EGFR is expressed on the cell surface of a substantial percentage of NSCLCs. Initial studies with the EGFR tyrosine kinase inhibitors (TKIs) gefitinib (Iressa) and erlotinib (Tarceva) demonstrated biologic and clinical activity in only a relatively limited subset of lung cancers.[4]
Further investigation demonstrated that the highest response rates to these TKIs were seen in patients with somatic mutations within the EGFR-TK domain, particularly exon 19 deletion, exon 21 L858R, and exon 18 G719X.[5]
By contrast, the exon 20 T790M mutation is associated with acquired resistance to TKI therapy.[6]
http://emedicine.medscape.com/article/1689988-overview
Further investigation demonstrated that the highest response rates to these TKIs were seen in patients with somatic mutations within the EGFR-TK domain, particularly exon 19 deletion, exon 21 L858R, and exon 18 G719X.[5]
By contrast, the exon 20 T790M mutation is associated with acquired resistance to TKI therapy.[6]
http://emedicine.medscape.com/article/1689988-overview
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