Abstract
AKT/PKB (Protein Kinase B) are central proteins mediating signals from receptor tyrosine kinases and phosphatidylinositol 3-kinase. AKT kinases are involved in a number of important cellular processes including cell proliferation and survival, cell size in response to nutrient availability, tumor invasion/metastasis, and angiogenesis. Various components of the AKT signaling pathway are encoded by tumor suppressor genes and oncogenes whose loss or activation, respectively, plays an important role in tumorigenesis. The growing body of evidence connecting deregulated AKT signaling with sporadic human cancers and inherited cancer predisposition syndromes is discussed. We also highlight new findings regarding the involvement of activating mutations of AKT1, AKT2, and AKT3 in somatic overgrowth disorders: Proteus syndrome, hypoglycemia with hypertrophy, and hemimegalencephaly, respectively. In addition, we review recent literature documenting the various ways the AKT signaling pathway is activated in human cancers and consequences for molecularly targeted therapies.
Keywords: AKT/PKB kinases, hemimegalencephaly, human malignancy, hypoglycemia, oncogenes, proteus syndrome, targeted therapies, tumor suppressor genes
Current Cancer Drug Targets
Title:Diverse Mechanisms of AKT Pathway Activation in Human Malignancy
Volume: 13 Issue: 3
Author(s): Mitchell Cheung and Joseph R. Testa
Affiliation:
Keywords: AKT/PKB kinases, hemimegalencephaly, human malignancy, hypoglycemia, oncogenes, proteus syndrome, targeted therapies, tumor suppressor genes
Abstract: AKT/PKB (Protein Kinase B) are central proteins mediating signals from receptor tyrosine kinases and phosphatidylinositol 3-kinase. AKT kinases are involved in a number of important cellular processes including cell proliferation and survival, cell size in response to nutrient availability, tumor invasion/metastasis, and angiogenesis. Various components of the AKT signaling pathway are encoded by tumor suppressor genes and oncogenes whose loss or activation, respectively, plays an important role in tumorigenesis. The growing body of evidence connecting deregulated AKT signaling with sporadic human cancers and inherited cancer predisposition syndromes is discussed. We also highlight new findings regarding the involvement of activating mutations of AKT1, AKT2, and AKT3 in somatic overgrowth disorders: Proteus syndrome, hypoglycemia with hypertrophy, and hemimegalencephaly, respectively. In addition, we review recent literature documenting the various ways the AKT signaling pathway is activated in human cancers and consequences for molecularly targeted therapies.
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Cite this article as:
Cheung Mitchell and R. Testa Joseph, Diverse Mechanisms of AKT Pathway Activation in Human Malignancy, Current Cancer Drug Targets 2013; 13 (3) . https://dx.doi.org/10.2174/1568009611313030002
DOI https://dx.doi.org/10.2174/1568009611313030002 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
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