Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page ( i" \. w9 j5 p- n7 ^
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Sub-category:
4 e, S3 s" N q0 x. yMolecular Targets % u5 B) N& t7 o% z, |8 {) v, T
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Category:& R- Z J/ S5 A' {# s
Tumor Biology / E$ p5 N2 ]3 [9 u( Z
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8 h9 O; t A8 G3 H1 L- _Meeting:$ y- T W7 l' Y% |
2011 ASCO Annual Meeting
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5 R: m2 x' E$ z" mSession Type and Session Title:$ I/ Y. M p$ D
Poster Discussion Session, Tumor Biology % S) H5 U3 g: K+ E9 h* G" Y
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Abstract No:
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Citation:1 J. c1 b3 Z9 e V
J Clin Oncol 29: 2011 (suppl; abstr 10517) ! S3 N @& s4 `3 _& K$ c8 `
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3 V: ?: x% k* H+ N/ @Author(s):% ^* Y- g n) v& ~
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 / U4 b1 W. H0 F1 ]
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\2 R% G+ g) B: p% X pAbstracts 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.5 I* N1 H/ a' s9 L; O
5 ~' E4 a. B& dAbstract Disclosures/ m! a: E' {. }2 m5 n! ~+ z/ q- n
( v# N$ A/ c2 y) i. t+ UAbstract:
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8 J8 h# d7 K1 P; r0 E. t) @9 N8 WBackground: 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.) C2 G* W* L; I9 x
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