Akt as a therapeutic target in cancer.

Abstract

BACKGROUND:

The phosphatidylinositol 3-kinase (PI3K)/phosphatase and tensin homolog (PTEN)/v-akt murine thymoma viral oncogene homolog (Akt)/mammalian target of rapamycin (mTOR) pathway is central in the transmission of growth regulatory signals originating from cell surface receptors.

OBJECTIVE:

This review discusses how mutations occur that result in elevated expression the PI3K/PTEN/Akt/mTOR pathway and lead to malignant transformation, and how effective targeting of this pathway may result in suppression of abnormal growth of cancer cells.

METHODS:

We searched the literature for articles which dealt with altered expression of this pathway in various cancers including: hematopoietic, melanoma, non-small cell lung, pancreatic, endometrial and ovarian, breast, prostate and hepatocellular.

RESULTS/CONCLUSIONS:

The PI3K/PTEN/Akt/mTOR pathway is frequently aberrantly regulated in various cancers and targeting this pathway with small molecule inhibitors and may result in novel, more effective anticancer therapies.

• Authors: Linda S Steelman, Kristin M Stadelman, William H Chappell, Stefan Horn, Jörg Bäsecke, Melchiorre Cervello, Ferdinando Nicoletti, Massimo Libra, Franca Stivala, Alberto M Martelli, James A McCubrey
• Journal: Expert opinion on therapeutic targets (Expert Opin Ther Targets) Vol. 12 Issue 9 Pg. 1139-65 (Sep 2008) ISSN: 1744-7631 [Electronic] England
• PMID: 18694380 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Antineoplastic Agents
• Proto-Oncogene Proteins c-akt

Topics

• Animals
• Antineoplastic Agents (pharmacology)
• Humans
• Mice
• Neoplasms (drug therapy)
• Proto-Oncogene Proteins c-akt (antagonists & inhibitors)