Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page + r! @% b' M' u
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Sub-category:2 F/ c# l Z. H3 A
Molecular Targets 1 f9 @3 j! V' }( A
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Category:# l' }4 I/ R. s
Tumor Biology . f* t- [ @' x# v
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! ?# o; f( v" r1 D$ Z0 }! r: z3 CMeeting:
6 ] r- ]6 K* z2011 ASCO Annual Meeting
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Session Type and Session Title:
7 S9 r3 l% C1 ~# x* ZPoster Discussion Session, Tumor Biology
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Abstract No:: d4 U1 U/ ]+ f
10517
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Citation:" O1 ]3 O2 K5 @- Z9 u$ _0 M7 W
J Clin Oncol 29: 2011 (suppl; abstr 10517) 2 v3 L- i% d4 u) g$ Y; i
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Author(s):$ X# _2 ^. I, H+ p7 l$ T
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.
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/ @: O' [, i+ T3 V/ F8 mAbstract Disclosures0 Q& p9 e; D3 A* m* `( C7 m+ X v$ e
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Abstract:# D: l: L; U- \' S- K0 K
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Background: 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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