Table 1. EGFR and KRAS Mutation Status in Lung Adenocarcinomas Sensitive or Refractory to Gefitinib or Erlotinib.

Lung tumors were examined for mutations in EGFR (exons 18–21) and KRAS (exon 2). In gefitinib-treated patients, six EGFR mutations involved exon 19 deletions that lacked the amino acids Leu-Arg-Glu-Ala, and two were exon 21 amino acid substitutions (L858R). A seventh case with an exon 19 deletion (involving 12 nucleotides) was detected by fluorescent capillary electrophoresis only, so exact sequence deletion information was unavailable (see Methods). In erlotinib-treated patients, three EGFR mutations were exon 19 deletions that lacked amino acids Leu-Arg-Glu-Ala, and five were exon 21 amino acid substitutions (L858R)

^a One erlotinib-sensitive tumor was unavailable for KRAS examination

^b The incidence of KRAS mutations in this cohort was low, probably because only cases involving bronchioloalveolar carcinoma were tested (see text)