Abstract
HER3, a member of the EGFR family of receptor tyrosine kinases coded by the ERBB3 gene, plays an important role in cancer, despite its lack of intrinsic kinase activity. As with genes coding for potential heterodimeric partners of HER3, EGFR, and HER2, oncogenic mutations of ERBB3 have been explored by several studies. In this review, we discuss the evidence presenting ERBB3 somatic mutations as potential tumoral drivers. We then show that ERBB3 mutations are not uncommon in many cancer types. Finally, we present the recent results of several studies evaluating different therapeutic approaches for treating patients with oncogenic ERBB3 mutations.
MeSH terms
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Animals
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Antibodies, Monoclonal / pharmacology
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Antibodies, Monoclonal / therapeutic use
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Antineoplastic Combined Chemotherapy Protocols / pharmacology*
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Antineoplastic Combined Chemotherapy Protocols / therapeutic use
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Carcinogenesis / drug effects
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Carcinogenesis / genetics*
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Cell Line, Tumor
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Clinical Trials as Topic
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Humans
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Mice
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Molecular Targeted Therapy / methods
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Mutation
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Neoplasms / drug therapy*
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Neoplasms / genetics
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Neoplasms / mortality
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Neoplasms / pathology
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Progression-Free Survival
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Protein Kinase Inhibitors / pharmacology*
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Protein Kinase Inhibitors / therapeutic use
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Protein Multimerization / drug effects
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Protein Multimerization / genetics
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Receptor, ErbB-2 / antagonists & inhibitors
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Receptor, ErbB-2 / genetics
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Receptor, ErbB-2 / metabolism
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Receptor, ErbB-3 / antagonists & inhibitors
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Receptor, ErbB-3 / genetics*
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Receptor, ErbB-3 / metabolism
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Signal Transduction / drug effects
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Signal Transduction / genetics
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Treatment Outcome
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Xenograft Model Antitumor Assays
Substances
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Antibodies, Monoclonal
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Protein Kinase Inhibitors
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ERBB2 protein, human
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ERBB3 protein, human
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Receptor, ErbB-2
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Receptor, ErbB-3