Correspondence
Somatic Mutations of EGFR in Colorectal Cancers and Glioblastomas
N Engl J Med 2004; 351:2883December 30, 2004
- Article
To the Editor:
Recent reports suggest that mutations in the epidermal growth factor receptor (EGFR) gene predict sensitivity to EGFR kinase inhibitors. In particular, patients with lung cancers containing mutations in the EGFR kinase domain have had responses to gefitinib.1,2 Are similar EGFR mutations present in a significant fraction of other tumor types for which gefitinib might be suitable therapy? To answer this question, we screened DNA from 293 colorectal tumors and 59 glioblastomas for alterations in the EGFR kinase domain (exons 17 to 24). These tumors were chosen for analysis because they have been linked to EGFR signaling: EGFR-targeted antibodies (cetuximab) have been approved for use in patients with colorectal cancer, and structural alterations of the EGFR gene (amplifications and rearrangements) have been described in glioblastomas.3 However, our analysis showed that only one of the colorectal cancers and none of the glioblastomas harbored a mutation. The single mutation was a G-to-S substitution at amino acid 719, which is identical to an activating mutation previously reported in lung tumors.2 Our results show EGFR mutations occur at a very low frequency in colorectal cancers and glioblastomas and suggest that gefitinib is unlikely to be effective in patients with these tumors. Furthermore, these data suggest that mutations in the EGFR kinase domain are unlikely to be responsible for the reported success of cetuximab against many colorectal cancers.4,5
5 ReferencesThomas D. Barber, Ph.D.
Bert Vogelstein, M.D.
Howard Hughes Medical Institute, Baltimore, MD 21231Kenneth W. Kinzler, Ph.D.
Victor E. Velculescu, M.D., Ph.D.
Sidney Kimmel Cancer Center at Johns Hopkins, Baltimore, MD 21231
velculescu@jhmi.edu 1
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Full Text | Web of Science | Medline
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