Abstract
In this issue of Cancer Cell, Schwartz and colleagues and Costa and colleagues demonstrate that inhibition of PI3Kα or PI3Kβ in cancer cells with hyperactivated PI3Kα or PI3Kβ, respectively, activates the other isoform, leading to a "rebound" of the PI3K activity through different compensation mechanisms.
Copyright © 2015 Elsevier Inc. All rights reserved.
MeSH terms
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Aniline Compounds / pharmacology*
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Animals
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Antineoplastic Combined Chemotherapy Protocols / pharmacology*
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Breast Neoplasms / drug therapy*
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Chromones / pharmacology*
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Class I Phosphatidylinositol 3-Kinases / metabolism*
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Female
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Humans
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Neoplasms / drug therapy*
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PTEN Phosphohydrolase / genetics*
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Phosphoinositide-3 Kinase Inhibitors*
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Protein Kinase Inhibitors / pharmacology*
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Pyrimidinones / pharmacology*
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Thiazoles / pharmacology*
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ortho-Aminobenzoates / pharmacology*
Substances
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2-(1-(7-methyl-2-morpholin-4-yl-4-oxo-4H-pyrido(1,2-a)pyrimidin-9-yl)ethylamino)benzoic acid
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AZD8186
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Aniline Compounds
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Chromones
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Phosphoinositide-3 Kinase Inhibitors
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Protein Kinase Inhibitors
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Pyrimidinones
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Thiazoles
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ortho-Aminobenzoates
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Alpelisib
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Class I Phosphatidylinositol 3-Kinases
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PTEN Phosphohydrolase