PI3K Inhibition Overcomes Trastuzumab Resistance: Blockade of ErbB2/ErbB3 Is Not Always Enough

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, wh...

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Veröffentlicht in:	Cancer cell 2009-05, Vol.15 (5), p.353-355
Hauptverfasser:	Hynes, Nancy E., Dey, Julien H.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Antibodies, Monoclonal - pharmacology Antibodies, Monoclonal, Humanized Antineoplastic Agents - pharmacology Breast Neoplasms - drug therapy Drug Resistance, Neoplasm - genetics Female Humans Mutation Phosphatidylinositol 3-Kinases - antagonists & inhibitors Phosphatidylinositol 3-Kinases - genetics Proto-Oncogene Proteins c-akt - metabolism Receptor, ErbB-2 - antagonists & inhibitors Receptor, ErbB-2 - metabolism Receptor, ErbB-3 - antagonists & inhibitors Receptor, ErbB-3 - metabolism Signal Transduction - drug effects Trastuzumab
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Zusammenfassung:	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.
ISSN:	1535-6108 1878-3686
DOI:	10.1016/j.ccr.2009.04.004