Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ( [8 R6 d$ v- S* N2 N) V* d& a
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/ Z4 J! k/ B5 m, H+ A8 M3 WMolecular Targets 2 Q+ H. m' F$ V( ~3 u
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+ G% K/ }4 n7 D& S" P1 KCategory:
+ z4 s4 D& ^3 cTumor Biology / Z; Y. ^2 K5 ^, V, k
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Meeting:
* i2 ]" A" F& u( k, p2011 ASCO Annual Meeting
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, v! b! B8 X0 o( x- j5 p' VSession Type and Session Title:
; f# b+ G2 J% d% q% y6 DPoster Discussion Session, Tumor Biology ' ]* r4 e: j/ j8 [! J0 o8 o( b! h
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. Q5 E7 _- t8 I5 \10517
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Citation:
! M$ [+ s- l: }% JJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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' O0 ]( d7 k1 X7 DAuthor(s):
! j1 l. Z! n" tJ. 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 ( E1 y. d {; Z
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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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* M7 g' t4 ~# ~! O+ mAbstract Disclosures) c5 }7 \1 ]* F& f
8 G. t I! \$ T, y8 u; F6 F% f vAbstract:
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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.6 ?. F' m3 \9 T6 a
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