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Annals of Oncology Advance Access originally published online on October 23, 2006
Annals of Oncology 2007 18(1):99-103; doi:10.1093/annonc/mdl323
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© 2006 European Society for Medical Oncology

lung cancer

EGFR and KRAS mutations as criteria for treatment with tyrosine kinase inhibitors: retro- and prospective observations in non-small-cell lung cancer

N van Zandwijk1,*, A Mathy1, L Boerrigter2, H Ruijter2, I Tielen2, D de Jong2, P Baas1, S Burgers1 and P Nederlof2

1 Department of Thoracic Oncology
2 Department of Pathology, The Netherlands Cancer Institute, Amsterdam, The Netherlands

* Correspondence to: Dr N. van Zandwijk, Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands. Tel: +31-20-512-2958; Fax: +31-20-512-2572; E-mail: n.v.zandwijk{at}nki.nl

Results of individualized therapy guided by mutational tumor profile of patients with non-small-cell lung cancer are presented. After confirming the importance of epidermal growth factor receptor (EGFR) and KRAS mutations for (non)response on gefitinib in a retrospective series of patients, EGFR mutations were looked for before—and were a condition for—treatment with gefitinib or erlotinib. To increase the chance to find such a mutation, we selected patients on the basis of smoking status, gender and histopathology. Out of 41 patients selected, 13 (32%) were found to harbor an EGFR mutation. In nine of them it concerned deletions in exon 19 and in none of them KRAS mutations were detected. All nine patients with an exon 19 deletion had a favorable and continuing response to tyrosine kinase inhibitors (TKIs), while four other patients with point mutations responded less favorably: stable disease or a response of short duration. These observations confirm the potential role of EGFR and KRAS mutations in predicting (non)response to TKIs. Exon 19 deletions that are associated with the best responses might be used for first-line treatment selection, while KRAS mutations could play a role in excluding patients from treatment with TKIs.

Key words: EGFR mutation, erlotinib, gefitinib, KRAS mutation, NSCLC


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