Epidermal growth factor receptor (EGFR) mutations in non-small-cell lung cancer (NSCLC) cells were first discovered in 2004 and most frequently occur in exons 18–21 of the tyrosine kinase domain.¹ EGFR mutations occur in 40–60% of South-East Asian patients compared with 10–20% of Caucasian patients with lung adenocarcinomas and are most frequently observed in never or light smokers.¹

An estimated 85% of activating EGFR mutations are exon 19 deletion or L858R point mutation in exon 21.² Both these mutations are sensitizing, meaning that tumors harboring these mutations are sensitive to EGFR tyrosine kinase inhibitors (TKIs).¹ A less common type of EGFR mutation is the in-frame insertion in exon 20.¹ Figure 1 shows the frequency of different types of EGFR mutations that can occur in patients with NSCLC.³

Information on acquired resistance mutations can be found in the section “EGFRm: Disease progression”.

Since the identification of EGFR mutations responsive to gefitinib in 2004, a range of TKIs have undergone clinical trials and been approved for patients with EGFR mutation-positive (EGFRm) advanced NSCLC.^1,4 A timeline of key approvals and events in this field can be seen in Figure 2.^4-21

Please refer to the full prescribing information for further information regarding each therapy.