PT  - JOURNAL ARTICLE
AU  - URAMOTO, HIDETAKA
AU  - UCHIUMI, TAKESHI
AU  - IZUMI, HIROTO
AU  - KOHNO, KIMITOSHI
AU  - OYAMA, TSUNEHIRO
AU  - SUGIO, KENJI
AU  - YASUMOTO, KOSEI
TI  - A New Mechanism for Primary Resistance to Gefitinib in Lung Adenocarcinoma: The Role of a Novel G796A Mutation in Exon 20 of EGFR
DP  - 2007 Jul 01
TA  - Anticancer Research
PG  - 2297--2303
VI  - 27
IP  - 4B
4099  - http://ar.iiarjournals.org/content/27/4B/2297.short
4100  - http://ar.iiarjournals.org/content/27/4B/2297.full
SO  - Anticancer Res2007 Jul 01; 27
AB  - Subsets of non-small cell lung cancer (NSCLC) patients who carry activating somatic mutations of the epidermal growth factor receptor (EGFR) have demonstrated an increased probability of obtaining objective responses to the receptor tyrosine kinase inhibitors (TKIs), gefitinib and erlotinib. However, a substantial proportion of the cases with somatic mutations, which suggest sensitivity to gefitinib, are primary resistant to it. A primary resistant case of lung adenocarcinoma that was found to carry both delE746-A750 and a G796A mutation in the EGFR is reported. In vitro, a stable clone of cells bearing the G796A mutation was approximately 50,000-fold less sensitive to gefitinib in comparison to cells carrying the delE746-A750 mutant EGFR. This study suggests that screening tumour samples for a range of EGFR mutations may improve our ability to identify the patients most likely to benefit from EFGR TKIs. Copyright© 2007 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved