of Clinical Oncology

Abstract

The protein kinase Akt is activated in a wide variety of cancers, and this activation results in enhanced resistance to apoptosis through multiple mechanisms. This article reviews the control of Akt activation by the opposing actions of the oncogene phosphoinositide 3-kinase (PI3-K) and the tumor suppressor phosphatase and tensin homolog deleted on chromosome 10. The activation of Akt by transforming mutations, such as the amplification of HER-2/neu in breast cancer and the formation of the BCR/ABL fusion gene in chronic myelogenous leukemia, seems to be essential for the transforming activity of these oncogenes. We discuss several of the proposed mechanisms for the antiapoptotic effect of activated Akt, including the inhibition of the proapoptotic protein Bad, downregulation of death receptors, and enhancement of the glycolytic rate. Increased glycolysis is seen in many malignancies and forms the basis for the increasing use of positron emission tomography imaging for diagnosis and staging. Finally, we discuss rapamycin and its analogs, which are now in trials as antineoplastic therapy; these agents show particular promise in tumors in which Akt has been activated.

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Metadata

Authors
Thompson, J. E., & Thompson, C. B.
Venue
Journal of Clinical Oncology
Published
2004-10-15
Volume
22
Issue
20
Pages
4217-4226
ISSN
  • 0732-183X (ISSN-L)
  • 1527-7755
OpenAlex
W2117666643
Cited by
206
References
9
FWCI
9.62
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Putting the Rap on Akt. https://app.cochat.ai/papers/10.1200/jco.2004.01.103
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Thompson, J. E., & Thompson, C. B. (2004). Putting the Rap on Akt. Journal of Clinical Oncology. https://doi.org/10.1200/jco.2004.01.103

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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.