Abstract
It is now well established that metastatic colorectal cancer patients without KRAS mutation (codon 12) benefit from treatment with an epidermal growth factor receptor monoclonal antibody (anti-EGFR mAb). Recently, EFGR and KRAS mutations have been shown to exist in patients who developed resistance to anti-EGFR mAb. We analyzed KRAS, BRAF V600E and EGFR S492R mutations in 37 post-anti-EGFR mAb tumor samples from 23 patients treated with chemotherapy plus anti-EGFR mAb. No EGFR S492R mutation was detected. A KRAS mutation was found after anti-EGFR mAb in only one tumor. Our results suggest that acquired EGFR S492R and KRAS mutations do not constitute the main mechanism of resistance to anti-EGFR mAb in combination with chemotherapy.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aged
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Antibodies, Monoclonal / adverse effects
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Antibodies, Monoclonal / therapeutic use
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Antineoplastic Agents / therapeutic use*
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Antineoplastic Combined Chemotherapy Protocols / therapeutic use
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Colorectal Neoplasms / drug therapy*
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Colorectal Neoplasms / genetics*
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Colorectal Neoplasms / pathology
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Combined Modality Therapy
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Disease Progression
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ErbB Receptors / genetics*
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ErbB Receptors / immunology*
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Female
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Humans
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Liver Neoplasms / secondary
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Male
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Middle Aged
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Mutation / genetics*
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Mutation / physiology*
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Neoplasm Metastasis
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Proto-Oncogene Proteins / genetics*
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Proto-Oncogene Proteins p21(ras)
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Treatment Outcome
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ras Proteins / genetics*
Substances
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Antibodies, Monoclonal
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Antineoplastic Agents
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KRAS protein, human
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Proto-Oncogene Proteins
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ErbB Receptors
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Proto-Oncogene Proteins p21(ras)
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ras Proteins