Somatic mutations of the epidermal growth factor receptor and non-small-cell lung cancer
- 1Division of Biomedical Sciences, Johns Hopkins Singapore, Singapore
- 2International Medical Centre, Johns Hopkins Singapore, Singapore
- Correspondence to: Dr X Zhang Division of Biomedical Sciences, Johns Hopkins Singapore, 31 Biopolis Way, #02-01, the Nanos, Singapore 138669, Singapore;
- Received 24 August 2006
- Accepted 14 November 2006
- Revised 13 November 2006
- Published Online First 8 December 2006
Frequent overexpression of epidermal growth factor receptor (EGFR) in non-small-cell lung cancer (NSCLC) makes EGFR a new therapeutic target. Two specific EGFR tyrosine kinase inhibitors, gefitinib (ZD1839, Iressa) and erlotinib (OSI-774, Tarceva), have been developed and approved by the US Food and Drug Administration for second-line and third-line treatment of advanced NSCLC. Clinical trials have shown considerable variability in the response rate between different patients with NSCLC, which led to the discovery of somatic EGFR-activating mutations. This brief review summarises the discovery and functional consequences of the mutations, their clinicopathological features and significant implications in the treatment and prognosis of NSCLC.
- EGF(R), epidermal growth factor (receptor)
- NSCLC, non-small cell lung cancer
- PCR, polymerase chain reaction
- SSCP, single-strand conformation polymorphism
- TKI, tyrosine kinase inhibitor
Competing interests: None.