Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page 5 [' M9 j( K c$ N2 t
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Sub-category:
9 T. z* D, @0 u; i, @1 c5 p" {Molecular Targets ' M6 L2 n. m; {$ A: h' y
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Category:. D. A: x8 Y* e
Tumor Biology
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Meeting:
8 P7 }9 q& W, t; r: F2011 ASCO Annual Meeting 4 M6 q* @2 m0 z- p
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Session Type and Session Title:/ h$ S2 c/ x e, s. J, g- P5 R
Poster Discussion Session, Tumor Biology , I7 I3 i* V3 ^8 W
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Abstract No:# M% H6 f: \% v
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7 W4 h. `9 R( q' AJ Clin Oncol 29: 2011 (suppl; abstr 10517) * Y8 {! w) b, ?# ?$ B5 N$ _1 x
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9 C& [, s1 r# k9 H/ Y7 VAuthor(s):
: t9 A# c* ^9 n9 C( Q \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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8 A' F6 G& z0 d& H/ XAbstract Disclosures* ?( Z3 n: M' P3 B0 U% B7 i5 q
! F+ E3 i3 @4 d4 V$ o. WAbstract:
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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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