Abstract
Anticancer targeted therapies are designed to exploit a particular vulnerability in the tumor, which in most cases results from its dependence on an oncogene and/or loss of a tumor suppressor. Genes in the phosphoinositide 3-kinase (PI3K)/AKT pathway are the most frequently altered in human cancers. Aberrant activation of this pathway, as a result of these somatic alterations, is associated with cellular transformation, tumorigenesis, cancer progression, and drug resistance. Several drugs targeting PI3K/ATK are currently in clinical trials, alone or in combination, in both solid tumors and hematologic malignancies. These drugs are the focus of this review.
Keywords:
breast cancer; lymphoproliferative disorders; mammalian target of rapamycin (mTOR); mutation; pathway inhibitors; phosphoinositide 3-kinase (PI3K)/AKT.
MeSH terms
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Antineoplastic Agents / therapeutic use*
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Breast Neoplasms / chemistry
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Breast Neoplasms / drug therapy*
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Female
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Humans
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Lymphoproliferative Disorders / drug therapy
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Molecular Targeted Therapy / methods*
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Phosphatidylinositol 3-Kinase / genetics
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Phosphatidylinositol 3-Kinase / metabolism
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Phosphoinositide-3 Kinase Inhibitors*
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Protein Kinase Inhibitors / therapeutic use*
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Proto-Oncogene Proteins c-akt / antagonists & inhibitors*
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Proto-Oncogene Proteins c-akt / genetics
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Proto-Oncogene Proteins c-akt / metabolism
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Receptor Protein-Tyrosine Kinases / metabolism
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Receptor, ErbB-2 / analysis
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Receptors, Estrogen / analysis
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Signal Transduction / drug effects*
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TOR Serine-Threonine Kinases / antagonists & inhibitors
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TOR Serine-Threonine Kinases / metabolism
Substances
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Antineoplastic Agents
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Phosphoinositide-3 Kinase Inhibitors
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Protein Kinase Inhibitors
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Receptors, Estrogen
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MTOR protein, human
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Phosphatidylinositol 3-Kinase
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ERBB2 protein, human
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Receptor Protein-Tyrosine Kinases
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Receptor, ErbB-2
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Proto-Oncogene Proteins c-akt
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TOR Serine-Threonine Kinases