Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page
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Molecular Targets 8 ?9 Z W$ [. W2 q; I8 h+ s; u
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Category:
( I6 d* w' q" \# C- t* D1 BTumor Biology * c# m6 N7 X: m2 p
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Meeting:
0 E% t* t* }& l, s2011 ASCO Annual Meeting 1 l) Z: w5 {& V1 H6 q, W; G$ R1 H
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% J, k+ z: l$ mSession Type and Session Title:
& N2 }& A: a% [Poster Discussion Session, Tumor Biology
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Abstract No:
. a% f I! j8 q* `10517
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0 o/ |% H3 K% [# S' X1 nCitation:
- T/ X0 v- ~3 |( G- k8 yJ Clin Oncol 29: 2011 (suppl; abstr 10517)
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Author(s):: P; z* w1 @ b7 V- v, a F' G6 c
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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. n/ l# d; X7 NAbstracts 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. ~$ m( x" Z+ l0 `
8 o( h/ q$ k2 W% HAbstract Disclosures b9 g1 k2 Z4 b: R/ K2 P
) F! q, @6 I/ v/ J: ?" {& XAbstract:. z5 ]3 M* ]6 p" W5 a% f* W
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* `( w% C. {) Y: ZBackground: 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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