Abstract
The most recently discovered PTEN tumor suppressor gene has been found to be defective in a large number of human cancers. In addition, germ-line mutations in PTEN result in the dominantly inherited disease Cowden syndrome, which is characterized by multiple hamartomas and a high proclivity for developing cancer. A series of publications over the past year now suggest a mechanism by which PTEN loss of function results in tumors. PTEN appears to negatively control the phosphoinositide 3-kinase signaling pathway for regulation of cell growth and survival by dephosphorylating the 3 position of phosphoinositides.
MeSH terms
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Cell Division
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Cell Survival
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Genes, Tumor Suppressor*
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Humans
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Neoplasms / genetics*
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Neoplasms / metabolism
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Neoplasms / pathology
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PTEN Phosphohydrolase
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Phosphatidylinositol 3-Kinases / metabolism*
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Phosphoric Monoester Hydrolases / genetics*
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Phosphoric Monoester Hydrolases / metabolism*
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Protein Serine-Threonine Kinases / metabolism*
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Proto-Oncogene Proteins c-akt
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Proto-Oncogene Proteins*
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Signal Transduction
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Tumor Suppressor Proteins*
Substances
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Proto-Oncogene Proteins
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Tumor Suppressor Proteins
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AKT1 protein, human
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-akt
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Phosphoric Monoester Hydrolases
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PTEN Phosphohydrolase
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PTEN protein, human