Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 5 L5 i0 K5 i6 _! Q
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Sub-category:
* n/ g8 g7 D) H' W0 I; UMolecular Targets . L0 F5 [% ]7 H7 v1 c2 B8 u6 E
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Tumor Biology
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- k# E; H. s& x8 U9 U4 TMeeting:
* A7 W9 A% ^ y1 t& T2011 ASCO Annual Meeting
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9 d2 ~9 {1 O& h6 l( h3 |$ VSession Type and Session Title:
# J$ i5 v/ d5 Q5 s+ FPoster Discussion Session, Tumor Biology . E! P8 r1 o; a7 b8 O" Z# u# k
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Abstract No:
4 ^0 F7 `7 c- G, w10517
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Citation:- u$ I; O1 L, s
J Clin Oncol 29: 2011 (suppl; abstr 10517) $ ~" o/ S5 S3 R5 k) I+ n" y/ S
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6 H/ M8 p! t. h& v( \+ qAuthor(s):
4 S" P) j9 A! B) F/ q" X h4 aJ. 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 / w: R3 ^$ a a' s {% k" c9 q
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& ^* G7 |2 ?4 cAbstracts 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.% {, Q: v. M! c
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Abstract Disclosures0 q: i* q; d0 G% n+ b1 R8 y
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Abstract:! M4 b; S0 D& Y
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- e9 Y) t; X) aBackground: 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.1 w: Q! c, n' Q! I' T ^( @6 e
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