Journal
LUNG CANCER
Volume 58, Issue 1, Pages 95-103Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.lungcan.2007.05.017
Keywords
epidermal growth; factor receptor; EGFR; mutation; tyrosine kinase; inhibitors; gefitinib; L858R; Exon 19 deletions; phase II trials; prospective; lung cancer; non-small cell lung cancer
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Funding
- NCI NIH HHS [P20 CA090578, P20 CA090578-01A10002, CA090578, P50 CA090578] Funding Source: Medline
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Purpose: Epidermal growth factor receptor (EGFR) mutations have been found in the majority of gefitinib-responsive non-small cell lung cancer (NSCLC) patients from retrospective studies. We sought to compile the available phase 11 and prospective trials of this EGFR tyrosine kinase inhibitor (TKI) to better understand the efficacy and safety of selecting patients to receive gefitinib based on their genotype. Design: We searched published trials involving EGFR-mutant patients and gefitinib. Five reports were identified (published between June 2006 and April 2007) in which gefitinib was given in a prospective manner to EGFR mutation positive patients at a dose of 250mg/day. Responses were determined by RECIST and toxicities by NCI-CTC. Results: A total of 101 patients were pooled from these studies. Fifty-nine received gefitinib as their first line of therapy and 42 after having received chemotherapy. The combined rate of complete and partial response (CR + PR) in the 99 measured patients was 80.8% (80/99) and only 7.1% (7/99) had progressive disease as best response. The response rate (CR + PR) for exon 19 deletion and L858R patients were 80.3% (53/66) and 81.8% (27/33), respectively. The median progression-free survival ranged from 7.7 to 12.9 months. Overall survival had not been reached in 4/5 reports and was 15.4 months in one of them. Gefitinib administration was safe (< 50% of patients developed grades 1-2 skin rash or diarrhea) and interstitial lung disease was only reported in two patients (2%), without deaths. Conclusions: Gefitinib monotherapy leads to objective responses in most patients with EGFR mutations. Both L858R and deletion 19 mutations derived similar clinical benefits. Small molecule TKIs are the new treatment paradigm for EGFR-mutant NSCLC. (c) 2007 Elsevier Ireland Ltd. All rights reserved.
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