The phosphatidylinositol 3-Kinase-AKT pathway in human cancer

One signal that is overactivated in a wide range of tumour types is the production of a phospholipid, phosphatidylinositol (3,4,5) trisphosphate, by phosphatidylinositol 3-kinase (PI3K). This lipid and the protein kinase that is activated by it -- AKT -- trigger a cascade of responses, from cell gro...

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Bibliographic Details
Published inNature reviews. Cancer Vol. 2; no. 7; pp. 489 - 501
Main Authors Sawyers, Charles L, Vivanco, Igor
Format Journal Article
LanguageEnglish
Published England Nature Publishing Group 01.07.2002
Subjects
Animals
Cancer
Cell Division
Cellular signal transduction
Control
Disease Models, Animal
Gene Deletion
Genetic aspects
Humans
Lipids
Mice
Models, Biological
Neoplasms - enzymology
Phenotype
Phosphatidylinositol 3-Kinases - metabolism
Phosphatidylinositol 3-Kinases - physiology
Phosphatidylinositol Phosphates - physiology
Physiological aspects
Protein Biosynthesis
Protein kinases
Protein-Serine-Threonine Kinases
Proto-Oncogene Proteins - metabolism
Proto-Oncogene Proteins c-akt
Signal Transduction
United States
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Summary:One signal that is overactivated in a wide range of tumour types is the production of a phospholipid, phosphatidylinositol (3,4,5) trisphosphate, by phosphatidylinositol 3-kinase (PI3K). This lipid and the protein kinase that is activated by it -- AKT -- trigger a cascade of responses, from cell growth and proliferation to survival and motility, that drive tumour progression. Small-molecule therapeutics that block PI3K signalling might deal a severe blow to cancer cells by blocking many aspects of the tumour-cell phenotype.
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ISSN:1474-1768
1474-175X
1474-1768
DOI:10.1038/nrc839