Abstract
Trastuzumab targets ErbB2 and is used for treating ErbB2-overexpressing breast cancers. In this issue of Cancer Cell, Junttila et al. show that trastuzumab disrupts ligand-independent ErbB2/ErbB3/PI3K complexes and blocks AKT signaling; if PI3K is mutated, complex disruption does not inhibit AKT, which explains why trastuzumab is ineffective in some tumors.
MeSH terms
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Animals
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Antibodies, Monoclonal / pharmacology*
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Antibodies, Monoclonal, Humanized
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Antineoplastic Agents / pharmacology*
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Breast Neoplasms / drug therapy
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Drug Resistance, Neoplasm* / genetics
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Female
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Humans
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Mutation
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Phosphatidylinositol 3-Kinases / genetics
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Phosphoinositide-3 Kinase Inhibitors*
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Proto-Oncogene Proteins c-akt / metabolism
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Receptor, ErbB-2 / antagonists & inhibitors*
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Receptor, ErbB-2 / metabolism
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Receptor, ErbB-3 / antagonists & inhibitors
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Receptor, ErbB-3 / metabolism
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Signal Transduction / drug effects
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Trastuzumab
Substances
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Humanized
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Antineoplastic Agents
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Phosphoinositide-3 Kinase Inhibitors
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Receptor, ErbB-2
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Receptor, ErbB-3
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Proto-Oncogene Proteins c-akt
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Trastuzumab