Abstract
A preclinical trial identified 4 of 20 (20%) gastric cancer (GC) patient-derived xenografts responded to cetuximab. Genome-wide profiling and additional investigations revealed that high EGFR mRNA expression and immunohistochemistry score (3+) are associated with tumor growth inhibition. Furthermore, EGFR amplification were observed in 2/4 (50%) responders with average copy number 5.8 and >15 respectively. Our data suggest that a GC subtype with EGFR amplification and overexpression benefit from cetuximab treatment.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antibodies, Monoclonal, Humanized / administration & dosage
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Antibodies, Monoclonal, Humanized / pharmacology*
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Antineoplastic Agents / administration & dosage
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Antineoplastic Agents / pharmacology*
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Cetuximab
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Disease Models, Animal
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ErbB Receptors / antagonists & inhibitors
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ErbB Receptors / genetics*
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ErbB Receptors / metabolism
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Female
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Gene Amplification*
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Gene Expression Profiling
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Gene Expression Regulation, Neoplastic
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Gene Expression*
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Humans
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Mice
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Mutation
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Stomach Neoplasms / drug therapy
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Stomach Neoplasms / genetics*
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Stomach Neoplasms / pathology
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Treatment Outcome
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Tumor Burden / drug effects
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Xenograft Model Antitumor Assays
Substances
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Antibodies, Monoclonal, Humanized
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Antineoplastic Agents
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ErbB Receptors
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Cetuximab