Abstract
Approximately forty percent of colorectal cancers (CRC) are characterized by activating mutations of the K-RAS gene. Determination of K-RAS mutational status as a predictive marker for anti-EGFR therapy is usually based on the assumption of intratumoral homogeneity. We present two cases of CRC in which morphologically distinct tumor components were associated with different activating mutations of K-RAS in one patient and a mutated and a non-mutated portion in the second patient, as demonstrated by laser microdissection and consecutive molecular analyses.
Copyright © 2011 Elsevier GmbH. All rights reserved.
MeSH terms
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Adult
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Antineoplastic Agents / 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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DNA Mutational Analysis
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ErbB Receptors / antagonists & inhibitors
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ErbB Receptors / metabolism
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Genetic Predisposition to Disease
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Humans
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Male
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Microdissection
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Middle Aged
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Molecular Targeted Therapy
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Mutation*
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Phenotype
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Protein Kinase Inhibitors / therapeutic use
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Proto-Oncogene Proteins / genetics*
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Proto-Oncogene Proteins p21(ras)
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ras Proteins / genetics*
Substances
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Antineoplastic Agents
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KRAS protein, human
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Protein Kinase Inhibitors
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Proto-Oncogene Proteins
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EGFR protein, human
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ErbB Receptors
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Proto-Oncogene Proteins p21(ras)
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ras Proteins