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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Published in	Nature reviews. Cancer Vol. 2; no. 7; pp. 489 - 501
Main Authors	Sawyers, Charles L, Vivanco, Igor
Format	Journal Article
Language	English
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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Abstract	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.
AbstractList	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.
Audience	Academic
Author	Vivanco, Igor Sawyers, Charles L
Author_xml	– sequence: 1 givenname: Charles L surname: Sawyers fullname: Sawyers, Charles L organization: Departments of Medicine, Molecular and Medical Pharmacology, Urology and Molecular Biology Institute, UCLA School of Medicine – sequence: 2 givenname: Igor surname: Vivanco fullname: Vivanco, Igor organization: Departments of Medicine, Molecular and Medical Pharmacology, Urology and Molecular Biology Institute, UCLA School of Medicine
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/12094235$$D View this record in MEDLINE/PubMed
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Snippet	One signal that is overactivated in a wide range of tumour types is the production of a phospholipid, phosphatidylinositol (3,4,5) trisphosphate, by...
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SubjectTerms	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
Title	The phosphatidylinositol 3-Kinase-AKT pathway in human cancer
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