Concomitant EGFR mutation and EML4-ALK gene fusion in non-small cell lung cancer. Print this page - L. T$ Y1 a8 \( G7 p7 Q% g6 b
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Sub-category:
8 B M$ I; {* `; ^3 j hMolecular Targets / q3 h7 y6 f- A: B: S) Z, R
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Category:5 _4 R; E7 d* F$ J+ ~% H9 k/ f$ C
Tumor Biology + o0 R5 |5 K$ t; `( e1 a
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1 T4 V. R- \8 n- E/ c$ \" VMeeting:
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& \8 S! ^7 W3 k% ESession Type and Session Title:
3 r- g# y& ]) @/ R% H" X: [9 BPoster Discussion Session, Tumor Biology 6 K& u ^; z' ~) z
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- I b" Y O; ], MAbstract No:
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J Clin Oncol 29: 2011 (suppl; abstr 10517)
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" m8 H2 l2 `9 Y* X. c- N0 Y& j7 wAuthor(s):
. j) M; E( A% C, ]7 D4 \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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9 X6 @1 }8 h+ ^, p C9 R( cAbstracts 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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Abstract Disclosures* [4 K4 d- x5 u1 H
3 M1 e' e1 n3 n6 h- [. }3 f. ~Abstract:4 I) t/ g! u- T* Y0 D
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7 ]9 v/ W. G% G- z) 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., A+ g# M/ [6 P! N7 h
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