Abstract
Two recent papers identify KRAS activation as a mechanism of acquired resistance to EGFR blockade in colorectal cancer. In doing so, they suggest that resistance to single-agent EGFR blockade will be unavoidable because these alterations exist as latent subclones within the tumor even prior to the initiation of therapy.
MeSH terms
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Antibodies, Monoclonal / therapeutic use*
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Antibodies, Monoclonal, Humanized / pharmacology
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use*
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Cell Line, Tumor
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Cetuximab
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Colorectal Neoplasms / drug therapy*
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Colorectal Neoplasms / metabolism
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Colorectal Neoplasms / pathology
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DNA, Neoplasm / blood
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Drug Resistance, Neoplasm / drug effects*
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ErbB Receptors / antagonists & inhibitors*
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ErbB Receptors / metabolism
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Humans
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Mutation
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Panitumumab
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ras Proteins / genetics
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ras Proteins / metabolism
Substances
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Antibodies, Monoclonal
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Antibodies, Monoclonal, Humanized
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Antineoplastic Agents
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DNA, Neoplasm
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Panitumumab
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ErbB Receptors
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ras Proteins
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Cetuximab