Abstract
This review presents some therapeutic interventions actually considered in prostate cancer therapy to compensate constitutive activation of the PI3K/Akt signalling pathway induced, particularly, by mutations of PTEN gene. Special emphasis is placed on applicability of EGF-R tyrosine kinase, COX-2, PDK-1, mTOR and farnesyltransferase inhibitors.
MeSH terms
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3-Phosphoinositide-Dependent Protein Kinases
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use*
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Cyclooxygenase 2 Inhibitors / metabolism
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Enzyme Inhibitors / pharmacology
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Enzyme Inhibitors / therapeutic use*
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ErbB Receptors / antagonists & inhibitors
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ErbB Receptors / metabolism
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Farnesyltranstransferase / antagonists & inhibitors
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Farnesyltranstransferase / metabolism
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Humans
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Male
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Mutation
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Phosphatidylinositol 3-Kinases / chemistry
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Phosphatidylinositol 3-Kinases / metabolism*
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Phosphoinositide-3 Kinase Inhibitors
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Prostatic Neoplasms / drug therapy*
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Prostatic Neoplasms / pathology
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Protein Kinases / metabolism
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Protein Serine-Threonine Kinases / antagonists & inhibitors
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Protein Serine-Threonine Kinases / metabolism
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Proto-Oncogene Proteins c-akt / antagonists & inhibitors
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Proto-Oncogene Proteins c-akt / metabolism*
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Signal Transduction
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TOR Serine-Threonine Kinases
Substances
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Antineoplastic Agents
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Cyclooxygenase 2 Inhibitors
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Enzyme Inhibitors
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Phosphoinositide-3 Kinase Inhibitors
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Farnesyltranstransferase
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Protein Kinases
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MTOR protein, human
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ErbB Receptors
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3-Phosphoinositide-Dependent Protein Kinases
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Protein Serine-Threonine Kinases
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Proto-Oncogene Proteins c-akt
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TOR Serine-Threonine Kinases