Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page + H& }$ q( K! |) f
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~* z! R" k+ m% O+ _4 L/ _) OMolecular Targets ; C7 Y7 u; |+ I- Q1 w
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Tumor Biology N4 g+ [! a6 z0 h( h8 p" ?" H5 ^% [
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# o8 k7 d5 Y G0 `Meeting:
' C& l4 C" Y' t2011 ASCO Annual Meeting
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Session Type and Session Title:
* u2 U) B6 Z$ tPoster Discussion Session, Tumor Biology
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( j8 `' j# Z# uAbstract No:! [, }7 u) I2 J) W
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Citation:0 W! N, ^: U3 d
J Clin Oncol 29: 2011 (suppl; abstr 10517) $ R( F# z& I7 ]5 A5 {+ _% c
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Author(s):/ Y( L' \& J" C: ^5 Y, \
J. Yang, X. Zhang, J. Su, H. Chen, H. Tian, Y. Huang, C. Xu, Y. L. Wu; Guangdong Lung Cancer Institute, Guangdong General Hospital & Guangdong Academy of Medical Sciences, Guangzhou, China; Guangdong Lung Cancer Institute, Medical Research Center of Guangdong General Hospital, Guangzhou, China; Guangdong Lung Cancer Institute, Guangzhou, China; Guangdong Lung Cancer Institute, Guangdong General Hospital & Guangdong Academy of Medical Sciences, Guangzhou, China
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Abstracts that were granted an exception in accordance with ASCO's Conflict of Interest Policy are designated with a caret symbol (^) here and in the printed Proceedings.1 d. u4 u% _" E1 G5 i- {
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Abstract Disclosures
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% {3 D- I% B7 |: T7 H- P& qAbstract:# z% V5 f9 x8 B9 \
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! G# X, m* M! qBackground: The fusion of the anaplastic lymphoma kinase (ALK) with the echinoderm microtubule-associated protein-like 4 (EML4) and epidermal growth factor receptor (EGFR) mutations are considered mutually exclusive. Advanced non-small cell lung cancer (NSCLC) patients with EML4-ALK did not benefit from EGFR tyrosine kinase inhibitors (TKIs). Methods: Multiplex reverse transcriptase-polymerase chain reaction (RT-PCR) followed by sequencing was performed for EML4-ALK fusion status detection. EGFR and KRAS mutations were determined by direct DNA sequencing. Positive results of EML4-ALK fusion were also confirmed by RACE-coupled PCR sequencing. Results: From April 2010 to January 2011, 412 patients (398 with NSCLC; 14 with SCLC) were tested for mutation status of EGFR, KRAS and EML4-ALK respectively. Frequency of EML4-ALK fusion was 10.6% (42/398) in NSCLC patients. No patients with SCLC were found to have positive EML4-ALK fusion. Frequency of concomitant EGFR and EML4-ALK gene mutations was 1.0% (4/398) in NSCLC patients, and their variants of EML4-ALK gene mutations were Variant 1 (3 patients) and Variant 6 (1 patient); being never smokers, all of them were diagnosed with advanced (3 with stage †W and 1 with stage IIIB) adenocarcinoma harbouring wild type KRAS. Two female stage †W patients with double gene mutations (1 with L858R and Variant 1; 1 with exon19 deletion and Variant 6) received first-line gefitinib which is one kind of EGFR TKIs and achieved partial response. Conclusions: Though being rare events, NSCLC patients harbouring concomitant EGFR mutation and EML4-ALK gene fusion are sensitive to first-line EGFR TKIs. Whether they could also benefit from ALK inhibition after failure to EGFR TKIs warranted further investigation.
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