RT Journal Article
SR Electronic
T1 A New Mechanism for Primary Resistance to Gefitinib in Lung Adenocarcinoma: The Role of a Novel G796A Mutation in Exon 20 of EGFR
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 2297
OP 2303
VO 27
IS 4B
A1 URAMOTO, HIDETAKA
A1 UCHIUMI, TAKESHI
A1 IZUMI, HIROTO
A1 KOHNO, KIMITOSHI
A1 OYAMA, TSUNEHIRO
A1 SUGIO, KENJI
A1 YASUMOTO, KOSEI
YR 2007
UL http://ar.iiarjournals.org/content/27/4B/2297.abstract
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