The phosphatidylinositol 3-kinase–AKT pathway in human cancer
I Vivanco, CL Sawyers - Nature Reviews Cancer, 2002 - nature.com
Nature Reviews Cancer, 2002•nature.com
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.
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.
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.
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