Journal
JOURNAL OF CLINICAL ONCOLOGY
Volume 23, Issue 11, Pages 2556-2568Publisher
AMER SOC CLINICAL ONCOLOGY
DOI: 10.1200/JCO.2005.07.799
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Purpose Gefitinib and erlotinib are small molecules that selectively inhibit epidermal growth factor receptor (EGFR) tyrosine kinase activity. When these drugs were introduced into the clinic, the specific targets affected in human tumors were unknown. In April 2004, two groups reported that mutations in the tyrosine kinase domain of EGFR are strongly associated with gefitinib sensitivity in patients with non-small-cell lung cancer (NSCLC). We subsequently extended these findings and showed that such mutations are also associated with sensitivity to erlotinib. Here, we present current knowledge about EGFR mutations in the context of clinical trials involving gefitinib and erlotinib in NSCLC. Design This article reviews the rationale for targeting EGFR, the development of gefitinib and erlotinib, the discovery of EGFR mutations, and subsequent studies to define the incidence, spectrum, and functions of EGFR mutations. Results The discovery of EGFR mutations promises to alter the ways in which we consider and treat NSCLC. Conclusion This information can guide practitioners and help them inform their patients about EGFR mutations and their impact on the treatment of NSCLC.
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