AKT in cancer: new molecular insights and advances in drug development

The phosphatidylinositol‐3 kinase (PI3K)–AKT pathway is one of the most commonly dysregulated pathways in all of cancer, with somatic mutations, copy number alterations, aberrant epigenetic regulation and increased expression in a number of cancers. The carefully maintained homeostatic balance of ce...

Full description

Saved in:
Bibliographic Details
Published in:British journal of clinical pharmacology 2016-10, Vol.82 (4), p.943-956
Main Authors: Mundi, Prabhjot S., Sachdev, Jasgit, McCourt, Carolyn, Kalinsky, Kevin
Format: Article
Language:English
Subjects:
Animals
Carcinogenesis - drug effects
clinical oncology
Humans
medical oncology
Molecular Targeted Therapy - methods
Neoplasms - drug therapy
Neoplasms - enzymology
Neoplasms - metabolism
Neoplasms - pathology
Phosphatidylinositol 3-Kinases - physiology
phosphatidylinositol 3‐kinases
protein kinase B
Proto-Oncogene Mas
Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Proto-Oncogene Proteins c-akt - physiology
proto‐oncogene proteins c‐AKT
proto‐oncogene proteins c‐AKT/genetics
proto‐oncogene proteins c‐AKT/metabolism
Review
Reviews
Signal Transduction - drug effects
signal transduction/physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The phosphatidylinositol‐3 kinase (PI3K)–AKT pathway is one of the most commonly dysregulated pathways in all of cancer, with somatic mutations, copy number alterations, aberrant epigenetic regulation and increased expression in a number of cancers. The carefully maintained homeostatic balance of cell division and growth on one hand, and programmed cell death on the other, is universally disturbed in tumorigenesis, and downstream effectors of the PI3K–AKT pathway play an important role in this disturbance. With a wide array of downstream effectors involved in cell survival and proliferation, the well‐characterized direct interactions of AKT make it a highly attractive yet elusive target for cancer therapy. Here, we review the salient features of this pathway, evidence of its role in promoting tumorigenesis and recent progress in the development of therapeutic agents that target AKT.
ISSN:0306-5251
1365-2125
DOI:10.1111/bcp.13021